The document discusses lipid metabolism disorders related to carnitine. It describes how carnitine transports long-chain fatty acids into mitochondria for breakdown (β-oxidation), a process called the carnitine shuttle. Deficiencies in carnitine can cause metabolic disorders by inhibiting fatty acid breakdown. The primary types are genetic deficiencies of carnitine palmitoyltransferases I and II, resulting in hypoglycemia, liver disease, and muscle issues. Secondary deficiencies occur with liver disease, malnutrition, or other medical conditions increasing carnitine needs. Diagnosis involves carnitine level testing, and treatment is carnitine supplementation.
Enzymes associated with the endoplasmic reticulum and outer mitochondrial membrane activate fatty acids by catalyzing their attachment to coenzyme A using ATP. Acyl-CoA synthases of different chain lengths esterify fatty acids. Long chain fatty acids are transported into mitochondria by the carnitine shuttle system, which involves transferring the fatty acid from coenzyme A to carnitine, then transporting carnitine-bound fatty acids across the inner mitochondrial membrane, and transferring the fatty acid back to coenzyme A. Deficiencies in carnitine can decrease the ability of tissues to use long chain fatty acids as energy.
Enzymes associated with the endoplasmic reticulum and outer mitochondrial membrane activate fatty acids by catalyzing their attachment to coenzyme A using ATP. Acyl-CoA is then transported into mitochondria and peroxisomes via the carnitine shuttle system, which involves transferring the fatty acid from CoA to carnitine, and then back to CoA after crossing the inner mitochondrial membrane. Deficiencies in carnitine transport can impair fatty acid breakdown, leading to metabolic disorders.
1) Lipids are a major class of biomolecules that serve important structural and energy storage roles. The main lipids include triacylglycerols, phospholipids, and steroids.
2) Lipids are metabolized through several key pathways. Triacylglycerols undergo hydrolysis to release fatty acids and glycerol. Fatty acids are transported and undergo beta-oxidation in the mitochondria to generate acetyl-CoA for the citric acid cycle.
3) Beta-oxidation is a four-step process occurring in the mitochondrial matrix that involves dehydrogenation, hydration, dehydrogenation, and thiolytic cleavage of fatty acyl-CoA molecules, shortening the
Medium Chain Acyl Coenzyme A Dehydrogenase DeficiencyDina m.
Medium-chain acyl-coenzyme A dehydrogenase deficiency (MCAD deficiency) is caused by defects in the MCAD enzyme, which is responsible for metabolizing medium chain fatty acids. This leads to an inability to convert these fatty acids into energy during periods without food intake. Symptoms include vomiting, lethargy and coma during illness when fasting, and it can cause sudden infant death. Diagnosis involves testing blood and urine for markers of medium chain fatty acid metabolism. Treatment focuses on avoiding fasting and providing adequate carbohydrates and calories during illnesses to prevent dangerous hypoglycemia.
Fatty Acids are Aliphatic carboxylic acids and each animal species will have characteristic pattern of fatty acid composition. Thus, human body fat contains 50% oleic acid, 25% palmitic acid, 10% linoleic acid and 5% stearic acid.
Disorders Associated with Fatty Acid Catabolismcoco_dawn_96
Disorders associated with fatty acid catabolism are caused by deficiencies in enzymes needed to break down fatty acids. This results in the buildup of fatty acid breakdown products and prevents the body from efficiently producing and using energy from fats. Specific disorders include medium-chain acyl-CoA dehydrogenase deficiency and carnitine uptake defect. Symptoms can include hypoglycemia, seizures, and delayed development. Treatment focuses on providing alternative energy sources and supplements.
This document provides an overview of lipid metabolism. It discusses β-oxidation of fatty acids, formation and utilization of ketone bodies, de novo fatty acid synthesis, the biological significance of cholesterol and its conversion to bile acids, steroid hormones and vitamin D. It also covers disorders of lipid metabolism like hypercholesterolemia and atherosclerosis. The key points are: β-oxidation breaks down fatty acids in the mitochondria, ketone bodies are energy sources formed from acetyl-CoA, and cholesterol is essential for cell membranes and is a precursor for other steroids.
Enzymes associated with the endoplasmic reticulum and outer mitochondrial membrane activate fatty acids by catalyzing their attachment to coenzyme A using ATP. Acyl-CoA synthases of different chain lengths esterify fatty acids. Long chain fatty acids are transported into mitochondria by the carnitine shuttle system, which involves transferring the fatty acid from coenzyme A to carnitine, then transporting carnitine-bound fatty acids across the inner mitochondrial membrane, and transferring the fatty acid back to coenzyme A. Deficiencies in carnitine can decrease the ability of tissues to use long chain fatty acids as energy.
Enzymes associated with the endoplasmic reticulum and outer mitochondrial membrane activate fatty acids by catalyzing their attachment to coenzyme A using ATP. Acyl-CoA is then transported into mitochondria and peroxisomes via the carnitine shuttle system, which involves transferring the fatty acid from CoA to carnitine, and then back to CoA after crossing the inner mitochondrial membrane. Deficiencies in carnitine transport can impair fatty acid breakdown, leading to metabolic disorders.
1) Lipids are a major class of biomolecules that serve important structural and energy storage roles. The main lipids include triacylglycerols, phospholipids, and steroids.
