This document discusses HDL metabolism and potential therapeutic targets to modify HDL. It provides an overview of HDL's role in reverse cholesterol transport and the various proteins involved. Potential pharmacologic therapies are described that aim to increase reverse cholesterol transport by targeting steps like apoA1 production, LCAT activity, and CETP inhibition. Clinical trials are summarized that tested acute therapies like apoA1-phospholipid complexes and longer-term therapies like CETP inhibitors, with mixed results on reducing atherosclerosis. Other anti-atherogenic properties of HDL beyond reverse cholesterol transport are also mentioned.
Lipoproteins are complexes of lipids and proteins that transport cholesterol, triglycerides, and fat-soluble vitamins throughout the body. They can be classified based on density and size into different classes, including chylomicrons, VLDLs, IDLs, LDLs, and HDLs. The major apolipoproteins associated with each lipoprotein class help to assemble particles and activate enzymes involved in lipoprotein metabolism. Disorders can cause abnormal accumulation of certain lipoprotein classes and are classified according to the Frederickson system.
Slideshow is from the University of Michigan Medical School's M1 Gastrointestinal / Liver sequence
View additional course materials on Open.Michigan:
http://openmi.ch/med-m1gastro
1) Lipids and proteins are metabolized through multi-step processes in the body. Lipids undergo absorption, lipolysis, beta-oxidation, and ketogenesis. Proteins are broken down through transamination and oxidative deamination.
2) Beta-oxidation of fatty acids in the mitochondria generates acetyl-CoA which enters the Krebs cycle to produce energy. Ketone bodies are formed from acetyl-CoA when carbohydrate intake is low.
3) Protein metabolism involves transferring amino groups through transamination and removing them via oxidative deamination, providing substrates for other metabolic pathways. The carbon skeletons are used for energy or substrate production.
medical #students #doctors #foodandnutrition #nurses #NEET #PCM #doctors #nutritioneducation #mscdfsm #dietician #nationaldieticians #RD #REGISTERED #DIETICIANS
#NUTRITIONIST #INTERNATIONAL DIETICIANS
This content is made for all student of medical ,nutrition ,doctors ,zoology ,chemistry ,medical who are still preparing for examination .feel free to give suggestion.
This document discusses lipoprotein metabolism. It defines lipoproteins as molecular complexes containing lipids and proteins that function to transport lipids in blood. There are five major classes of lipoproteins: chylomicrons, VLDL, LDL, HDL, and FFA bound to albumin. The classes are separated by ultracentrifugation or electrophoresis. Chylomicrons transport exogenous lipids from the intestine. VLDL transports endogenous lipids from the liver and intestine. LDL transports cholesterol from the liver to tissues. HDL transports cholesterol from tissues back to the liver in a process called reverse cholesterol transport. Apolipoproteins are the protein components of lipoproteins that serve structural, enzymatic, and receptor binding functions
This document summarizes key aspects of fatty acid metabolism from Chapter 22 of a biochemistry textbook. It discusses four main metabolic steps in fatty acid breakdown including lipase-mediated triglyceride hydrolysis producing fatty acids. It then describes three steps of triglyceride degradation involving beta-oxidation in the mitochondria to ultimately form acetyl-CoA. Beta-oxidation cycles are explained along with production of ATP. Fatty acid biosynthesis is also summarized involving fatty acid synthase and NADPH. Regulation of steps like acetyl-CoA carboxylase is covered.
The document discusses lipid metabolism and β-oxidation of fatty acids. It notes that triacylglycerols are broken down into free fatty acids and glycerol in the gut. Fatty acids are transported via lipoproteins or albumin and undergo β-oxidation in the mitochondria to generate acetyl-CoA. β-Oxidation involves four steps per fatty acid: dehydrogenation, hydration, second dehydrogenation, and thiolysis. This shortens the fatty acid by two carbons, producing acetyl-CoA and reducing equivalents.
The document discusses fatty acid oxidation (β-oxidation) which involves the breakdown of fatty acids into acetyl-CoA in the mitochondria. It describes the steps prior to β-oxidation including fatty acid transport into the cell and activation. It then explains the steps of β-oxidation which sequentially cleaves two-carbon units from acyl-CoA. The document also discusses the metabolism of ketone bodies which are produced from acetyl-CoA during periods of fasting or diabetes to be used as fuel by other tissues.
Lipoproteins are complexes of lipids and proteins that transport cholesterol, triglycerides, and fat-soluble vitamins throughout the body. They can be classified based on density and size into different classes, including chylomicrons, VLDLs, IDLs, LDLs, and HDLs. The major apolipoproteins associated with each lipoprotein class help to assemble particles and activate enzymes involved in lipoprotein metabolism. Disorders can cause abnormal accumulation of certain lipoprotein classes and are classified according to the Frederickson system.
Slideshow is from the University of Michigan Medical School's M1 Gastrointestinal / Liver sequence
View additional course materials on Open.Michigan:
http://openmi.ch/med-m1gastro
1) Lipids and proteins are metabolized through multi-step processes in the body. Lipids undergo absorption, lipolysis, beta-oxidation, and ketogenesis. Proteins are broken down through transamination and oxidative deamination.
2) Beta-oxidation of fatty acids in the mitochondria generates acetyl-CoA which enters the Krebs cycle to produce energy. Ketone bodies are formed from acetyl-CoA when carbohydrate intake is low.
3) Protein metabolism involves transferring amino groups through transamination and removing them via oxidative deamination, providing substrates for other metabolic pathways. The carbon skeletons are used for energy or substrate production.
medical #students #doctors #foodandnutrition #nurses #NEET #PCM #doctors #nutritioneducation #mscdfsm #dietician #nationaldieticians #RD #REGISTERED #DIETICIANS
#NUTRITIONIST #INTERNATIONAL DIETICIANS
This content is made for all student of medical ,nutrition ,doctors ,zoology ,chemistry ,medical who are still preparing for examination .feel free to give suggestion.
This document discusses lipoprotein metabolism. It defines lipoproteins as molecular complexes containing lipids and proteins that function to transport lipids in blood. There are five major classes of lipoproteins: chylomicrons, VLDL, LDL, HDL, and FFA bound to albumin. The classes are separated by ultracentrifugation or electrophoresis. Chylomicrons transport exogenous lipids from the intestine. VLDL transports endogenous lipids from the liver and intestine. LDL transports cholesterol from the liver to tissues. HDL transports cholesterol from tissues back to the liver in a process called reverse cholesterol transport. Apolipoproteins are the protein components of lipoproteins that serve structural, enzymatic, and receptor binding functions
This document summarizes key aspects of fatty acid metabolism from Chapter 22 of a biochemistry textbook. It discusses four main metabolic steps in fatty acid breakdown including lipase-mediated triglyceride hydrolysis producing fatty acids. It then describes three steps of triglyceride degradation involving beta-oxidation in the mitochondria to ultimately form acetyl-CoA. Beta-oxidation cycles are explained along with production of ATP. Fatty acid biosynthesis is also summarized involving fatty acid synthase and NADPH. Regulation of steps like acetyl-CoA carboxylase is covered.
The document discusses lipid metabolism and β-oxidation of fatty acids. It notes that triacylglycerols are broken down into free fatty acids and glycerol in the gut. Fatty acids are transported via lipoproteins or albumin and undergo β-oxidation in the mitochondria to generate acetyl-CoA. β-Oxidation involves four steps per fatty acid: dehydrogenation, hydration, second dehydrogenation, and thiolysis. This shortens the fatty acid by two carbons, producing acetyl-CoA and reducing equivalents.
