This document provides information on various types of lipoproteins:
- It defines lipoproteins as biochemical assemblies containing both lipids and proteins that allow fats to move through water.
- It classifies lipoproteins based on density, electrophoretic mobility, and apolipoprotein content into chylomicrons, VLDL, IDL, LDL, and HDL.
- It describes the structure of lipoproteins consisting of a nonpolar lipid core surrounded by a surface layer of amphipathic lipids and proteins.
- It details the functions and metabolism of various lipoproteins including their role in transporting lipids between tissues and organs.
The high risks of lipids and its relevance towards the development of different cardiovascular diseases has been known to all where this present slide focuses on that only along with the different treatment procedures,.
The high risks of lipids and its relevance towards the development of different cardiovascular diseases has been known to all where this present slide focuses on that only along with the different treatment procedures,.
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.
Hyperlipidemia , dyslipidemia , and drug therapy
also Fat transport and metabolisim and pathophysiology of lipoprotein
clincal importance of
1. Hypertriglycredemia
2. Hypercholesterolemia
3.Combined hyperlipidemia
4. Some other lipoprotein disorders
Including disorder of HDL_C
the aim of sharing this material to help students and provide delayed information regarding topic.You all are most welcome for you suggestion to make i more easy, graspable and attractive.(easy to learn in creative way)
Coronary heart disease due to atherosclerotic process is the major cause of death.Lipids have been implicated for enhanced atherosclerosis. The major lipids involved are triacy glycerol and cholesterol which are transported in the plasma by lipoproteins. So a better understanding of lipid transport and its abnormalities is essential for medical and health professional students.
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.
Hyperlipidemia , dyslipidemia , and drug therapy
also Fat transport and metabolisim and pathophysiology of lipoprotein
clincal importance of
1. Hypertriglycredemia
2. Hypercholesterolemia
3.Combined hyperlipidemia
4. Some other lipoprotein disorders
Including disorder of HDL_C
the aim of sharing this material to help students and provide delayed information regarding topic.You all are most welcome for you suggestion to make i more easy, graspable and attractive.(easy to learn in creative way)
Coronary heart disease due to atherosclerotic process is the major cause of death.Lipids have been implicated for enhanced atherosclerosis. The major lipids involved are triacy glycerol and cholesterol which are transported in the plasma by lipoproteins. So a better understanding of lipid transport and its abnormalities is essential for medical and health professional students.
Lipoprotein introduction, their general characteristics, exogenous and endogenous metabolism focusing on chylomicron and vldl metabolism, ldl metabolism and HDL metabolism , reverse cholesterol transport.
Lipid Profile Tests.A lipid profile is a blood test that measures the concentrations of fats and cholesterol in the blood and can be used to assess so-called 'good cholesterol' versus 'bad cholesterol levels.
lipoproteins transfer lipids such as triacylglycerol, cholestryl ester, fat soluble vitamins in the body. there are 5 categories of lipoproteins which includes chylomicrone, VLDL, IDL, LDL and HDL. LDL-cholesterol is called bad cholestrol while HDL-cholesterol is called good cholesterol.
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.
A complete cholesterol test — also called a lipid panel or lipid profile — is a blood test that can measure the amount of cholesterol and triglycerides in your blood
Introduction
General structure of lipoprotein
Apo lipoprotein
Classification of lipoprotein
Chylomicron
LDL- low density lipoprotein
HDL- high density lipoprotein
VLDL- very low density lipoprotein
IDL- intermediate density lipoprotein
Clinical disorders
Preventive measures
Lipoprotein analysis
Diet , cholesterol and lipoprotein
Etiopathogenesis and pharmacotherapy of hyperlipidemias
a. the pathophysiology of selected disease states and the rationale for drug therapy;
b. the therapeutic approach to management of these diseases;
c. the controversies in drug therapy;
d. the importance of preparation of individualised therapeutic plans based on diagnosis;
e. needs to identify the patient-specific parameters relevant in initiating drug therapy,
and monitoring therapy (including alternatives, time-course of clinical and laboratory
indices of therapeutic response and adverse effects);
f. describe the pathophysiology of selected disease states and explain the rationale for
drug therapy;
g. summarise the therapeutic approach to management of these diseases including
reference to the latest available evidence;
h. discuss the controversies in drug therapy;
i. discuss the preparation of individualised therapeutic plans based on diagnosis; and
j. identify the patient-specific parameters relevant in initiating drug therapy, and
monitoring therapy (including alternatives, time-course of clinical and laboratory indices of therapeutic response and adverse effects).