2) Lipids are metabolized through several key pathways. Triacylglycerols undergo hydrolysis to release fatty acids and glycerol. Fatty acids are transported and undergo beta-oxidation in the mitochondria to generate acetyl-CoA for the citric acid cycle.
3) Beta-oxidation is a four-step process occurring in the mitochondrial matrix that involves dehydrogenation, hydration, dehydrogenation, and thiolytic cleavage of fatty acyl-CoA molecules, shortening the
Medium Chain Acyl Coenzyme A Dehydrogenase DeficiencyDina m.
Medium-chain acyl-coenzyme A dehydrogenase deficiency (MCAD deficiency) is caused by defects in the MCAD enzyme, which is responsible for metabolizing medium chain fatty acids. This leads to an inability to convert these fatty acids into energy during periods without food intake. Symptoms include vomiting, lethargy and coma during illness when fasting, and it can cause sudden infant death. Diagnosis involves testing blood and urine for markers of medium chain fatty acid metabolism. Treatment focuses on avoiding fasting and providing adequate carbohydrates and calories during illnesses to prevent dangerous hypoglycemia.
Fatty Acids are Aliphatic carboxylic acids and each animal species will have characteristic pattern of fatty acid composition. Thus, human body fat contains 50% oleic acid, 25% palmitic acid, 10% linoleic acid and 5% stearic acid.
Disorders Associated with Fatty Acid Catabolismcoco_dawn_96
Disorders associated with fatty acid catabolism are caused by deficiencies in enzymes needed to break down fatty acids. This results in the buildup of fatty acid breakdown products and prevents the body from efficiently producing and using energy from fats. Specific disorders include medium-chain acyl-CoA dehydrogenase deficiency and carnitine uptake defect. Symptoms can include hypoglycemia, seizures, and delayed development. Treatment focuses on providing alternative energy sources and supplements.
This document provides an overview of lipid metabolism. It discusses β-oxidation of fatty acids, formation and utilization of ketone bodies, de novo fatty acid synthesis, the biological significance of cholesterol and its conversion to bile acids, steroid hormones and vitamin D. It also covers disorders of lipid metabolism like hypercholesterolemia and atherosclerosis. The key points are: β-oxidation breaks down fatty acids in the mitochondria, ketone bodies are energy sources formed from acetyl-CoA, and cholesterol is essential for cell membranes and is a precursor for other steroids.
The document discusses the intestinal glands and their role in digestion and absorption. It describes the various secretions of the intestinal glands including intestinal juice, enzymes, mucus, and their functions. It also summarizes the digestion and absorption of carbohydrates, proteins, fats, and water. Key points covered include the roles of pancreatic and intestinal enzymes in breaking down macronutrients into smaller units for absorption, and the mechanisms of absorption such as active transport and formation of micelles. Conditions that can lead to malabsorption syndrome due to impaired digestion or absorption are also briefly mentioned.
1) Fatty acids are oxidized through beta-oxidation, where two-carbon fragments are removed from the carboxyl end in the mitochondrial matrix, producing acetyl-CoA, NADH, and FADH2.
2) Fatty acids are activated to fatty acyl-CoAs in the cytosol then transported into the mitochondria by the carnitine shuttle.
3) Beta-oxidation occurs through four steps - oxidation, hydration, oxidation, and thiolysis - shortening the fatty acyl chain by two carbons each cycle to generate energy.
Nutrient sensing and metabolic disturbanceshelix1661
This document summarizes potential causes of metabolic syndrome and insulin resistance, including ectopic fat accumulation, impaired fat oxidation, defects in mitochondrial function, and impaired lipid metabolism. It also discusses adipose tissue as an endocrine organ and the roles of adipocytokines like adiponectin and resistin. Finally, it examines nutrient sensing pathways such as AMPK that regulate cellular energy levels and metabolism.
This document summarizes various screening models for diabetes, including in vivo and in vitro models. For in vivo models, it describes chemically-induced diabetes models using alloxan and streptozotocin in rodents, as well as spontaneous genetic rodent models like BB rats and KK mice. In vitro models discussed include isolated pancreatic islet cells, cultured human myotubes for glucose uptake studies, and the Gluc-HET chick embryo model for assessing insulin mimetic compounds. The document provides details on the procedures, advantages and limitations of each type of screening model.
Ketone bodies, or simply ketones are substances produced by the liver during gluconeogenesis, a process which creates glucose in times of fasting and starvation. There are three ketone bodies produced by the liver. They are acetoacetate, beta-hydroxybutyrate, and acetone. These compounds are used in healthy individuals to provide energy to the cells of the body when glucose is low or absent in the diet.
This document provides information on the digestion, absorption, and metabolism of lipids. It discusses how dietary lipids are broken down by lipases in the mouth, stomach, and small intestine. Pancreatic lipase plays a major role in digesting triglycerides into fatty acids and monoacylglycerides. These products are absorbed via micelles in the small intestine and resynthesized into triglycerides for transport to the liver and peripheral tissues. The document also outlines the pathways of beta-oxidation of fatty acids in mitochondria, ketogenesis in the liver from fatty acids, and utilization of ketone bodies by extrahepatic tissues.
