Lipid Metabolism Flashcards
(5 cards)
Describe the physiological functions of cholesterol i.e. as a component of biological membranes and as a precursor for steroid and bile salt synthesis.
Cholesterol is a lipid molecule essential for many physiological processes. It is both obtained from the diet and synthesized in the body (mainly in the liver).
Functions:
Component of Cell Membranes:
Stabilizes and regulates membrane fluidity and integrity.
Reduces permeability to small water-soluble molecules.
Embedded among phospholipids in the lipid bilayer.
Precursor for Steroid Hormones:
Cholesterol is the starting molecule for synthesis of:
Glucocorticoids (e.g. cortisol)
Mineralocorticoids (e.g. aldosterone)
Sex hormones (e.g. estrogen, testosterone)
Precursor for Bile Acids and Bile Salts:
Bile acids (e.g., cholic acid) are synthesized from cholesterol in the liver.
Aid in fat digestion and absorption in the intestine by emulsifying dietary lipids.
Precursor for Vitamin D:
7-dehydrocholesterol (a derivative of cholesterol) in the skin converts to vitamin D upon exposure to UV light.
Describe and provide examples of saturated and unsaturated fatty acids and their relevance in human health.
Fatty Acids are hydrocarbon chains with a terminal carboxylic group.
Saturated Fatty Acids (SFAs):
No double bonds between carbon atoms.
Solid at room temperature.
Found in animal fats, butter, coconut oil.
Examples:
Palmitic acid
Stearic acid
Health Impact:
Excess intake may increase LDL (“bad”) cholesterol.
Associated with higher risk of cardiovascular disease (CVD).
Unsaturated Fatty Acids:
One or more double bonds in the chain.
Liquid at room temperature.
Types:
Monounsaturated (MUFA) – one double bond (e.g., oleic acid in olive oil).
Polyunsaturated (PUFA) – multiple double bonds (e.g., linoleic acid, omega-3, and omega-6).
Health Impact:
Reduce LDL and may increase HDL (“good”) cholesterol.
Anti-inflammatory effects (especially omega-3s).
Protective against CVD.
Describe the physical and chemical properties of free cholesterol and cholesterol esters in relation to their distribution in the body and transport in the plasma.
Free (Unesterified) Cholesterol:
Amphipathic: has both hydrophilic (hydroxyl group) and hydrophobic parts.
Found in cell membranes and lipoprotein surfaces (e.g., HDL, LDL).
Can move between membranes and blood.
Cholesteryl Esters:
Formed when cholesterol is esterified with a fatty acid.
Fully hydrophobic.
Stored in lipid droplets, transported inside lipoprotein cores (especially in LDL and VLDL).
Inert and cannot be used directly by cells without being hydrolyzed.
Distribution & Transport:
In blood, cholesterol is carried by lipoproteins:
HDL: picks up cholesterol from tissues (“good cholesterol”).
LDL: delivers cholesterol to tissues (“bad cholesterol”).
LCAT (lecithin–cholesterol acyltransferase) converts free cholesterol to esters in HDL for transport.
Outline the process of cholesterol synthesis, the role of HMG-CoA reductase and its inhibitors in health and ischaemic heart disease
Synthesis:
Mainly occurs in the liver and intestines.
Key steps:
Acetyl-CoA → HMG-CoA
HMG-CoA → Mevalonate (rate-limiting step, catalyzed by HMG-CoA reductase)
Multiple steps → Squalene → Lanosterol → Cholesterol
HMG-CoA Reductase:
Rate-limiting enzyme in cholesterol biosynthesis.
Regulated by feedback inhibition (by cholesterol), hormones (insulin ↑, glucagon ↓), and gene expression.
Inhibitors (Statins):
Drugs like atorvastatin and simvastatin inhibit HMG-CoA reductase.
Lower LDL levels by reducing synthesis and increasing LDL receptor expression on liver cells.
Used in treatment and prevention of ischemic heart disease and hypercholesterolemia.
Describe the process of fatty acid synthesis and their hormonal control in human body.
Site:
Mainly occurs in liver, adipose tissue, and lactating mammary glands.
Takes place in the cytoplasm.
Process:
Acetyl-CoA (from mitochondria) is transported to cytoplasm as citrate.
Acetyl-CoA carboxylase (ACC) converts acetyl-CoA to malonyl-CoA.
Fatty acid synthase complex elongates the chain by adding two-carbon units to form palmitic acid (16:0).
Can be elongated/desaturated in the endoplasmic reticulum.
Hormonal Regulation:
Insulin: activates ACC and promotes fatty acid synthesis after a meal.
Glucagon and epinephrine: inhibit synthesis during fasting/stress.
