Fatty acid transport/Obesity Flashcards
(43 cards)
What are the main dietary lipids?
Triglycerides (60-100g/day), cholesterol, and phospholipids
How are triglycerides digested and absorbed?
Broken down by lipases in the small intestine into monoacylglycerols and fatty acids → reassembled into triglycerides in intestinal cells.
How is cholesterol absorbed?
Solubilized by bile salts and transported via lipoproteins.
What is the structure of lipoproteins?
Hydrophobic core (triglycerides, cholesterol esters) and hydrophilic surface (phospholipids, apolipoproteins).
Chylomicrons
Function: Transport dietary triglycerides from intestine to tissues (muscle/adipose).
Key Apolipoprotein: ApoB-48.
Unique Feature: Largest lipoprotein; present only post-meal
VLDL (Very Low-Density Lipoprotein):
Function: Liver → transports endogenous triglycerides to tissues.
Key Apolipoprotein: ApoB-100.
Fate: Loses triglycerides → becomes IDL → LDL.
LDL (Low-Density Lipoprotein):
Function: Delivers cholesterol to peripheral tissues via LDL receptors.
Clinical Link: High LDL → atherosclerosis. Mnemonic: “LDL = Lethal.”
HDL (High-Density Lipoprotein):
Function: Reverse cholesterol transport (tissues → liver).
Clinical Link: High HDL reduces heart disease risk. Mnemonic: “HDL = Healthy.”
IDL (Intermediate-Density Lipoprotein):
Origin: VLDL after triglyceride loss.
Fate: Taken up by liver or converted to LDL.
Fed State:
Process:
Chylomicrons deliver triglycerides to tissues.
Lipoprotein lipase (activated by ApoC-II) releases fatty acids.
Cholesterol transferred to HDL → liver uptake as chylomicron remnants (via ApoE).
Fasted State:
Process:
Liver produces VLDL → releases triglycerides.
VLDL → IDL → LDL.
HDL collects cholesterol from tissues → liver for excretion.
Clinical Aspects
Familial Hypercholesterolemia:
Cause: Defective LDL receptors → high LDL → atherosclerosis.
Symptoms: Xanthomas, early heart disease.
Role of Lipoprotein Lipase:
Function: Hydrolyzes triglycerides in chylomicrons/VLDL. Activated by ApoC-II.
HDL and Cholesterol Ester Transfer:
Process: LCAT (lecithin-cholesterol acyltransferase) esterifies cholesterol for HDL transport.
Atherosclerosis Risk Factors:
Key Players: Oxidized LDL → foam cells → plaques.
Lipoprotein Density Order:
“Chylomicrons Very Large, In Line, HDL Helps” (Chylomicrons → VLDL → IDL → LDL → HDL).
SAQ Practice
Q1: Describe the journey of a chylomicron from formation to clearance.
Formed in intestinal cells → lymphatic system → bloodstream → lipoprotein lipase (ApoC-II) releases fatty acids to tissues → remnant (rich in cholesterol) taken up by liver via ApoE receptors.
Q2: Contrast LDL and HDL functions.
A2: LDL delivers cholesterol to tissues (atherogenic), HDL removes cholesterol to the liver (protective).
Define obesity and discuss the limitations of BMI as a measurement tool.
Obesity is a disorder of energy balance where excess energy is stored as fat. BMI (weight/height²) is commonly used but flawed—it doesn’t distinguish fat from muscle (e.g., athletes with high BMI) and may miss high body fat in individuals with sarcopenia (muscle loss).
Why is waist-to-hip ratio (WHR) a better indicator of health risks?
WHR >1.0 (men) or >0.8 (women) indicates central (visceral) obesity, which is strongly linked to metabolic diseases (e.g., diabetes, CVD) compared to subcutaneous fat.
Explain the energy balance equation and its implications.
ΔBody weight = Energy intake – Energy expenditure. Obesity arises from prolonged positive energy balance. However, obese individuals often have higher resting metabolic rates (RMR) due to larger body mass, but RMR decreases post-weight loss, necessitating sustained dietary control.
Discuss the role of leptin in obesity.
Leptin, produced by adipose tissue, signals satiety and increases energy expenditure. Obese individuals are leptin-resistant, blunting its effects. Rare leptin deficiency (as in mice) causes severe obesity, but in humans, resistance is more common, driven by genetic/epigenetic factors.
What are “thrifty genes,” and how do they contribute to obesity?
Thrifty genes evolved to favor fat storage during famine. In modern environments with abundant food, these genes predispose to obesity (e.g., Pima Indians). Polygenic obesity involves multiple genes with small effects, complicating GWAS identification.
How does epigenetics influence obesity risk?
Heritable changes (e.g., DNA methylation, histone modifications) from parental obesity can alter gene expression in offspring. Drosophila and twin studies show epigenetic transmission of metabolic traits, linking environment to genetic regulation.