The document discusses fatty acid oxidation (β-oxidation) which involves the breakdown of fatty acids into acetyl-CoA in the mitochondria. It describes the steps prior to β-oxidation including fatty acid transport into the cell and activation. It then explains the steps of β-oxidation which sequentially cleaves two-carbon units from acyl-CoA. The document also discusses the metabolism of ketone bodies which are produced from acetyl-CoA during periods of fasting or diabetes to be used as fuel by other tissues.
The document summarizes the biosynthesis of fatty acids in plants. It discusses that fatty acids are synthesized from acetyl-CoA in plastids using the fatty acid synthase complex. This complex contains multiple enzyme domains that catalyze the sequential condensation of acetyl-CoA and malonyl-CoA units to form saturated fatty acid chains in a repetitive four-step cycle, requiring NADPH and ATP. The process results in the most common end product of palmitic acid (C16). Key enzymes involved include acetyl-CoA carboxylase and fatty acid synthase.
The document summarizes the process of beta oxidation, where fatty acids are broken down in the mitochondria to generate acetyl-CoA. There are four steps: 1) activation of fatty acids to fatty acyl-CoA in the cytosol, 2) transport into the mitochondrial matrix using carnitine shuttle, 3) beta oxidation proper involving oxidation, hydration, and thiolytic cleavage reactions to remove two-carbon acetyl-CoA units, 4) repetition of steps 3 until the fatty acid is fully broken down to acetyl-CoA, which feeds into the citric acid cycle. The process generates large amounts of ATP through production of FADH2 and NADH. Deficiencies in enzymes involved can
1) Fatty acids are oxidized through beta-oxidation in the mitochondria to generate acetyl-CoA units and energy in the form of ATP.
2) Beta-oxidation involves four steps - dehydrogenation, hydration, dehydrogenation, and thiolysis - that occur in a recurring cycle to shorten the fatty acid by two carbons each time.
3) Fatty acid oxidation provides the major source of energy during periods of fasting or low carbohydrate availability and yields substantial ATP through the electron transport chain.
Glycolysis is the first stage of cellular respiration where glucose is broken down. It occurs in the cytosol and involves 10 enzyme-catalyzed reactions that convert glucose into two pyruvate molecules, ATP, and NADH. Glycolysis harvests a small amount of energy by producing two ATP and two NADH but requires an initial investment of two ATP. It is an ancient pathway that was the earliest form of energy transfer from organic molecules to ATP.
1. Haem is synthesized through 8 enzymatic steps involving 8 molecules of succinyl CoA and glycine.
2. The pathway involves both cytosolic and mitochondrial enzymes with the rate-limiting step being ALA synthase which is inhibited by haem and glucose.
3. Deficiencies in the enzymes can lead to various porphyrias like acute intermittent porphyria or erythropoietic protoporphyria.
The document summarizes fatty acid oxidation pathways. Fatty acids undergo beta-oxidation where they are sequentially shortened by two carbons into acetyl-CoA. This occurs through activation, transport into mitochondria via carnitine shuttle, and four steps of beta-oxidation. Alpha-oxidation removes the alpha carbon for certain fatty acids like phytanic acid to allow beta-oxidation. Abnormalities in fatty acid oxidation can cause clinical conditions.
This document summarizes the oxidation of fatty acids. Fatty acids are stored as triglycerides in tissues and are released into the blood by the intestines, liver, and adipose tissue. They are transported bound to lipoproteins or albumin. Fatty acids are taken up by cells and activated by binding to CoA before being oxidized in the mitochondria or peroxisomes. The major pathway of fatty acid oxidation is beta-oxidation, which occurs through four reactions in the mitochondrial matrix and removes two carbon units in acetyl-CoA per cycle. This process continues until an acetyl-CoA remains. Beta-oxidation generates substantial ATP. Defects can occur in any step of this process
Fatty acid breakdown occurs via beta-oxidation, which takes place in four steps catalyzed by specific enzymes. This process generates acetyl-CoA molecules that can enter the citric acid cycle to produce energy. Unsaturated and odd-numbered fatty acids require additional reactions for complete breakdown. Regulation of fatty acid oxidation occurs via controlling import of fatty acids into mitochondria. Ketone bodies are formed from acetyl-CoA and exported from the liver as an alternative fuel for other tissues.
Riboflavin,flavoproteins and their clinical applicationsrohini sane
A presentation in lucid-style on Riboflavin (vitamin B2), Flavoproteins and their clinical applications for MBBS , BDS , B Pham and Biotechnology students to facilitate easy leaning.
The document summarizes the process of beta oxidation, which is the pathway by which fatty acids are broken down in the mitochondria to generate acetyl-CoA molecules. It involves four key steps: 1) oxidation of the alpha and beta carbons to form a double bond, producing FADH2. 2) Addition of a water molecule to form a beta-hydroxy group. 3) Oxidation of the beta-hydroxy group to a ketone. 4) Cleavage of the fatty acid chain between the alpha and beta carbons, producing acetyl-CoA. This repetitive process degrades acyl-CoA molecules into acetyl-CoA, releasing energy molecules FADH2 and NADH.
This ppt has been presented as seminar in Department of Biochemistry ,C.C.S. university, Meerut.in front of all faculty members for the detailed discussion on this topic. Hope this will help you to go through the concept in an easy manner.
This document summarizes beta oxidation, the pathway for catabolism of fatty acids. It discusses that beta oxidation occurs at the beta-carbon of fatty acids. Triglycerides are the most abundant dietary lipids and are stored with a glycerol backbone and three fatty acids. Lipases hydrolyze triglycerides to release fatty acids. Glycerol is converted to glycolysis intermediates. Beta oxidation occurs in both peroxisomes of animals and plants, though plant peroxisomes are the main site of fatty acid oxidation. Seeds store high amounts of fats and oils. The enzymes of beta oxidation are arranged in eukaryotes. Multiple rounds of beta oxidation can occur to fully break down fatty
This document provides an overview of fatty acid metabolism. It discusses the three stages of fatty acid utilization: mobilization of triglycerides from adipose tissue, activation and transport of fatty acids into mitochondria, and breakdown of fatty acids to acetyl-CoA. It also covers fatty acid oxidation pathways in mitochondria and peroxisomes, ketone body formation, fatty acid synthesis, and regulation of fatty acid metabolism.
Vitamin A chemistry, functions and deficiencyNamrata Chhabra
1) Vitamin A plays an essential role in vision, immune function, cell growth and differentiation. It exists in two forms - retinoids found in animal foods and carotenoids which are plant-derived provitamin A compounds.
2) Dietary vitamin A is absorbed in the intestine and transported to the liver where it is stored. It is then circulated bound to retinol-binding protein.
3) Deficiency can result from inadequate intake or malabsorption and causes xerophthalmia, night blindness, susceptibility to infection and increased mortality in children.
Where are we going and how are we going to get there?David De Roure
The document discusses the myExperiment virtual research environment for sharing workflows. Some key points:
1. myExperiment is a social network and repository for research workflows and methods. It currently has over 1800 users and hundreds of shared workflows.
2. The site allows fine-grained privacy controls, grouping of related content into "packs", and integration with other systems through federation.
3. Analysis found that most workflows and other content are shared publicly, and some users actively build upon other users' shared workflows. The most viewed workflow has over 1500 views.
4. The principles behind myExperiment's design focus on empowering scientists by enabling new forms of collaboration and sharing without forcing changes to workflows. The
This document discusses lipoprotein metabolism and summarizes the key points. It notes that plasma consists of triglycerides, phospholipids, cholesterol, and other components. There are four major classes of lipoproteins that transport lipids in plasma: chylomicrons, VLDL, LDL, and HDL. The document outlines the formation and catabolism of chylomicrons and VLDL, which involves lipoprotein lipase, and the metabolism of LDL and HDL. Abnormalities in lipoprotein metabolism can lead to hypo- or hyperlipoproteinemia and diseases like atherosclerosis.