Nutritional ketosis condition and specific ketogenic diet, may benefit cancer...banafsheh61
Cancer is the second leading cause of death in the United States. Researchers estimate that 595,690 Americans will die from cancer in 2017. That means approximately 1,600 deaths per day on average.39 Cancer is most commonly treated with a combination of surgery, chemotherapy and radiation. Many different diet strategies have been studied, but none have been particularly effective. Interestingly, there is some applied research suggesting that a very low-carb ketogenic diet may help.40, 41, 42 According to Otto Warburg hypothesis, the cause of cancer is the change in the metabolism of mitochondrion in human cells. Low oxygen in tissues in combination with high blood glucose will change the cell respiration from aerobic to anaerobic which leads to fermentation type of respiration. In this perspective and prospective research, I have shown the very low carbohydrate ketogenic diet and mostly ketosis, may benefit cancer patients in reducing and weakening cancer cells. Although further researches are needed, this perspective article could be beneficial in future perspective of alternative treatments of cancer.
This document discusses ketone bodies, their metabolism, and conditions of excess ketone body production. Ketone bodies are produced in the liver from acetyl-CoA when fatty acid breakdown exceeds the ability of the citric acid cycle to process acetyl-CoA. They can be used as an energy source by other tissues. Excess ketone body production occurs in starvation and uncontrolled diabetes, leading to ketosis or ketoacidosis as ketone levels rise and pH decreases due to ketone acid buildup.
The document discusses ketone bodies, their production through ketogenesis in the liver from acetyl-CoA, and their utilization as an energy source by extrahepatic tissues. It notes that ketone body production is regulated by lipolysis in adipose tissue and the availability of acetyl-CoA. Conditions like starvation and uncontrolled diabetes can result in diabetic or starvation ketoacidosis if ketone bodies are produced in excess, overwhelming the body's pH buffering mechanisms and leading to metabolic acidosis.
Lipid metabolism is the synthesis and degradation of lipids in cells.
It involves the breakdown or storage of fats for energy and the synthesis of structural and functional lipids, such as those involved in the construction of cell membranes.
In animals, these fats are obtained from food or synthesized by the liver.
This document provides information about live cell therapy and stem cell nutrition therapy presented by Dr. Shebendra. It discusses what live cell therapy and stem cells are, and how stem cell nutrition therapy works by providing less cooked foods, green foods, herbal foods, herbal medicinal foods and herbal medicines. The document also describes the products Astashine Silver and OptiGision Gold, including their active ingredients like astaxanthin and L-carnitine-L-tartrate. It discusses the benefits of these ingredients for antioxidant support, weight management, male fertility, cardiovascular health and more. Finally, it provides details on olive leaf extract and broccoli extract ingredients.
This document discusses lipid metabolism and fatty acid synthesis and oxidation. It begins by explaining that triacylglycerols (TGs), consisting of fatty acids esterified to glycerol, are the main form in which lipids are stored in the body as an energy reserve. The pathways of fatty acid synthesis and oxidation, which occur in the cytoplasm and mitochondria respectively, are then outlined. Key processes like elongation, desaturation, and the carnitine shuttle for transporting long-chain fatty acids into mitochondria are also summarized. Alternative pathways for unsaturated fatty acids and the production of ketone bodies during fasting are briefly mentioned.
This document discusses live cell therapy and stem cell nutrition. It presents on astashine silver and moringalite supplements. Astashine silver contains natural astaxanthin and L-carnitine-L-tartrate to support energy production, fat metabolism, and antioxidant benefits. Moringalite contains nutrients from moringa oleifera including protein, vitamins, minerals, and antioxidants to provide energy and support overall health and vitality. The presentation provides details on the ingredients, benefits, and recommended usage of these supplements.
Astashine silver & Moringalite are two natural products are marketed by PUGOS CO.in Bangladesh. Astashine silver a trade name of Astaxanthin & L-Carnitine, L-Tartrate. Astaxanthin is a molecule of Red & Pink color pigment which naturally have from hard shall animal like Lobster,Crab,Shrimp,feather,Horn etc.Bulk amount of Astaxanthin is found in Hematococcus Pluvialis a microalgae. Astshine contains Astaxanthin from Hematococcus Pluvialis. AstaReal Inc. a subsidiary company of Fuji Chemical Industries Ltd.Japan produces natural Astaxanthin commercially.
Carnipure’s L- Carnitine-L-Tartrate is high quality special grade L-carnitine manufactured by Lonza, Switzerland. It is a salt of 68% L- Carnitine and 32% tartaric acid, which is highest L-Carnitine concentration of any commercially available hygroscopic salt form. L- Carnitine-L-Tartrate in ASTASHINE Silver. Carnipure’s L- carnitine by lonza is the biggest supplier of L-Carnitine with more than 30 years of research in various clinical studies and continued scientific support.
Dr.Shebendra karmakar
Honorary PhD, IUM-USA
Member:
MedShr,London, UK.
Adipose tissue functions as an endocrine organ that secretes hormones and cytokines involved in energy metabolism and physiological processes. White adipose tissue stores excess energy as fat, while brown adipose tissue generates heat. Adipocytes secrete factors such as leptin, adiponectin, resistin, visfatin, and omentin that regulate appetite, glucose levels, inflammation, and fatty acid breakdown in target tissues. Dysregulation of these adipokines is associated with obesity, diabetes, and cardiovascular disease. Measurement of adipokine levels provides insight into metabolic and endocrine functions of adipose tissue.