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
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
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
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NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
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.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
3. Lipoprotein:
➢ Lipids absorbed from the diet and synthesized by the liver and
adipose tissue must be transported between various cells and organs
for utilization and storage.
➢ Lipids are insoluble in water, the problem of transportation in the
aqueous plasma is solved by associating nonpolar lipids
(triacylglycerol's and cholesteryl esters) with amphipathic lipids
(phospholipids and cholesterol) and proteins to make water-
miscible lipoproteins.
4. Definition:
A lipoprotein is a biochemical assembly that contains both proteins
and lipids, bound to the proteins , which allow fats to move through
the water inside and outside cells.
The proteins serve to emulsify the lipid molecules.
Many enzymes, transporters, structural proteins, antigens, and toxins
are lipoproteins.
6. Structure
Lipoproteins consist of a nonpolar core and a single surface layer of
amphipathic lipids
The nonpolar lipid core consists of mainly triacylglycerol and cholesteryl
ester and is surrounded by a single surface layer of amphipathic
phospholipid and cholesterol molecules
These are oriented so that their polar groups face outward to the aqueous
medium
The protein moiety of a lipoprotein is known as an apolipoprotein or
apoprotein.
7.
8. Classification
Lipoproteins can be classified in three ways-
1) Based on density-
They are separated by Ultracentrifugation.
Depending upon the floatation constant (Sf), Five major groups of
lipoproteins have been identified that are important physiologically
and in clinical diagnosis.
✓ Chylomicrons,
✓ VLDL
✓ IDL
✓ LDL
✓ HDL
9. (i)Chylomicrons,
-derived from intestinal absorption of triacylglycerol and other lipids;
-Density < 0.95 while
-mean diameter 100- 500 nm
(ii)Very low density lipoproteins (VLDL),
-derived from the liver for the export of triacylglycerol;
-density 0.95- 1.006
-mean diameter 30-80 nm.
(iii)Intermediate density lipoproteins (IDL)
- derived from the catabolism of VLDL,
-density 1.006-1.019
-mean 25-50nm.
10. iv) Low-density lipoproteins (LDL),
-representing a final stage in the catabolism of VLDL;
-density1.019-1.063
-mean diameter 18-28 nm
(iv) High-density lipoproteins (HDL),
-involved in cholesterol transport and also in VLDL and chylomicron
metabolism.
-Density 1.063-1.121
-mean diameter 5-15 nm.
11.
12. 2) Based on electrophoretic mobilities
➢ Lipoproteins may be separated according to their electrophoretic
properties into - pre β, β, and broad beta lipoproteins.
➢ The mobility of a lipoprotein is mainly dependent upon protein
content.
➢ Those with higher protein content will move faster towards the
anode and those with minimum protein content will have
minimum mobility.
13. ▪ HDL are -α , VLDL pre- β, LDL-β , and IDL are broad beta
lipoproteins.
▪ Free fatty acid and albumin complex although not a lipoprotein is
an important lipid fraction in serum and is the fastest moving
fraction.
▪ Chylomicrons remain at the origin since they have more lipid
content.
▪ VLDLs with less protein content than LDL move faster than
LDL, this is due to nature of apoprotein present.