Fundamentals of HDL (first 4 chapters only) - GodseHammam
In electronics, a hardware description language (HDL) is a specialized computer language used to program the structure, design and operation of electronic circuits, and most commonly, digital logic circuits.
The document discusses lipoproteins, which are complexes of lipids and proteins that transport lipids in the bloodstream. It defines the main classes of lipoproteins - chylomicrons, VLDL, LDL, HDL - and describes their composition, size, density, functions, and roles in lipid transport. Diseases associated with abnormalities in lipoprotein metabolism are also summarized, such as hyperlipoproteinemias which result from defects in the synthesis or catabolism of specific lipoproteins.
The document summarizes the biosynthesis of fatty acids in plants. It discusses that fatty acids are synthesized from acetyl-CoA in plastids using the fatty acid synthase complex. This complex contains multiple enzyme domains that catalyze the sequential condensation of acetyl-CoA and malonyl-CoA units to form saturated fatty acid chains in a repetitive four-step cycle, requiring NADPH and ATP. The process results in the most common end product of palmitic acid (C16). Key enzymes involved include acetyl-CoA carboxylase and fatty acid synthase.
The document summarizes the process of beta oxidation, where fatty acids are broken down in the mitochondria to generate acetyl-CoA. There are four steps: 1) activation of fatty acids to fatty acyl-CoA in the cytosol, 2) transport into the mitochondrial matrix using carnitine shuttle, 3) beta oxidation proper involving oxidation, hydration, and thiolytic cleavage reactions to remove two-carbon acetyl-CoA units, 4) repetition of steps 3 until the fatty acid is fully broken down to acetyl-CoA, which feeds into the citric acid cycle. The process generates large amounts of ATP through production of FADH2 and NADH. Deficiencies in enzymes involved can
1) Fatty acids are oxidized through beta-oxidation in the mitochondria to generate acetyl-CoA units and energy in the form of ATP.
2) Beta-oxidation involves four steps - dehydrogenation, hydration, dehydrogenation, and thiolysis - that occur in a recurring cycle to shorten the fatty acid by two carbons each time.
3) Fatty acid oxidation provides the major source of energy during periods of fasting or low carbohydrate availability and yields substantial ATP through the electron transport chain.
Glycolysis is the first stage of cellular respiration where glucose is broken down. It occurs in the cytosol and involves 10 enzyme-catalyzed reactions that convert glucose into two pyruvate molecules, ATP, and NADH. Glycolysis harvests a small amount of energy by producing two ATP and two NADH but requires an initial investment of two ATP. It is an ancient pathway that was the earliest form of energy transfer from organic molecules to ATP.
1. Haem is synthesized through 8 enzymatic steps involving 8 molecules of succinyl CoA and glycine.
2. The pathway involves both cytosolic and mitochondrial enzymes with the rate-limiting step being ALA synthase which is inhibited by haem and glucose.
3. Deficiencies in the enzymes can lead to various porphyrias like acute intermittent porphyria or erythropoietic protoporphyria.
The document summarizes fatty acid oxidation pathways. Fatty acids undergo beta-oxidation where they are sequentially shortened by two carbons into acetyl-CoA. This occurs through activation, transport into mitochondria via carnitine shuttle, and four steps of beta-oxidation. Alpha-oxidation removes the alpha carbon for certain fatty acids like phytanic acid to allow beta-oxidation. Abnormalities in fatty acid oxidation can cause clinical conditions.
This document summarizes the oxidation of fatty acids. Fatty acids are stored as triglycerides in tissues and are released into the blood by the intestines, liver, and adipose tissue. They are transported bound to lipoproteins or albumin. Fatty acids are taken up by cells and activated by binding to CoA before being oxidized in the mitochondria or peroxisomes. The major pathway of fatty acid oxidation is beta-oxidation, which occurs through four reactions in the mitochondrial matrix and removes two carbon units in acetyl-CoA per cycle. This process continues until an acetyl-CoA remains. Beta-oxidation generates substantial ATP. Defects can occur in any step of this process
Fatty acid breakdown occurs via beta-oxidation, which takes place in four steps catalyzed by specific enzymes. This process generates acetyl-CoA molecules that can enter the citric acid cycle to produce energy. Unsaturated and odd-numbered fatty acids require additional reactions for complete breakdown. Regulation of fatty acid oxidation occurs via controlling import of fatty acids into mitochondria. Ketone bodies are formed from acetyl-CoA and exported from the liver as an alternative fuel for other tissues.
Riboflavin,flavoproteins and their clinical applicationsrohini sane
A presentation in lucid-style on Riboflavin (vitamin B2), Flavoproteins and their clinical applications for MBBS , BDS , B Pham and Biotechnology students to facilitate easy leaning.
The document summarizes the process of beta oxidation, which is the pathway by which fatty acids are broken down in the mitochondria to generate acetyl-CoA molecules. It involves four key steps: 1) oxidation of the alpha and beta carbons to form a double bond, producing FADH2. 2) Addition of a water molecule to form a beta-hydroxy group. 3) Oxidation of the beta-hydroxy group to a ketone. 4) Cleavage of the fatty acid chain between the alpha and beta carbons, producing acetyl-CoA. This repetitive process degrades acyl-CoA molecules into acetyl-CoA, releasing energy molecules FADH2 and NADH.
This ppt has been presented as seminar in Department of Biochemistry ,C.C.S. university, Meerut.in front of all faculty members for the detailed discussion on this topic. Hope this will help you to go through the concept in an easy manner.
This document summarizes beta oxidation, the pathway for catabolism of fatty acids. It discusses that beta oxidation occurs at the beta-carbon of fatty acids. Triglycerides are the most abundant dietary lipids and are stored with a glycerol backbone and three fatty acids. Lipases hydrolyze triglycerides to release fatty acids. Glycerol is converted to glycolysis intermediates. Beta oxidation occurs in both peroxisomes of animals and plants, though plant peroxisomes are the main site of fatty acid oxidation. Seeds store high amounts of fats and oils. The enzymes of beta oxidation are arranged in eukaryotes. Multiple rounds of beta oxidation can occur to fully break down fatty
This document provides an overview of fatty acid metabolism. It discusses the three stages of fatty acid utilization: mobilization of triglycerides from adipose tissue, activation and transport of fatty acids into mitochondria, and breakdown of fatty acids to acetyl-CoA. It also covers fatty acid oxidation pathways in mitochondria and peroxisomes, ketone body formation, fatty acid synthesis, and regulation of fatty acid metabolism.
Vitamin A chemistry, functions and deficiencyNamrata Chhabra
1) Vitamin A plays an essential role in vision, immune function, cell growth and differentiation. It exists in two forms - retinoids found in animal foods and carotenoids which are plant-derived provitamin A compounds.
2) Dietary vitamin A is absorbed in the intestine and transported to the liver where it is stored. It is then circulated bound to retinol-binding protein.
3) Deficiency can result from inadequate intake or malabsorption and causes xerophthalmia, night blindness, susceptibility to infection and increased mortality in children.
Where are we going and how are we going to get there?David De Roure
The document discusses the myExperiment virtual research environment for sharing workflows. Some key points:
1. myExperiment is a social network and repository for research workflows and methods. It currently has over 1800 users and hundreds of shared workflows.
2. The site allows fine-grained privacy controls, grouping of related content into "packs", and integration with other systems through federation.