This document provides an overview of carbohydrates, including their classification, structures, functions, and histological staining properties. Carbohydrates are classified as simple carbohydrates or glycoconjugates. Glycogen and mucin are two important carbohydrates for histological analysis. Glycogen stains with PAS, Best's carmine, and other techniques. Mucins include acid and neutral forms that stain differently with Alcian blue, PAS, and other histochemical stains depending on their composition. Carbohydrates play important roles in cellular metabolism and structure.
This seminar presentation covered carbohydrates, including their structure, functions, sources, classification, absorption, metabolism, and related diseases. Carbohydrates contain carbon, hydrogen, and oxygen, serve as an important energy source, and are connected by glycosidic bonds. They are classified as monosaccharides, disaccharides, and polysaccharides. Carbohydrates are broken down into monosaccharides in the small intestine and absorbed actively via SGLT-1 or passively via GLUT transporters. Glucose is metabolized through glycolysis, the Krebs cycle, and oxidative phosphorylation to produce ATP. Diseases related to carbohydrate deficiency or excess include diabetes, galactosemia, and heart disease.
This document discusses coagulants and anticoagulants used in medicinal chemistry. It provides background on blood coagulation pathways and factors. Coagulants discussed include vitamin K, fibrinogen, antihaemophilic factor, desmopressin, and others. Vitamin K is important for the synthesis of clotting factors and its deficiency can cause bleeding. Anticoagulants lower blood coagulability and include heparins, low molecular weight heparins, danaparoid, lepirudin, ancrod, and oral coumarin derivatives like warfarin.
This document summarizes ketone bodies and their synthesis during periods of starvation or uncontrolled diabetes. It notes that ketone bodies are normally a negligible source of energy but their levels can increase up to 500mg/dl during prolonged fasting as fatty acids are broken down and converted to ketone bodies in the liver. The key ketone bodies, acetoacetate and 3-hydroxybutyrate, can then be used as an energy source by tissues like cardiac muscle when glucose levels are low. The document also explains that ketone body synthesis is regulated by the lipolysis of fatty acids from adipose tissue and their conversion to acetyl-CoA in the liver mitochondria.
Ketogenic diet as a treatment of cancer somayeh zaminpira - sorush niknamianbanafsheh61
This document discusses how a ketogenic diet may benefit cancer patients by changing the metabolic state of cancer cells. It begins by providing background on cancer prevalence and treatments. It then discusses ketosis and how a ketogenic diet very low in carbs and high in fat induces a metabolic state where the body produces ketones from fat for energy instead of glucose. Cancer cells rely on glucose for energy and proliferation. Several animal studies show that a ketogenic diet reduces tumor growth and improves survival rates. The diet may benefit cancer patients by starving cancer cells of glucose, lowering insulin levels, and preventing cancer cells from using ketones for fuel.
বাংলাদেশের অর্থনৈতিক সমীক্ষা ২০২৪ [Bangladesh Economic Review 2024 Bangla.pdf] কম্পিউটার , ট্যাব ও স্মার্ট ফোন ভার্সন সহ সম্পূর্ণ বাংলা ই-বুক বা pdf বই " সুচিপত্র ...বুকমার্ক মেনু 🔖 ও হাইপার লিংক মেনু 📝👆 যুক্ত ..
আমাদের সবার জন্য খুব খুব গুরুত্বপূর্ণ একটি বই ..বিসিএস, ব্যাংক, ইউনিভার্সিটি ভর্তি ও যে কোন প্রতিযোগিতা মূলক পরীক্ষার জন্য এর খুব ইম্পরট্যান্ট একটি বিষয় ...তাছাড়া বাংলাদেশের সাম্প্রতিক যে কোন ডাটা বা তথ্য এই বইতে পাবেন ...
তাই একজন নাগরিক হিসাবে এই তথ্য গুলো আপনার জানা প্রয়োজন ...।
বিসিএস ও ব্যাংক এর লিখিত পরীক্ষা ...+এছাড়া মাধ্যমিক ও উচ্চমাধ্যমিকের স্টুডেন্টদের জন্য অনেক কাজে আসবে ...
The document discusses the intestinal glands and their role in digestion and absorption. It describes the various secretions of the intestinal glands including intestinal juice, enzymes, mucus, and their functions. It also summarizes the digestion and absorption of carbohydrates, proteins, fats, and water. Key points covered include the roles of pancreatic and intestinal enzymes in breaking down macronutrients into smaller units for absorption, and the mechanisms of absorption such as active transport and formation of micelles. Conditions that can lead to malabsorption syndrome due to impaired digestion or absorption are also briefly mentioned.
1) Fatty acids are oxidized through beta-oxidation, where two-carbon fragments are removed from the carboxyl end in the mitochondrial matrix, producing acetyl-CoA, NADH, and FADH2.
2) Fatty acids are activated to fatty acyl-CoAs in the cytosol then transported into the mitochondria by the carnitine shuttle.
3) Beta-oxidation occurs through four steps - oxidation, hydration, oxidation, and thiolysis - shortening the fatty acyl chain by two carbons each cycle to generate energy.
Nutrient sensing and metabolic disturbanceshelix1661
This document summarizes potential causes of metabolic syndrome and insulin resistance, including ectopic fat accumulation, impaired fat oxidation, defects in mitochondrial function, and impaired lipid metabolism. It also discusses adipose tissue as an endocrine organ and the roles of adipocytokines like adiponectin and resistin. Finally, it examines nutrient sensing pathways such as AMPK that regulate cellular energy levels and metabolism.