14. 3) Based on nature of Apo- protein content
❑One or more apolipoproteins (proteins or polypeptides) are present
in each lipoprotein.
❑The major apolipoproteins of HDL (α-lipoprotein) are designated A.
❑The main apolipoprotein of LDL (β -lipoprotein) is apolipoprotein B (B-
100), which found also in VLDL.
❑Chylomicrons contain a truncated form of apo B (B-48) that is
synthesized in the intestine, while B-100 is synthesized in the liver.
❑Apo E is found in VLDL, HDL, Chylomicrons.
17. ✓ They are products of VLDL and IDL metabolism, and the most
cholesterol rich of all lipoproteins.
Low density lipoprotein is sometimes called "bad cholesterol“
LDL are the principal cholesterol and fat transporter in human
blood thatcarries cholesterol from the liver to the body tissues
and cells.
Function of LDLs :
18. Despite cholesterol's negative reputation, it's nevertheless an
important biomolecule that serves a number of vital purposes in
the body.
Appropriate levels of LDL cholesterol can positively impact health in
many ways.
In metabolism their function is mediating by cellular uptake via
receptor - mediated endocytosis followed by lysosomal degradation ,
and is strongly dependent on the lipid distribution .
19. Apart from their well-established role as lipid transporter,
LDL particles are intimately involved in the progression of
cardiovascular diseases such as atherosclerosis or stroke, which are
among the most prevalent causes ofdeath.
Raised plasma levels of LDL are linked to an increased risk for disease.
20. Metabolism of LDL
➢ About 40 to 60% of all LDL are cleared by the liver in a process
mediated by apo B and hepatic LDL receptors.
➢ The rest are taken up by either hepatic LDL or non-hepatic non-
LDL (scavenger) receptors.
Hepatic LDL receptors are down-regulated by :
delivery of cholesterol to the liver by chylomicrons, and by
increased dietary saturated fat.
They can be up-regulated by decreased dietary fat andcholesterol.
21. Non-hepatic scavenger receptors
most notably on macrophages.
take up excess oxidized circulating LDL not processed by hepatic
receptors.
Monocytes rich in oxidized LDL migrate into the sub-endothelial
space and become macrophages.
These macrophages are then take up more oxidized LDL and
form foamcells within atherosclerotic plaques .
23. HDL type is the smallest of the lipoprotein particles.
It is the densest because it contains the highest proportion of protein
to lipids.
Its most abundant apolipoproteins .
24. FUNCTION OF HDL:
High density lipoprotein (HDL) particles are protective particles that
have functions in the body.
They :
➢ Play a key role in protecting against heart disease via their role in
reverse cholesterol transport, or the transport of excess
cholesterol out of the body.
➢ Are also part of the innate immune system due to their ability to
bind a number of toxic substances in the blood.
25. HDL is synthesized and secreted from both liver and intestine .
However, apo C and apo E are synthesized in the liver and
transferred from liver HDL to intestinal HDL when the latterenters
the plasma.
A major function of HDL is to act as a repository for the apo C and
apo E required for the metabolism of chylomicrons and VLDL.
Synthesis of HDL
26. LCAT and the LCAT activator apo A-I—bind to the discoidal
particles, and the surface phospholipid and free cholesterol are
converted into cholesteryl esters and lysolecithin .
The nonpolar cholesteryl esters move into the hydrophobic interior
of the bilayer, whereas lysolecithin is transferred to plasma
albumin.
Thus, a nonpolar core is generated, forming a spherical,
pseudomicellar HDL covered by a surface film of polar lipids
and apolipoproteins.
This aids the removal of excess unesterified cholesterol from
lipoproteins and tissues .
27. Chylomicron
Chylomicron (from the Greek chylø, meaning juice or milky
fluid, and micron, meaning small particle) are lipoprotein particles
that consist of:
Triglycerides (85–92%),
Phospholipids (6–12%),
Cholesterol (1–3%),
Proteins (1–2%).