3. Analysis found that most workflows and other content are shared publicly, and some users actively build upon other users' shared workflows. The most viewed workflow has over 1500 views.
4. The principles behind myExperiment's design focus on empowering scientists by enabling new forms of collaboration and sharing without forcing changes to workflows. The
This document discusses lipoprotein metabolism and summarizes the key points. It notes that plasma consists of triglycerides, phospholipids, cholesterol, and other components. There are four major classes of lipoproteins that transport lipids in plasma: chylomicrons, VLDL, LDL, and HDL. The document outlines the formation and catabolism of chylomicrons and VLDL, which involves lipoprotein lipase, and the metabolism of LDL and HDL. Abnormalities in lipoprotein metabolism can lead to hypo- or hyperlipoproteinemia and diseases like atherosclerosis.
Fundamentals of HDL (first 4 chapters only) - GodseHammam
In electronics, a hardware description language (HDL) is a specialized computer language used to program the structure, design and operation of electronic circuits, and most commonly, digital logic circuits.
The document discusses lipoproteins, which are complexes of lipids and proteins that transport lipids in the bloodstream. It defines the main classes of lipoproteins - chylomicrons, VLDL, LDL, HDL - and describes their composition, size, density, functions, and roles in lipid transport. Diseases associated with abnormalities in lipoprotein metabolism are also summarized, such as hyperlipoproteinemias which result from defects in the synthesis or catabolism of specific lipoproteins.
Lipoprotein metabolism - (transport of lipids in the Blood)Ashok Katta
This presentation explains metabolism of lipoproteins (Chylomicron, VLDL, LDL, HDL) in very simple way. The presentation contains lots of animation to explain metabolism of individual lipoproteins.
This document discusses LDL metabolism and structure. It notes that LDL transports cholesterol from the liver to tissues, contains one apolipoprotein, and has a half-life of 2 days. LDL is taken up by tissues through receptor-mediated endocytosis, and defects in LDL receptors can lead to familial hypercholesterolemia. High LDL levels are a risk factor for cardiovascular disease by contributing to atherosclerotic plaque formation. The document also summarizes HDL metabolism and functions, noting it transports cholesterol from tissues to the liver in a reverse transport process.
This document discusses lipoprotein metabolism and structure. It describes the different lipoproteins including chylomicrons, VLDL, IDL, LDL, and HDL. It outlines the roles of apoproteins and how lipoproteins transport triglycerides and cholesterol through the body. The pathways of exogenous and endogenous cholesterol are summarized along with lipoprotein processing and targets for treating dyslipidemia.
This document summarizes lipids that are important physiologically and their roles in health and disease. It discusses major lipids like fatty acids, triglycerides, phospholipids, sterols, and lipoproteins. Specific fatty acids like saturated, unsaturated, omega-3 and omega-6 are explained. The roles of lipids in brain development, cancer prevention and various lipid-related disorders are highlighted. Atherosclerosis and its pathological progression are also diagrammatically represented.
Lipoproteins- structure, classification, metabolism and clinical significanceNamrata Chhabra
Lipoproteins transport lipids between cells and tissues. They consist of a nonpolar lipid core surrounded by a surface layer of phospholipids and proteins. Lipoproteins are classified based on density into chylomicrons, VLDL, IDL, LDL, and HDL. Chylomicrons transport dietary lipids from the intestine. The liver secretes VLDL, which circulates and is converted to IDL and LDL through lipolysis. HDL transports cholesterol from tissues to the liver. Apolipoproteins associated with each lipoprotein determine its function and metabolism.
Lipoproteins are complexes of protein and lipids that transport lipids in the bloodstream. There are four main types of lipoproteins: chylomicrons, very low-density lipoproteins (VLDL), low-density lipoproteins (LDL), and high-density lipoproteins (HDL). Each type has a specific function in lipid transport and metabolism. Chylomicrons transport dietary lipids from the intestine to other tissues, VLDL transports endogenous lipids from the liver, LDL delivers cholesterol to tissues, and HDL transports cholesterol from tissues back to the liver. The apolipoproteins associated with each lipoprotein complex help determine its structure and function in lipid transport and metabolism.
Lipoproteins: Structure, classification, metabolism and significanceenamifat
This document discusses lipoproteins and their role in transporting lipids like triglycerides and cholesterol in the body. It describes the different types of lipoproteins, including chylomicrons, VLDL, LDL, and HDL. Chylomicrons transport dietary lipids from the intestine to tissues, while VLDL transports endogenous lipids from the liver. VLDL is converted to LDL as it delivers lipids to tissues. HDL transports cholesterol from tissues back to the liver in a process called reverse cholesterol transport. The document provides details on the composition and metabolism of each lipoprotein class and their role in lipid transport.
This document discusses lipid and lipoprotein metabolism. Key points include:
1) Cholesterol is synthesized in tissues and absorbed from the diet, while triglycerides are absorbed after dietary fat is broken down.
2) Lipoproteins like LDL and HDL transport lipids in the blood and are composed of a lipid core surrounded by proteins and phospholipids.
3) The liver plays a central role in lipid homeostasis, regulating cholesterol synthesis and bile acid production.
4) Derangements in lipid metabolism can occur in conditions like metabolic syndrome and increase disease risk. Reverse cholesterol transport via HDL is an important protective process.
This document summarizes cholesterol metabolism and dyslipidemia management. It discusses triglycerides, free fatty acids, and cholesterol as lipids in the blood and the lipoproteins that transport them such as chylomicrons, VLDL, IDL, LDL, and HDL. It then covers the enzymes, receptors, and transporters involved in lipoprotein metabolism and how different conditions can lead to secondary hyperlipidemias. Treatment options for managing dyslipidemias are also briefly mentioned.
This document discusses lipid and lipoprotein metabolism. It covers cholesterol and triglyceride synthesis and absorption, the roles of various apolipoproteins and enzymes, reverse cholesterol transport, and how derangements can lead to conditions like metabolic syndrome. Key lipoproteins like LDL, HDL, VLDL, and lipoprotein(a) are examined, as well as their roles in health and disease.
This document discusses lipid and lipoprotein metabolism. It covers cholesterol and triglyceride synthesis and absorption, the roles of various apolipoproteins and enzymes, reverse cholesterol transport, and derangements associated with metabolic syndrome. Key lipoproteins like LDL, HDL, VLDL and their metabolic pathways are explained in detail.
This document discusses lipid and lipoprotein metabolism. It covers cholesterol and triglyceride synthesis and absorption, the roles of various apolipoproteins and enzymes, reverse cholesterol transport, and derangements associated with metabolic syndrome. Key lipoproteins like LDL, HDL, VLDL and their metabolic pathways are explained in detail.
Lipoproteins are complexes of lipids and proteins that transport lipids through the bloodstream. There are four main types of plasma lipoproteins - chylomicrons, VLDL, LDL, and HDL - which differ in size, density, and lipid/protein composition. Chylomicrons carry dietary lipids from the intestine to other tissues, VLDL transports endogenous lipids from the liver, LDL carries cholesterol, and HDL transports cholesterol from tissues to the liver for processing or excretion. The metabolism and interactions between these lipoproteins, such as the transfer of lipids between them, are tightly regulated and essential for maintaining lipid homeostasis.
The document outlines lipoprotein structure and function, including:
- Lipoproteins are protein-lipid complexes that transport lipids between tissues. They have a hydrophobic core of triglycerides and cholesterol esters surrounded by a hydrophilic surface.
- The main classes of lipoproteins are chylomicrons, VLDL, IDL, LDL, and HDL. They differ in size, density, and protein/lipid content.