This document summarizes various screening models for diabetes, including in vivo and in vitro models. For in vivo models, it describes chemically-induced diabetes models using alloxan and streptozotocin in rodents, as well as spontaneous genetic rodent models like BB rats and KK mice. In vitro models discussed include isolated pancreatic islet cells, cultured human myotubes for glucose uptake studies, and the Gluc-HET chick embryo model for assessing insulin mimetic compounds. The document provides details on the procedures, advantages and limitations of each type of screening model.
Ketone bodies, or simply ketones are substances produced by the liver during gluconeogenesis, a process which creates glucose in times of fasting and starvation. There are three ketone bodies produced by the liver. They are acetoacetate, beta-hydroxybutyrate, and acetone. These compounds are used in healthy individuals to provide energy to the cells of the body when glucose is low or absent in the diet.
This document provides information on the digestion, absorption, and metabolism of lipids. It discusses how dietary lipids are broken down by lipases in the mouth, stomach, and small intestine. Pancreatic lipase plays a major role in digesting triglycerides into fatty acids and monoacylglycerides. These products are absorbed via micelles in the small intestine and resynthesized into triglycerides for transport to the liver and peripheral tissues. The document also outlines the pathways of beta-oxidation of fatty acids in mitochondria, ketogenesis in the liver from fatty acids, and utilization of ketone bodies by extrahepatic tissues.
Nutritional ketosis condition and specific ketogenic diet, may benefit cancer...banafsheh61
Cancer is the second leading cause of death in the United States. Researchers estimate that 595,690 Americans will die from cancer in 2017. That means approximately 1,600 deaths per day on average.39 Cancer is most commonly treated with a combination of surgery, chemotherapy and radiation. Many different diet strategies have been studied, but none have been particularly effective. Interestingly, there is some applied research suggesting that a very low-carb ketogenic diet may help.40, 41, 42 According to Otto Warburg hypothesis, the cause of cancer is the change in the metabolism of mitochondrion in human cells. Low oxygen in tissues in combination with high blood glucose will change the cell respiration from aerobic to anaerobic which leads to fermentation type of respiration. In this perspective and prospective research, I have shown the very low carbohydrate ketogenic diet and mostly ketosis, may benefit cancer patients in reducing and weakening cancer cells. Although further researches are needed, this perspective article could be beneficial in future perspective of alternative treatments of cancer.
This document discusses ketone bodies, their metabolism, and conditions of excess ketone body production. Ketone bodies are produced in the liver from acetyl-CoA when fatty acid breakdown exceeds the ability of the citric acid cycle to process acetyl-CoA. They can be used as an energy source by other tissues. Excess ketone body production occurs in starvation and uncontrolled diabetes, leading to ketosis or ketoacidosis as ketone levels rise and pH decreases due to ketone acid buildup.
The document discusses ketone bodies, their production through ketogenesis in the liver from acetyl-CoA, and their utilization as an energy source by extrahepatic tissues. It notes that ketone body production is regulated by lipolysis in adipose tissue and the availability of acetyl-CoA. Conditions like starvation and uncontrolled diabetes can result in diabetic or starvation ketoacidosis if ketone bodies are produced in excess, overwhelming the body's pH buffering mechanisms and leading to metabolic acidosis.
Lipid metabolism is the synthesis and degradation of lipids in cells.
It involves the breakdown or storage of fats for energy and the synthesis of structural and functional lipids, such as those involved in the construction of cell membranes.
In animals, these fats are obtained from food or synthesized by the liver.
This document provides information about live cell therapy and stem cell nutrition therapy presented by Dr. Shebendra. It discusses what live cell therapy and stem cells are, and how stem cell nutrition therapy works by providing less cooked foods, green foods, herbal foods, herbal medicinal foods and herbal medicines. The document also describes the products Astashine Silver and OptiGision Gold, including their active ingredients like astaxanthin and L-carnitine-L-tartrate. It discusses the benefits of these ingredients for antioxidant support, weight management, male fertility, cardiovascular health and more. Finally, it provides details on olive leaf extract and broccoli extract ingredients.
This document discusses lipid metabolism and fatty acid synthesis and oxidation. It begins by explaining that triacylglycerols (TGs), consisting of fatty acids esterified to glycerol, are the main form in which lipids are stored in the body as an energy reserve. The pathways of fatty acid synthesis and oxidation, which occur in the cytoplasm and mitochondria respectively, are then outlined. Key processes like elongation, desaturation, and the carnitine shuttle for transporting long-chain fatty acids into mitochondria are also summarized. Alternative pathways for unsaturated fatty acids and the production of ketone bodies during fasting are briefly mentioned.
This document discusses live cell therapy and stem cell nutrition. It presents on astashine silver and moringalite supplements. Astashine silver contains natural astaxanthin and L-carnitine-L-tartrate to support energy production, fat metabolism, and antioxidant benefits. Moringalite contains nutrients from moringa oleifera including protein, vitamins, minerals, and antioxidants to provide energy and support overall health and vitality. The presentation provides details on the ingredients, benefits, and recommended usage of these supplements.