28. Function of chylomicron
✓ Chylomicrons transport lipids absorbed from the intestine to adipose,
cardiac and skeletal muscle tissue, where their triglyceride components are
hydrolyzed by the activity of lipoprotein lipase and the released free fatty
acids are absorbed by the tissue.
✓ When a large portion of the triacylglycerol core have been hydrolyzed,
chylomicron remnants are formed and are taken up by the liver, hereby
transferring dietary fat also to the liver.
✓ It transports dietary fats and cholesterol from intestines to tissues.
29. Metabolism of chylomicron
The enzyme lipoprotein lipase, with apolipoprotein (apo)C-II as a co-factor,
hydrolyzes chylomicron triglyceride allowing the delivery of free fatty acids
to muscle and adipose tissue.
As a result, a new particle called a chylomicron remnant is formed. This
particle is enriched in cholesteryl ester and fat-soluble vitamins and contains
apoB-48 andapoE.
It is rapidly removed from the circulation by the liver. ApoE is the moiety
required forrapid hepatic removal.
Its activity is inhibited by C apolipoproteins, especially apoC-I.
30. The particle must first achieve a size that allows it to be "sieved" through the
endothelial fenestre
Here, it may
1) be removed directly by LDL receptors.
2) acquire additional apoE that is secreted free into the space, and then be
removed directly by the LDL receptor-related protein (LRP);
3) it may be sequestered in the space. Sequestration occurs by binding of
apoE to heparan sulfate proteoglycans and/or binding of apoB to hepatic
lipase.
32. Function of VLDL
• VLDL transports endogenous triglycerides, phospholipids, cholesterol, and
cholesteryl esters.
• It functions as the body's internal transport mechanism for lipids.
• In addition it serves for long-range transport of hydrophobic intercellular
messengers, like the morphogen.
33. Metabolism of VLDL
VLDL metabolism is very similar to Chylomicrons metabolism.
The main lipid found in VLDL is also triacylglycerol, but in this case triacylglycerols come
from excess fatty acids on diet or an increase in the hepatic synthesis of fatty acids as a
consequence of excess carbohydrates in diet.
Fats coming from the hepatocytes uptake of Chylomicrons remnants are also a source of
triacylglycerols for VLDL.
Additionally to triacylglycerols, VLDL contains around 35 % of free and esterified
cholesterol, 35 % of phospholipids, and various apoproteins, including ApoB-100.
VLDL, in the same way than Chylomicrons, acquires in the blood stream Apo C-II and Apo E.
The functions of these apoproteins in VLDL are similar to their functions in Chylomicrons:
Apo C-II activates Lipoprotein Lipase and as a consequence, VLDL triacylglycerols are
hydrolyzed, so the proportion of cholesterol increases.
34. IDL (intermediate density lipoprotein)
-It’s formed from the degradation of very low-density lipoproteins.
Their size is, in general, 25 to 35 nm in diameter, and they contain primarily
a range of triacylglycerols and cholesterol esters.
35. Function of IDL
It enables fats and cholesterol to move within the water-based
solution of thebloodstream.
Each native IDL particle consists of protein that encircles various
fatty acids, enabling, as a water - soluble particle, these fatty
acids to travel in the aqueous blood environment as part of the fat
transport system within the body.
In general, IDL, somewhat similar to low-density lipoprotein (LDL),
transports a variety of triglyceride fats and cholesterol and, like
LDL, can also promote the growth ofatheroma.
41. Hyperlipoproteinemia
It is also known as hyperlipidaemia or hyperlipoproteinemia
In this case it is defined as a presence of raised or abnormal levels of
lipids and/or lipoproteins in the blood
This is abnormality is common in the general population, and is one of the
most important modifiable risk factors for coronary heart disease (CHD).