- Apolipoproteins associated with each lipoprotein help with structure and regulate metabolism. Chylomicrons contain apoB-48 and transport dietary lipids. VLDL contains apoB-100 and transports endogenous lipids.
There are six major classes of lipoproteins in blood that are classified based on their density. Different analytical techniques separate lipoproteins based on properties like density, size, and electric charge. The major lipoproteins are chylomicrons, very low density lipoproteins (VLDL), intermediate density lipoproteins (IDL), low density lipoproteins (LDL), and high density lipoproteins (HDL). Apolipoproteins associated with each lipoprotein particle help maintain their structure and facilitate their metabolism and clearance from circulation.
1) Chylomicrons are assembled in the intestines and carry dietary lipids through the lymphatic system and bloodstream to tissues. They are formed when apo B-48 is loaded with lipids by MTP in the ER and Golgi.
2) Nascent chylomicrons acquire apo C and E from HDL in the bloodstream. Lipoprotein lipase on capillary walls hydrolyzes chylomicron triglycerides, providing fatty acids to tissues.
3) Remnant chylomicrons are taken up by the liver via apo E binding to hepatic receptors, where lipids are metabolized and reused or stored.
This document discusses lipoprotein metabolism. Lipoproteins are particles that carry lipids like triglycerides and cholesterol through the water-based bloodstream. They are composed of a hydrophobic core of lipids surrounded by a surface layer of phospholipids and apolipoproteins. The main lipoproteins are chylomicrons, VLDL, IDL, LDL, and HDL. The document details how these lipoproteins are formed, the lipids they carry, their roles in lipid transport, and regulation of their metabolism by factors like diet, exercise, and enzymes. Maintaining healthy lipoprotein levels is important for cardiovascular health.
Lipoproteins are biochemical assemblies containing both proteins and lipids that transport fats like triglycerides through the water-based plasma. They consist of a nonpolar lipid core surrounded by a layer of amphipathic lipids and proteins. Lipoproteins can be classified based on density, electrophoretic mobility, and apolipoprotein content. They transport lipids between tissues and are involved in lipid metabolism through interactions with enzymes like lipoprotein lipase. Defects in lipoprotein metabolism can cause diseases like atherosclerosis and coronary artery disease.
1. High-density lipoprotein (HDL) transports cholesterol from tissues like arteries back to the liver, helping to reduce atherosclerosis.
2. HDL has protective effects including inhibiting oxidation, inflammation, and endothelial activation which contribute to atherosclerosis.
3. Lifestyle factors like exercise and diet can help raise HDL levels, while medications like niacin and fibrates are also used to increase HDL.
Lipoproteins are complexes of lipids and proteins that transport hydrophobic lipid molecules in blood plasma. They play key roles in lipid absorption, transport, and reverse cholesterol transport. Lipoproteins are classified based on their density and include chylomicrons, VLDL, LDL, IDL, and HDL. They contain characteristic amounts of triglycerides, cholesterol, phospholipids, and apolipoproteins such as Apo B, Apo E, and differ in size, density, and function. Abnormal lipoprotein metabolism can lead to dyslipidemias and diseases like atherosclerosis.
Plasma lipids include triglycerides, cholesterol, phospholipids, and free fatty acids. They are transported in the form of lipoproteins which contain a core of triglycerides and cholesterol esters surrounded by a layer of phospholipids and proteins. The main classes of lipoproteins are chylomicrons, VLDL, LDL, and HDL, which differ in their size, lipid content, and apolipoprotein composition. Lipoproteins transport lipids through the blood and deliver them to tissues, playing important roles in lipid metabolism.
Lipids are insoluble in water, the problem of transportation in the aqueous plasma is solved by associating nonpolar lipids (triacylglycerols and cholesteryl esters) with amphipathic lipids (phospholipids and cholesterol) and proteins to make water-miscible lipoproteins.
lipoproteins types and classication in the body and role of them in diagnosis...ROOPAR45
The document discusses different classes of lipoproteins, including chylomicrons, very low density lipoproteins (VLDL), intermediate density lipoproteins (IDL), low density lipoproteins (LDL), and high density lipoproteins (HDL). It describes the separation techniques, composition, sites of synthesis, functions, and disorders associated with each class. Characteristics such as density, diameter, electrophoretic mobility, major lipids, and apolipoproteins are compared among the different classes.
Similar to HDL: Where are we and where are we going? (20)
Simposio ALAD Avances en la prevención y el tratamiento de la diabetes tipo 2...rdaragnez
This document summarizes research on diabetes treatment and outcomes from several long-term clinical trials. It finds that intensive glucose control early in type 2 diabetes can significantly reduce cardiovascular and renal complications long-term. However, rapidly lowering glucose in those with existing cardiovascular disease may increase mortality risk. Multifactorial treatment including blood pressure and glucose control provides substantial benefits and is recommended for all type 2 diabetes patients.
Simposio ALAD Avances en la prevención y el tratamiento de la diabetes tipo 2...rdaragnez
El documento trata sobre la prevención de la nefropatía diabética. Explica que la nefropatía se desarrolla en alrededor del 20-35% de los pacientes diabéticos y que existen factores de riesgo genéticos y ambientales. Recomienda realizar exámenes anuales de microalbuminuria a partir del diagnóstico de diabetes tipo 2 y a los 5 años en diabetes tipo 1 para detección temprana, así como control glucémico, de presión arterial y lípidos para prevenir la progresión de la
Simposio ALAD Avances en la prevención y el tratamiento de la diabetes tipo 2...rdaragnez
Este documento presenta las recomendaciones de la Asociación Latinoamericana de Diabetes (ALAD) para el tratamiento de la diabetes tipo 2. Propone iniciar el tratamiento con cambios en el estilo de vida y metformina. Si la metformina está contraindicada, se recomiendan otras opciones como tiazolidinedionas, inhibidores de DPP-IV o sulfonilureas. Para niveles más altos de glucosa o HbA1c, se sugiere agregar insulina u otras combinaciones de fármacos. El objetivo es lograr un control glucé
Pharmacological Treatment of Type 2 Diabetesrdaragnez
- Pharmacological treatment of type 2 diabetes involves reducing A1C, blood pressure, and cholesterol levels to prevent complications. Monotherapy often fails and multiple medications are usually required.
- Lifestyle interventions and metformin were shown to be more effective than placebo at preventing diabetes in pre-diabetic patients. Metformin worked best in those with higher BMIs, ages under 60, and fasting plasma glucose over 110 mg/dL.
- Pioglitazone treatment was able to delay the onset of type 2 diabetes by over 80% compared to placebo in pre-diabetic patients over 2.6 years of follow up. Intensive glucose control was not shown to reduce cardiovascular events compared to standard treatment in
The Metabolic Syndrome and Cardiovascular Riskrdaragnez
This document discusses the metabolic syndrome and its relationship to cardiovascular risk. It begins with an overview of type 2 diabetes as a progressive disease driven by insulin resistance and declining beta cell function. It then discusses how insulin resistance, hyperinsulinemia, hypertension, dyslipidemia and other factors associated with the metabolic syndrome contribute to increased cardiovascular risk in those with type 2 diabetes or prediabetes. The document reviews various criteria and definitions for diagnosing the metabolic syndrome, and discusses the prevalence of the metabolic syndrome in the United States. It also summarizes several studies examining the predictive value of the metabolic syndrome for future diabetes and cardiovascular disease.