Astashine silver & Moringalite are two natural products are marketed by PUGOS CO.in Bangladesh. Astashine silver a trade name of Astaxanthin & L-Carnitine, L-Tartrate. Astaxanthin is a molecule of Red & Pink color pigment which naturally have from hard shall animal like Lobster,Crab,Shrimp,feather,Horn etc.Bulk amount of Astaxanthin is found in Hematococcus Pluvialis a microalgae. Astshine contains Astaxanthin from Hematococcus Pluvialis. AstaReal Inc. a subsidiary company of Fuji Chemical Industries Ltd.Japan produces natural Astaxanthin commercially.
Carnipure’s L- Carnitine-L-Tartrate is high quality special grade L-carnitine manufactured by Lonza, Switzerland. It is a salt of 68% L- Carnitine and 32% tartaric acid, which is highest L-Carnitine concentration of any commercially available hygroscopic salt form. L- Carnitine-L-Tartrate in ASTASHINE Silver. Carnipure’s L- carnitine by lonza is the biggest supplier of L-Carnitine with more than 30 years of research in various clinical studies and continued scientific support.
Dr.Shebendra karmakar
Honorary PhD, IUM-USA
Member:
MedShr,London, UK.
Adipose tissue functions as an endocrine organ that secretes hormones and cytokines involved in energy metabolism and physiological processes. White adipose tissue stores excess energy as fat, while brown adipose tissue generates heat. Adipocytes secrete factors such as leptin, adiponectin, resistin, visfatin, and omentin that regulate appetite, glucose levels, inflammation, and fatty acid breakdown in target tissues. Dysregulation of these adipokines is associated with obesity, diabetes, and cardiovascular disease. Measurement of adipokine levels provides insight into metabolic and endocrine functions of adipose tissue.
This document provides an overview of carbohydrates, including their classification, structures, functions, and histological staining properties. Carbohydrates are classified as simple carbohydrates or glycoconjugates. Glycogen and mucin are two important carbohydrates for histological analysis. Glycogen stains with PAS, Best's carmine, and other techniques. Mucins include acid and neutral forms that stain differently with Alcian blue, PAS, and other histochemical stains depending on their composition. Carbohydrates play important roles in cellular metabolism and structure.
This seminar presentation covered carbohydrates, including their structure, functions, sources, classification, absorption, metabolism, and related diseases. Carbohydrates contain carbon, hydrogen, and oxygen, serve as an important energy source, and are connected by glycosidic bonds. They are classified as monosaccharides, disaccharides, and polysaccharides. Carbohydrates are broken down into monosaccharides in the small intestine and absorbed actively via SGLT-1 or passively via GLUT transporters. Glucose is metabolized through glycolysis, the Krebs cycle, and oxidative phosphorylation to produce ATP. Diseases related to carbohydrate deficiency or excess include diabetes, galactosemia, and heart disease.
This document discusses coagulants and anticoagulants used in medicinal chemistry. It provides background on blood coagulation pathways and factors. Coagulants discussed include vitamin K, fibrinogen, antihaemophilic factor, desmopressin, and others. Vitamin K is important for the synthesis of clotting factors and its deficiency can cause bleeding. Anticoagulants lower blood coagulability and include heparins, low molecular weight heparins, danaparoid, lepirudin, ancrod, and oral coumarin derivatives like warfarin.
This document summarizes ketone bodies and their synthesis during periods of starvation or uncontrolled diabetes. It notes that ketone bodies are normally a negligible source of energy but their levels can increase up to 500mg/dl during prolonged fasting as fatty acids are broken down and converted to ketone bodies in the liver. The key ketone bodies, acetoacetate and 3-hydroxybutyrate, can then be used as an energy source by tissues like cardiac muscle when glucose levels are low. The document also explains that ketone body synthesis is regulated by the lipolysis of fatty acids from adipose tissue and their conversion to acetyl-CoA in the liver mitochondria.
Ketogenic diet as a treatment of cancer somayeh zaminpira - sorush niknamianbanafsheh61
This document discusses how a ketogenic diet may benefit cancer patients by changing the metabolic state of cancer cells. It begins by providing background on cancer prevalence and treatments. It then discusses ketosis and how a ketogenic diet very low in carbs and high in fat induces a metabolic state where the body produces ketones from fat for energy instead of glucose. Cancer cells rely on glucose for energy and proliferation. Several animal studies show that a ketogenic diet reduces tumor growth and improves survival rates. The diet may benefit cancer patients by starving cancer cells of glucose, lowering insulin levels, and preventing cancer cells from using ketones for fuel.
বাংলাদেশের অর্থনৈতিক সমীক্ষা ২০২৪ [Bangladesh Economic Review 2024 Bangla.pdf] কম্পিউটার , ট্যাব ও স্মার্ট ফোন ভার্সন সহ সম্পূর্ণ বাংলা ই-বুক বা pdf বই " সুচিপত্র ...বুকমার্ক মেনু 🔖 ও হাইপার লিংক মেনু 📝👆 যুক্ত ..
আমাদের সবার জন্য খুব খুব গুরুত্বপূর্ণ একটি বই ..বিসিএস, ব্যাংক, ইউনিভার্সিটি ভর্তি ও যে কোন প্রতিযোগিতা মূলক পরীক্ষার জন্য এর খুব ইম্পরট্যান্ট একটি বিষয় ...তাছাড়া বাংলাদেশের সাম্প্রতিক যে কোন ডাটা বা তথ্য এই বইতে পাবেন ...
