1. The document describes the role of HDL in plasma lipid transport between tissues like the liver and adipose tissue.
2. Lipids like triglycerides, cholesterol, and fatty acids are transported from the liver via VLDL particles and taken up by tissues through lipoprotein lipase.
3. HDL plays a role in reverse cholesterol transport, ferrying cholesterol from tissues back to the liver for processing or excretion.
ALT is an enzyme present in liver, heart skeletal muscles, highest concentration is present in Liver. it value increases when there is abnormality in liver, ALT is an amino transferase which transfer one amino group from an amino acid and transfer to another substance for production of non essential amino acid
biological characteristics of the enzyme. How it works, what it is, how it is measured, interferences to the tests and applications in clinical pathology
Diagnostic enzymology
Enzymes are normally intracellular and LOW concentration in blood
Enzyme release (leakage)in the blood indicates cell damage (cell –death, hypoxia, intracellular toxicity)
Quantitative measure of cell/tissue damage
Organ specificity- but not absolute specificity inspite of same gene content.
Most enzymes are present in most cells-differing amounts
Liver function tests (LFT’s) are groups of laboratory blood assays designed to give information about the state of patients liver
They include
Liver enzymes (SGOT, SGPT, ALP, GGT etc.,)
Bilirubin(Direct and indirect)
Albumin
Prothrombin time / INR
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.
ALT is an enzyme present in liver, heart skeletal muscles, highest concentration is present in Liver. it value increases when there is abnormality in liver, ALT is an amino transferase which transfer one amino group from an amino acid and transfer to another substance for production of non essential amino acid
biological characteristics of the enzyme. How it works, what it is, how it is measured, interferences to the tests and applications in clinical pathology
Diagnostic enzymology
Enzymes are normally intracellular and LOW concentration in blood
Enzyme release (leakage)in the blood indicates cell damage (cell –death, hypoxia, intracellular toxicity)
Quantitative measure of cell/tissue damage
Organ specificity- but not absolute specificity inspite of same gene content.
Most enzymes are present in most cells-differing amounts
Liver function tests (LFT’s) are groups of laboratory blood assays designed to give information about the state of patients liver
They include
Liver enzymes (SGOT, SGPT, ALP, GGT etc.,)
Bilirubin(Direct and indirect)
Albumin
Prothrombin time / INR
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.
synthesis and lipolysis is explained in detail. enzymes involved and their differences are tabulated. adipose tissue metabolism is also included. Fatty liver causes are explained in detail. obesity is briefly described.
1. Plasma Lipid Transport
Role of HDL
Philip Barter, MBBS, FRACP, PhD
Professor and Director
The Heart Research Institute, Sydney,
Source: International Chair on Cardiometabolic Risk
www.cardiometabolic-risk.org
Australia
Cholesterol of dietary origin is taken up by the liver where it combines with cholesterol newly synthesised in the liver. This cholesterol is subsequently esterified. Triglyceride is formed in the liver either from newly synthesis fatty acids or from free fatty acids (FFA) released from adipose tissue. The cholesteryl esters and triglyceride are incorporated into VLDL.
The VLDL (and the cholesterol they contain) are subsequently secreted into plasma.
Once in plasma the triglyceride in VLDL is broken down by lipoprotein lipase, releasing free fatty acids for uptake by tissues.
As it loses its triglyceride, the VLDL particle becomes progressively smaller and, in a complex series of reactions, is ultimately converted into a triglyceride-poor, cholesterol-rich LDL particle.
The cholesterol in LDL is subsequently delivered to tissues following binding of the particles to LDL receptors. Since the level of expression of the LDL receptor is increased in cells that are depleted of cholesterol and decreased in cells that are overloaded with cholesterol, this process ensures that the cholesterol in LDL is delivered precisely where it is needed, whether this is a return of the cholesterol to the liver or an uptake of cholesterol by cells in extrahepatic tissues.
New synthesis also contributes to cellular cholesterol.
Only the liver and those endocrine tissues that synthesise steroid hormones have the ability to metabolise the cholesterol molecule. Other tissues are totally dependent on an efflux to acceptors in the extracellular space to remove their surplus cholesterol. The predominant extracellular acceptors are HDLs. There are at least three distinct processes (mediated by activities of ABCA1, ABG1 and SR-B1) that promote the efflux of cholesterol from cells. Lecithin:cholesterol acyltransferase (LCAT) esterifies cholesterol on the surface of HDL particles in a process that moves the cholesterol into the inside of the particle.
Once the cholesterol has been transferred from cells to HDLs in the extracellular space, it may be delivered to the liver in a process involving binding of HDLs to SR-B1.
The cholesterol taken up by the liver may be recycled into VLDL.
The cholesterol taken up by the liver may also be released into bile, either as unchanged cholesterol or after being converted into bile acids.
In some species, including humans, non-human primates and rabbits, the cholesterol in HDL may also be delivered to the liver by an indirect pathway involving the cholesteryl ester transfer protein-mediated transfer of HDL cholesteryl esters to the VLDL/LDL fractions, with delivery to the liver then being achieved by the receptor-mediated uptake of LDL.
In diabetes and the metabolic syndrome there is an increase in release of free fatty acids (FFA) from adipose tissue. A proportion of this is taken up by the liver and converted into triglyceride.
This leads to an increased synthesis and secretion of VLDL and an increase in concentration of VLDL triglyceride in plasma.
There is also a decreased activity of lipoprotein lipase resulting in a decreased rate of breakdown of triglyceride and a further increase in the concentration of triglyceride in plasma.
A decrease in delivery of cell cholesterol to HDL has the capacity to decrease the concentration of HDL cholesterol.
An increase in the cholesteryl ester transfer protein-mediated transfer of cholesterol from HDL to the expanded VLDL pool further reduces the concentration of HDL cholesterol.