Diabetes Tipo 2 del niño y adolescente. ¿Igual que en el adulto?rdaragnez
El documento presenta los resultados preliminares de un estudio clínico que compara tres regímenes de tratamiento para la diabetes tipo 2 en adolescentes y jóvenes: metformina más placebo, metformina más rosiglitazona, y metformina más modificación intensiva del estilo de vida. El objetivo principal es comparar el efecto a largo plazo en el control glucémico. Algunos objetivos secundarios importantes incluyen la seguridad, la preservación de la función de las células beta, y los factores de riesgo cardiovascular.
Documento - Dipeptidyl peptidase-4 inhibitors and the management of type 2 di...rdaragnez
1) Oral dipeptidyl peptidase-4 (DPP-4) inhibitors improve glucose control in type 2 diabetes by increasing levels of the incretin hormones GLP-1 and GIP.
2) Clinical trials show that the DPP-4 inhibitors sitagliptin and vildagliptin modestly lower glycated hemoglobin (HbA1c) as monotherapy and in combination with other agents, without weight gain or hypoglycemia.
3) DPP-4 inhibitors appear to have a benign safety profile and may help preserve pancreatic beta-cell function, but long-term studies are still needed to determine if they can modify the progression of type
Documento - Estrategías de insulinización en la diabetes mellitus tipo 2rdaragnez
Este documento describe estrategias de tratamiento con insulina para la diabetes tipo 2. La diabetes tipo 2 se caracteriza por resistencia a la insulina y deterioro progresivo de la función de las células beta pancreáticas, lo que requiere tratamiento con insulina para muchos pacientes. El documento revisa opciones para iniciar o intensificar la terapia con insulina, como añadir análogos de insulina de acción prolongada a tratamientos orales previos, usar insulina premezclada o terapia basal-bolus. El objetivo es lograr un
Riesgo Cardiometabolico: Papel de la Hipertension (1)rdaragnez
Este documento resume la relación entre la hipertensión y el riesgo cardiometabólico. La hipertensión es común en pacientes con diabetes tipo 2 y aumenta drásticamente la morbilidad y mortalidad cardiovascular en estas personas. El control de la presión arterial y los lípidos es peor en pacientes con síndrome metabólico. Finalmente, la resistencia a la insulina e inflamación son factores que contribuyen a la hipertensión arterial en personas con obesidad.
Riesgo Cardiometabolico: Papel de la Hipertension (2)rdaragnez
Este estudio encontró que los niveles de PCR se correlacionan con la definición del Síndrome Metabólico según el ATP III en 14,719 mujeres estadounidenses aparentemente sanas. El ATP III define el Síndrome Metabólico como la presencia de 3 o más de las siguientes características: obesidad central, triglicéridos altos, HDL bajo, hipertensión o intolerancia a la glucosa. Cuanto mayor era el número de características del Síndrome Metabólico presentes, mayores eran
Riesgo Cardiometabolico: Papel de la Hipertension (3)rdaragnez
1) Blocking the renin-angiotensin-aldosterone system (RAAS) through ACE inhibitors or ARBs reduces oxidative stress, improves endothelial function, and lowers rates of atherosclerosis progression compared to other antihypertensives.
2) RAAS blockade improves glucose metabolism by increasing nitric oxide, reducing angiotensin II levels, and enhancing insulin sensitivity and glucose transport in skeletal muscle. Clinical trials show reduced cardiovascular events and nephropathy in diabetes patients treated with ACE inhibitors.
3) Multiple clinical trials demonstrate that targeting lower diastolic blood pressure goals or using RAAS blockade reduces cardiovascular events and new onset diabetes compared to other antihypertensive classes.
Riesgo Cardiometabolico: Papel de la Hipertension (4)rdaragnez
Este documento describe el tratamiento integral del paciente hipertenso con síndrome metabólico. Se discuten diversas estrategias de tratamiento como cambios en el estilo de vida, tratamiento farmacológico y quirúrgico. Se analizan los mecanismos de acción de diferentes fármacos y sus efectos en factores de riesgo cardiovascular.
Consenso Latinoamericano de la Asociación Latinoamericana de Diabetes (ALAD) ...rdaragnez
Este documento presenta las directrices de la Asociación Latinoamericana de Diabetes sobre el síndrome metabólico. Define el síndrome metabólico y discute su relación con la diabetes y las enfermedades cardiovasculares. Presenta los criterios diagnósticos del síndrome metabólico según la Federación Internacional de Diabetes y el ATP III. También analiza la epidemiología del síndrome metabólico en América Latina y ofrece recomendaciones sobre el manejo clínico, control metabólico y tratamiento de los pacientes con este sí
Obesidad: ¿Enfermedad Quirurgica? Efectos Metabólicos de la Cirugía Bariátric...rdaragnez
This document summarizes research on the effects of bariatric surgery on metabolic parameters and type 2 diabetes. It shows that bariatric surgery leads to significant and sustained weight loss, improved glycemic control, reduced insulin resistance, normalization of lipid profiles and other metabolic markers. The surgery favors an anorectic hormone state that facilitates weight loss and metabolic improvements. Over time, bariatric surgery can result in remission or significant improvement of type 2 diabetes in many patients by addressing the underlying causes of insulin resistance and beta cell dysfunction.
Dislipidemia 2009: Is there something new?rdaragnez
The document discusses research on the role of Scavenger Receptor Class B Type I (SR-BI) in cholesterol transport and human health. Studies found that variants in the SR-BI gene are associated with HDL cholesterol levels and subclinical atherosclerosis. In vitro work also suggests low SR-BI levels may be linked to reduced progesterone production and female infertility.
Este documento presenta información sobre la diabetes en las Américas. Resume datos sobre la prevalencia, incidencia y mortalidad de la diabetes, así como sobre la capacidad nacional para prevenirla y controlarla. También describe el proyecto VIDA para mejorar la calidad de la atención a la diabetes a través de intervenciones como entrenamiento y educación. El documento concluye que la diabetes genera altos costos y que es necesario desarrollar iniciativas multisistema para prevenirla y controlarla.
La conferencia discutió la epidemia creciente de síndrome metabólico y nefropatía diabética. Se proyectó que el número de personas con diabetes aumentará dramáticamente en todo el mundo para 2030, especialmente en China e India. La diabetes se ha convertido en una de las principales causas de insuficiencia renal crónica en México. La nefropatía diabética progresa de microalbuminuria a nefropatía franca y finalmente a insuficiencia renal terminal. El control glucémico y de la presión arterial pueden ayud
Simposio ALAD Nefropatia Diabetica - Nefropatia Diabetica: Razones para su Tr...rdaragnez
Este documento describe las razones para tratar la nefropatía diabética. La nefropatía diabética afecta al 35% de personas con diabetes y es la principal causa de enfermedad renal en etapa terminal. Los estudios RENAAL y otros muestran que el tratamiento con losartán reduce significativamente la duplicación de la creatinina sérica y la progresión a enfermedad renal en etapa terminal en personas con nefropatía diabética. Por lo tanto, el tratamiento de la nefropatía diabética es crucial para prevenir complic
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Adhd Medication Shortage Uk - trinexpharmacy.comreignlana06
The UK is currently facing a Adhd Medication Shortage Uk, which has left many patients and their families grappling with uncertainty and frustration. ADHD, or Attention Deficit Hyperactivity Disorder, is a chronic condition that requires consistent medication to manage effectively. This shortage has highlighted the critical role these medications play in the daily lives of those affected by ADHD. Contact : +1 (747) 209 – 3649 E-mail : sales@trinexpharmacy.com
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by...Donc Test
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HDL: Where are we and where are we going?
1. HDL: Where are we and
where are we going?