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9
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Date: May 29, 2024
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1. LIPID METABOLISM DISORDERS
RELATED TO CARNITINE
Sir. Stymass Kasty
SOKOINE UNIVERSITY OF AGRICULTURE
MOROGORO-TANZANIA
1/22/2018 Sir. Stymass Kasty 1
2. CONTENTS
INTRODUCTION.
β-OXIDATION OF FATTY ACIDS.
TRANSPORT OF FATTY ACIDS IN TO THE MITOCHONDRIA.
CARNITINE SHUTTLE
FATE OF ACYL-CARNITINE IN MITOCHONDRIA
INHIBITOR OF THE CARNITINE SHUTTLE
METABOLIC DISORDERS ASSOCIATED WITH CARNITINE
EPIDEMIOLOGY
DIAGNOSIS
LABORATORY FINDING
TREATMENT
CONCLUSION
REFFERENCES
1/22/2018 Sir. Stymass Kasty 2
3. INTRODUCTION
CARNITINE Is a specialized carrier protein (Low
molecular weight compound), which transports the
long chain fatty acyl groups from the cytosol in to the
mitochondrial matrix.
SOURCES OF CARNITINE IN THE BODY
From the diet, primarily in Meat products.
Synthesis from amino acids, LYSINE and
METHIONINE by the enzymatic pathway found in
the liver and kidney.
1/22/2018 Sir. Stymass Kasty 3
4. β-OXIDATION OF FATTY ACIDS
This is a mitochondrial pathway; a major
pathway of the Catabolism of fatty acids in which
two-carbon fragments are successively removed
from the carboxyl group or end of the fatty Acyl
CoA, producing Acety CoA, NADH and FADH2.
Example of fatty acyl CoA is shown below,
[CH3-(CH2)x-CH2-CH2-C=O-S-CoA]
The energy yield from the β-oxidation
pathway is high.
1/22/2018 Sir. Stymass Kasty 4
5. TRANSPORT OF FATTY ACIDS IN TO THE
MITOCHONDRIA
Because β-oxidation occurs in the mitochondrial
matrics, the fatty acid must be transported across
the inner mitochondrial membrane that is
impermeable to Coenzme A (CoA).
After a long chain fatty acids enters a cell, they
are converted in the cytosol to its CoA
derivative by long-chain fatty acyl CoA
synthetase (thiokinase), an enzyme of the outer
mitochondrial membrane.
1/22/2018 Sir. Stymass Kasty 5
6. TRANSPORT OF FATTY ACIDS IN TO THE
MITOCHONDRIA
Fatty acids shorter than 12 Carbons gets activated
to their CoA derivatives inside the mitochondria
by matrix enzymes, and are oxidized.
The entry of short and medium chain fatty acids
in to the mitochondria do not require the help of
membrane transporters.
Those fatty acids with 14-Carbon or more can not
pass directly through the mitochondria
membrane.
1/22/2018 Sir. Stymass Kasty 6
7. TRANSPORT OF FATTY ACIDS IN TO THE
MITOCHONDRIA
The transport of long chain fatty acids (LCFA)
in to the mitochondria requires a specialized
carriers. These carriers are called CARNITINE.
This rate limiting transport process is called
CARNITINE SHUTTLE.
Carnitine deficiency leads to the occurance of
among of the LIPID METABOLISM DISORDERS.
1/22/2018 Sir. Stymass Kasty 7
8. CARNITINE SHUTTLE
Three enzymatic reactions are involved.
1st Reaction; The acyl group is transferred
from CoA to carnitine by Carnitine
acyltransferase-I (CAT-I). This reaction forms
acylcarnitine and regenerate free CoA.
2nd Reaction; The Acylcarnitine is transported
in to the mitochondrial matrix in exchange for
free carnitine by carnitine-acylcarnitine
translocase (Facilitated diffusion).
1/22/2018 Sir. Stymass Kasty 8
9. CARNITINE SHUTTLE
3rd Reaction; Carnitine acyltransferase-II an
enzyme of the inner mitochondrial membrane
catalyses the transfer of the acyl group from
carnitine to CoA in to the mitochondrial
matrix in which free Carnitine is regenerated.
1/22/2018 Sir. Stymass Kasty 9
11. FATE OF ACYL-CARNITINE IN
MITOCHONDRIA
Once in the mitochondrial matrix,acyl-
carnitine is converted to the acyl-CoA and
regenerating carnitine.
The enzyme involved is carnitine
acyltransferase II.
Then carnitine move from matrix to the
cytosol for transporting another LCFA.
The acyl-CoA enter the β-Oxidation.
1/22/2018 Sir. Stymass Kasty 11
12. INHIBITOR OF THE CARNITINE
SHUTTLE
Malonyl CoA inhibits Carnitine
acyltransferase-I (CAT-I) thus preventing the
entry of Long chain acyl groups in to the
mitochondrial matrix.
Example; Newly made palmitate in the cytosol
can not be transferred in to the mitochondria
and dagraded in the presence of Malonyl CoA.
1/22/2018 Sir. Stymass Kasty 12
14. CARNITINE DEFICIENCIES
These can be broadly classified in to two
groups;
Primary carnitine deficiencies and
Secondary carnitine deficienices.