Dyslipidaemia is generally characterized by increased fasting
concentrations of total cholesterol (TC), LDL cholesterol (LDL-C), and
triglycerides (TG), in conjunction with decreased concentrations of HDL
cholesterol (HDL-C)
42. On diagnosing hyperlipoproteinemia, hyperlipidaemic status
should be evaluated to determine whether it is primary lipoprotein
disorder or secondary to any of a variety of metabolic diseases.
The diagnosis of primary hyperlipoproteinemia is made after
secondary causes have been excluded.
43. Hereditary Hyperlipoproteinemia's
✓ Familial Lipoprotein lipase deficiency (Type I Hyperlipoproteinemia).
✓ Characterized by high levels of chylomicrons and triglycerides and a
deficiency of lipoprotein lipase, an enzyme that accelerates the
breakdown of lipoproteins.
✓ Disease onset is usually in infancy.
✓ Type 1 has a pure elevation of triglycerides in the chylomicron fraction.
✓ These people sometimes get pancreatitis and abdominal pains, but they
do not seem to have an increase in vascular disease
44. Type II, broken into two subtypes, type II-a and type II-b.
Have elevated cholesterol.
Some have elevated triglycerides also.
The familial (genetic) versions of Type 2 often develop
xanthomas, which are yellow fatty deposits under the skin of the
knuckles, elbows, buttocks or heels.
They may also have smaller yellow patches on the eyelids.
Both subtypes display high levels of blood cholesterol.
People with type II-b also have high levels of triglycerides in their
blood. Disease onset is usually after age 20.
Type II Familial hypercholesterolemia
45.
46. DYSBETALIPOPROTEINEMIA
▪ also called broad beta disease.
▪ Accumulation of IDL, VLDL and chylomicron remnant.
▪ Elevated level of total cholesterol and triglycerides
▪ The disorder caused by Apo-E or Apo-E receptor.
▪ Diabetes, hypothyroidism are associated with type III
disorders.
▪ Type 3 appears in one in 10,000 people and elevates both
triglycerides and cholesterol with consequent vascular disease,
▪ Disease onset is usually in adults.
47. Abetalipoproteinemia
✓ Elevates only triglycerides and does not increase the risk of vascular
disease
✓ Genetic defect in the synthesis of Apo-B.
✓ Both chylomicron and VLDL are affected.
✓ Fat malabsorption occurs because chylomicron can not be formed by
intestine.
✓ Disease onset is usually during puberty or early adulthood.
48. Secondary hyperlipoproteinemia
Diabetes mellitus, because it alters the way the body handles its energy
needs, also affects the way it handles fats. The result is elevated triglycerides
and reduced HDL cholesterol. This effect is amplified by obesity
Hypothyroidisms a common cause of lipid abnormalities. The thyroid hormone
affects the rate of many chemical processes in the body, including the clearing of
fats from the blood. The consequence is usually an elevation of cholesterol
Kidney disease affects the blood's proteins and consequently the composition
of the fat packages. It usually raises the LDLs
Liver disease, depending on its stage and severity, can raise or lower any of the
blood fats
Alcohol raises triglycerides
Cigarettes smoking lowers HDL cholesterol, as does malnutrition and obesity.
49. ➢ Usually high lipid levels are asymptomatic
➢ Occasionally when fat levels are high, it can be deposited in skin and
tendons forming bumps called xanthomas (eyes and Achilles tendon)
➢ Very high triglyceride levels may cause liver to enlarge
➢ High lipids increase the risk of developing pancreatitis, which causes
severe abdominal pain and is sometimes fatal
➢ Human coronary atherosclerosis is a chronic inflammatory disease that is
superimposed on a background of lipid abnormalities.
➢ In humans, oxidized LDL in plasma and within atherosclerotic lesions is
strongly associated with coronary artery disease, acute coronary
syndromes, and vulnerable plaques
50. Factors
Levels of lipoproteins and lipids (LDL) increase slightly with age.
Other factors associated with increase of these are:
familial history
Obesity
diet high in saturated fat
Inactivity
alcohol consumption