Annabelle Rodriguez, MD
Johns Hopkins School of Medicine
Division of Endocrinology
Slide Source
Lipids Online Slide Library
www.lipidsonline.org
2. CAD Risk as a Function of LDL-C and
HDL-C in Men (Ages 50 to 70 Years
Old): Framingham Heart Study
Coronary Artery Disease (CAD)
3
Relative Risk
2
25 0.65
1 45 1.16
65 1.68
0 85 2.2
220 160 100 mg/dL
5.69 4.14 2.58 mmol/L
LDL Cholesterol (LDL-C)
Slide Source
Modified from Castelli WP. Can J Cardiol 1988;4:5A10A. Lipids Online Slide Library
www.lipidsonline.org
3. HDL Metabolism
Nascent HDL (lipid-poor apolipoprotein A1 [Apo A1]) is produced
by the liver and intestine
intestine
liver
particle
LPL uptake
TGRL
selective
uptake
apo A1
HDL2
CETP
ABC1 SR-BI
peripheral cells HL, EL
LCAT
HDL3 PLTP
pre- surface
cubilin HDL remnants
kidney
Slide Source
Von Eckardstein A et al. Curr Opin Lipidol 2000;11:627637. Lipids Online Slide Library
www.lipidsonline.org
4. Potential Targets to Modify HDL
Increase apolipoprotein A1 (apo A1) production
Increase anti-inflammatory effect of high-density
lipoprotein (HDL)
Infuse apo A1 phospholipid complexes
PPAR alpha, delta and gamma
LXR agonists
Upregulate ABCA1 or ABCG1
Enhance LCAT activity
Inhibit CETP
Modify Hepatic Holoparticle uptake of HDL (niacin
receptor agonist)
PPAR=peroxisome proliferator-activated receptor; LXR=liver X receptor; ABCA1=ATP-binding
cassette transporter A1; ABCG1=ATP-binding cassette transporter G1; LCAT=lecithin
Slide Source
cholesterol acyltransferase; CETP=cholesteryl ester transfer protein Lipids Online Slide Library
www.lipidsonline.org
5. Pharmacologic Therapy to Promote
Reverse Cholesterol Transport
Bile Feces
A1
A1 CE
FC
CE LCAT
FC FC
CE
SR-BI Nascent Macrophage
HDL
Liver Mature
HDL
CE=cholesterol ester ;FC=free cholesterol; SR-BI=scavenger receptor class-B, type I;
A1=apolipoprotein A1; LCAT=lecithin cholesterol acyltransferase; HDL=high-density
Slide Source
lipoprotein Lipids Online Slide Library
www.lipidsonline.org
6. Normal Apo A1 and Apo A1 Milano Dimer
Lipid Binding In
Vivo Catabolism
35
143 187
99
243
A1
1
25 209 220
66 121 165
A1=apolipoprotein A1
LCAT Activation Receptor A1m=apolipoprotein A1 Milano
Cholesterol Efflux Binding LCAT=lecithin cholesterol acyl-
transferase
243 243
A1m/A1m 173 173
1 ss 1
Slide Source
Franceschini G. Eur J Clin Invest 1996;26:733746. Lipids Online Slide Library
www.lipidsonline.org
7. HDL Metabolism as a Therapeutic
Target: Potential Strategies
Acute (parenteral) therapies
– Apo A1 Milano/phospholipid complexes
– Apo A1 mimetic peptides
– Large unilamellar vesicles (LUVs)
– Delipidated HDL
– Apo A1 isolated from human plasma and
phosphatidylcholine derived from soybean
Slide Source
HDL=high-density lipoprotein; Apo A1=apolipoprotein A1 Lipids Online Slide Library
www.lipidsonline.org
9. ERASE Trial: Primary Endpoint
Percent Change in Atheroma Volume from
Baseline to 6 weeks
Change in Atheroma Volume (%)
1% The primary endpoint
CSL-111 Placebo
of percent change in
0% atheroma volume from
baseline to 6 weeks did
-1% not differ between
treatment groups
-2% −1.6% (−3.4% in the CSL-111
group vs.
-3% p = 0.48 −1.6% in the placebo
−3.4% group, p=0.48)
-4%
Slide Source
Tardif JC et al. JAMA 2007;297:16751682. Lipids Online Slide Library
www.lipidsonline.org
10. Mechanisms Other Than
Reverse Cholesterol Transport by which
HDL May Be Anti-atherogenic
Anti-oxidant effects
Anti-inflammatory effects
Anti-coagulant effects
Improve endothelial function
Slide Source
HDL=high-density lipoprotein Lipids Online Slide Library
www.lipidsonline.org
11. Conversion of Anti-Inflammatory
and Pro-Inflammatory HDL
Myeloperoxidase
HDL=high-density lipoprotein
Nitrotyrosine
Chlortyrosine
Apo A1
Paraoxonase,
other factors
Apo A1 Pro-inflammatory
factors, other
factors
Anti-inflammatory Pro-inflammatory
Modified from Ansell BJ et al. J Am Coll Cardiol 2005;46:1792 Slide Source
1798. Lipids Online Slide Library
www.lipidsonline.org
12. Regulation of Cholesterol Efflux
in the Macrophage by LXR
A1
CE
ABCG1
LXR
Chol
A1
ABCA1
LXR=liver X receptor; CE=cholesterol ester;A1=apolipoprotein A1; ABCA1=ATP-binding
Slide Source
cassette transporter A1; ABCG1=ATP-binding cassette transporter G1 Lipids Online Slide Library
www.lipidsonline.org
13. Pharmacologic Manipulation of
ABCA1 and Macrophage Cholesterol
Efflux
Fibrates, TZDs, dual PPARs,
new agents
PPAR
PPAR
PPAR
A1
FC LXR/RXR
ABCA1
New
agents
?New
ABCA1=ATP-binding cassette transporter
A1; A1=apolipoprotein A1; FC=free
agents
cholesterol; LXR=liver X receptor;
RXR=retinoid X receptor; PPAR=
peroxisome proliferator-activated Slide Source
receptor; TZD=thiazolidinedione Lipids Online Slide Library
www.lipidsonline.org
14. FIELD Study: Primary Endpoint
Nonfatal MI or CHD death at 5 years
5.9%
6% Full study cohort:
5.2% – Fenofibrate (n=4895)
– Placebo (n=4900)
5%
The primary end point of
nonfatal MI or CHD death was
4% not significantly lower in the
fenofibrate group compared
with the placebo group
3%
P = .16 Nonfatal MI and revascularization
were significantly lower in the
2% fenofibrate group compared with
the placebo group
Patients in the placebo group
1% were treated more frequently
with lipid-lowering therapy
0%
Fenofibrate Placebo MI=myocardial infarction
CHD=coronary heart disease
(n=256) (n=288)
Slide Source
Keech A et al. Lancet 2005;366:18491861. Lipids Online Slide Library
www.lipidsonline.org
15. Total CVD in Subgroups
Feno- Favors Favors HR
Interaction Placebo fibrate Fenofibrate Placebo (95% CI) P
HDL-C P % %
15.1
Low (ATPIII) 13.0 0.02 0.3
2.1%
12.3
High 11.8 0.6
0.5%
Triglycerides
15.4
>1.7 mM 13.6 0.07 0.8
2.8%
12.4
<1.7 11.3 0.2
1.1%
Dyslipidemia (low HDL-C + high TG)
16.3
Yes 14.0 0.06 0.6
2.3%
12.6
No 11.6 0.2
1.0%
CVD=cardiovascular disease 0.5 0.6 0.7 0.8 0.9 1 1.1 1.2 1.3 1.4 1.5
Slide Source