These deficiencies result in a decreased
ability of the tissues to use long-chain fatty
acids (LCFA) as a metabolic fuel.
1/22/2018 Sir. Stymass Kasty 14
15. PRIMARY CARNITINE DEFICIENCY
Congenital deficiencies in one of the
Carnitine-acyltransferase (CAT) system which is also
known as Carnitine palmitoyltransferase (CPT)
system or Mutations in the SLC22A5 gene (making
of OCTN2 protein-transport Carnitine in to cells)
Genetic Carnitine palmitoyl transferase I (or CAT-
1) deficiency which affects the liver. This result in
a decreased or inability of the liver to synthesize
glucose during a fast.
1/22/2018 Sir. Stymass Kasty 15
16. PRIMARY CARNITINE DEFICIENCY
This can lead to;
i. Severe hypoglycemia
ii. Coma and
iii. Death
Genetic Carnitine palmitoyltransferase-II (or
CAT-II) deficiency which occur primarly in
Cardiac and Skeletal muscles.
1/22/2018 Sir. Stymass Kasty 16
17. PRIMARY CARNITINE DEFICIENCY
There are three main forms of CAT-II based on tissue-
specific symptomology and age of onset.
1.MYOPATHIC FORM.
Most common form of the disorder.
Mild to severe adult form with the following
symptoms.
Rhabdomyolysis (release of myoglobin due to
breakdown of muscle fibers).
Myalgia (muscle pain) and weakness.
Myoglobinuria (myoglobin in urine).
.
1/22/2018 Sir. Stymass Kasty 17
18. PRIMARY CARNITINE DEFICIENCY
2.MULTISYSTEMIC FORM.
It is severe infantile form.
Involves multiple organ systems
Symptoms occur between 6 and 24 months of
age.
Characterized by the following symptoms.
Hypoketotic
Acute liver failure.
Hepatomegaly.
Cardiomyopathy.
1/22/2018 Sir. Stymass Kasty 18
19. PRIMARY CARNITINE DEFICIENCY
3.NEONATAL FORM.
It is a lethal form in neonatal.
It is the least common clinical presentation of
this disorder.
Symptoms occur just hours after birth to
within 4 days of life
Symptoms are; Encephalopathy, confusion,
Hypoglycemia, liver failure, Cardiomyopathy
and muscle weakness.
1/22/2018 Sir. Stymass Kasty 19
20. SECONDARY CARNITINE DEFICIENCY
This may occur in many situations, such as;
A patient with liver disease causing decreased
synthesis of Carnitine.
Individual suffering from malnutrition and those
on strictly vegetarian diets.
Those with an increased requirements for
carnitine as a result of, for instance, Pregnancy,
severe infection, burns or trauma
Those undergoing Haemodialysis, which removes
carnitine from the blood.
1/22/2018 Sir. Stymass Kasty 20
21. EPIDEMIOLOGY
Primary systemic carnitine deficiency was
estimated in Japan to occur in 1 per 40,000
births (1:40,000).
In Australia, the incidence has been estimated to
be between 1:37,000 to 1:100,000 newborns
The frequent of this condition is not known
However, in UK the previous report identified 4
affected mothers in 62,004 infants screened, with
a frequency of 1 per 15,500 (1:15,500).
1/22/2018 Sir. Stymass Kasty 21
22. DIAGNOSIS
In neonates, carnitine palmitoyltransferase
deficiency (CPT) is diagnosed using mass
spectrometry to screen blood.
Prenatal diagnosis may be possible using
amniotic villous cells.
In adults, the definitive diagnosis is based on
acylcarnitine levels in serum, urine, and
tissues(muscle and liver for systemic deficiency;
muscle only for myopathic deficiency).
1/22/2018 Sir. Stymass Kasty 22
24. TREATMENT
Avoid prolonged fast
Adopting a diet high in carbohydrate
Adopting a diet low in Long-chain fatty acids
Supplements with medium chain fatty acids
and Carnitine. This is because their oxidation
is not dependent on CPT-I hence it is not
subject to inhibition by malonyl CoA.
Treated by giving L-carnitine 25mg/kg per 6
hours.
1/22/2018 Sir. Stymass Kasty 24
25. PROGNOSIS
Infantile metabolic and childhood myopathic
forms of the conditions can be FATAL if
untreated.
Long-term prognosis is exellent with oral
Carnitine supplimentation.
If the disorder is not recognised for a long
time, death can occur due to Cardiac failure,
hypoglycemia and arrhythmias or sudden
death.
1/22/2018 Sir. Stymass Kasty 25
26. CONCLUSION
Carnitine is thus considered as a
“conditionally essential nutrient” since
individuals requirements might exceed dietary
intake during specific disease states.
1/22/2018 Sir. Stymass Kasty 26
27. REFERENCES
• Richard H & Denise F. (2011).Lippincott’s Illustrated
Reviews: Biochemistry, 5th ed.
• Ayman W El-Hattab. Systemic primary carnitine
deficiency. GeneReviews .November 3,2016;
• Carnitine transporter defficiency. Screening,
Technology and Research in Genetics
(STARG).2/20/2016;
• Agnetti A, Bitton L, Techana B, Raymond A and
Caranon. Primary carnitine deficiency dilated
cardiomyopathy:28 years follow-up. Jun 2 2012;
1/22/2018 Sir. Stymass Kasty 27