Keech A et al. Lancet 2005;366:1849-1861. Lipids Online Slide Library
www.lipidsonline.org
17. CHICAGO: Mean Change in CIMT
0.020 p=0.017
LS Mean Change from Baseline
0.015 Glimepiride
Posterior Wall CIMT (mm)
0.010 0.012 Pioglitazone
0.005
0.000
-0.005
−0.001
-0.010
Baseline CIMT GLM (N=186) PIO (N=175) Treatment group difference,
LS Mean (SE) 0.779 (0.0085) mm 0.771 (0.0085) mm Final Visit
−0.013 (95% CI: −0.024,−0.002)
CIMT=carotid intima-media thickness
Slide Source
Adapted from Mazzone T et al. JAMA 2006;296:25722581. Lipids Online Slide Library
www.lipidsonline.org
18. HDL Cholesterol Changes
8
Glimepiride Pioglitazone
LS Mean Change from Baseline,
6
HDL-C (mg/dL)
12.8%
4
2
−1.1%
*p<0.0001
0
-2
Baseline 24 48 72
No. of Observations Week
Glimepiride 206 203 206 206
Pioglitazone 201 198 201 201
Slide Source
Mazzone T et al. JAMA 2006;296:2572−2581. Lipids Online Slide Library
www.lipidsonline.org
19. HDL Metabolism: Role of CETP
Bile
A1
FC A1 CE
CE FC LCAT
FC FC
CE ABCA1
SR-BI
Macrophage
Liver CETP
LDLR A1=apolipoprotein A1
ABCA1=ATP-binding cassette transporter A1
CE=cholesterol ester
CETP=cholesterol ester transfer protein
CE FC=free cholesterol
B TG LCAT=lecithin cholesterol acyltransferase
LDL=low-density lipoprotein
LDLR=LDL receptor
SR-BI=scavenger receptor class-B, type I
TG=triglyceride
VLDL/LDL VLDL=very low density lipoprotein
Slide Source
Lipids Online Slide Library
www.lipidsonline.org
20. CETP Deficiency is Associated with
Markedly Increased HDL-C Levels
Bile A1
FC FC A1 CE
CE LCAT
CE FC FC
SR-BI ABCA1
Macrophage
Liver
LDLR
X
CETP A1=apolipoprotein A1
ABCA1=ATP-binding cassette transporter A1
CE=cholesterol ester
CETP=cholesterol ester transfer protein
FC=free cholesterol
CE LCAT=lecithin cholesterol acyltransferase
B TG LDL=low-density lipoprotein
LDLR=LDL receptor
SR-BI=scavenger receptor class-B, type I
TG=triglyceride
VLDL/LDL VLDL=very low density lipoprotein
Slide Source
Lipids Online Slide Library
HDL-C=high-density lipoprotein cholesterol www.lipidsonline.org
21. Torcetrapib: Pharmacodynamic
Effect on HDL-C in Phase 1
Phase I Summary of Lipid and Lipoprotein Changes
100 91 70
80 Base HDL-C 73 60
Base HDL-C (mg/dL)
50
60 62
% Change
% HDL-C
40
40 % Apo A1
28 27 27
24 30
16
20 11 12
20
0 10
−3 −2
-20 0
PBO 10 30 60 120 240 (bid)
Daily Dose
Changes are following 2 weeks of treatment; n=6 per active dose group; n=9 placebo (PBO)
Created from Clark RW et al. Arterioscler Thromb Vasc Biol 2004; Slide Source
Lipids Online Slide Library
24:490497. www.lipidsonline.org
22. Torcetrapib (Study A3071007)
Consistent HDL-C Raising by Gender and
Baseline HDL-C
Mean % Change: 58% 55% 45% 42%
Torcetrapib 120 mg qd
140
130 Male Female
120
110
100
HDL-C 90
(mg/dL) 80
70
60
50
40
30
20
Week: 0 8 0 8 0 8 0 8
Baseline HDL-C: Low High Low High
Slide Source
Created from Bamberger MJ et al. Circulation 2005;112:II-179. Lipids Online Slide Library
www.lipidsonline.org
23. ILLUSTRATE Trial: Primary Endpoint
Percent change in atheroma volume from baseline
0.3 p=0.72
Change in Atheroma Volume
The percent
change in
from Baseline (%)
0.19%
0.2 atheroma volume
did not differ
0.12% between
0.1 treatment groups
0
Torcetrapib Placebo
N = 591 N = 597
Slide Source
Nissen SE et al. N Engl J Med 2007;356:13041316. Lipids Online Slide Library
www.lipidsonline.org
25. Coronary Drug Project:
Clinical Outcomes*
35 −14
30 Placebo
25
Event Rate (%)
Niacin
20 −27
15 −26
10 −47
5
0
Nonfatal MI/ Nonfatal MI Stroke/TIA CV Surgery
CHD Death
MI=myocardial infarction; CHD=coronary heart disease; TIA=transient ischemic attack;
CV=cardiovascular
*Total follow-up, adjusted for baseline characteristics, p<0.05, 5-year rate Source
Slide
Coronary Drug Project Research Group. JAMA 1975;231:360381. Lipids Online Slide Library
www.lipidsonline.org
26. ARBITER 3:
Changes in CIMT – Pooled, 12-Month Data
CIMT=carotid intima-media thickness; ERN=extended-release niacin
Placebo + statin phase
0.075
n = 61
Overall CIMT
regression Significant CIMT progression
Aggregate Change in CIMT for
0.05
Initial 12 months ERN + statin
All Drug Periods (mm)
ANOVA p<0.001 n = 125
0.025 Pooled ARBITER 2 and 3
−0.027 0.011
results
−0.041 0.021
0 Net CIMT regression
−0.027 ± 0.011 mm
p<0.001 vs.
-0.025
placebo
24 month ERN + statin effect
-0.05 n = 57
Mean ± SEM Continuous ERN treatment
-0.075 CIMT regression
Placebo First 12 mos. Total 24 mos.
−0.041 ± 0.021 mm
Phase ERN (+ statin) ERN
(+ Statin) Treatment Period (+ statin) p<0.001 vs. placebo
Slide Source
Taylor AJ et al. Curr Med Res Opin 2006;22:22432250. Lipids Online Slide Library
www.lipidsonline.org
27. MK-0524 (laropiprant)
Suppresses Niacin-Induced Increases in Skin
Blood Flow
1.4
9
Laser Doppler Perfusion Imaging
1.2
Laropiprant 30mg + ER niacin 1500 mg
Placebo-Corrected LDPI
1 Laropiprant 100 mg + ER niacin 1500 mg
Measurement (Volt)
Laropiprant 300 mg + ER niacin 1500 mg
0.8 Aspirin 325 mg Pretreatment + ER niacin 1500 mg
ER niacin 1500 mg
0.6
0.4
0.2
0
2 0
0 30 60 90 120 150 180 210 240 270 300 330 360
ER=extended-release Time (minute, post dose)
Slide Source
Lai E et al. Clin Pharmacol Ther 2007;81:849-857. Lipids Online Slide Library
www.lipidsonline.org
28. Summary
LDL-C remains the primary goal of lipid-treatment but novel
therapies that affect reverse cholesterol transport are on
the horizon
Novel strategies to improve reverse cholesterol transport
include infusions of synthetic HDL or phospholipids, nuclear
receptor agonists to enhance LXR gene regulation, apo A1
peptides to enhance the anti-inflammatory aspects of HDL
and DP-1 antagonists in combination with niacin to improve
compliance
Even small increases in HDL-C may confer substantial
benefit
Intervention to raise HDL-C levels should be considered in
high-risk patients
Slide Source
Lipids Online Slide Library
www.lipidsonline.org