Introduction to lipids Flashcards
Function of lipids (6)
Phospholipids and cholesterol in cell membranes
Triglyceride is a key energy store
Steroids and fatty acids play regulatory roles as hormones, vitamins and bile acids
Fat serves as thermal insulator
Lipid coating around nerves acts as electrical insulator
Oil/ wax on surface of skin repel water
Energy storage in cells
Cellular is stored short term:
- ATP
- redox agents (NADH, FADH2)
- ionic transmembrane gradients
Energy stored long term as large, stable, efficient energy precursors:
- carbohydrates
- fats
Beta oxidation
Pathway from fatty acids to acetyl CoA
Fatty acid —> Acetyl CoA + e-(ATP)
Lipogenesis
Pathway from acetyl CoA to fatty acids
Depends on fatty acid synthase
Acetyl CoA + ATP + e-(ATP) —> fatty acid + CO2 + CoA
Carbohydrate as energy
Starch is digested into sugars in the gut
Sugars absorbed from gut into blood stream
Sugars absorbed by liver and stored as glycogen
Sugars stored throughout body as glycogen
Glycogen broken down to glucose when needed
Fatty acids
Simple straight carbon chains and COOH
In humans mostly 16-20 carbons long
Monounsaturates
One carbon carbon double bond
Polyunsaturates
Two or more carbon carbon double bonds
Essential fatty acids
Must be in the diet as cannot be made by mammals
Triglycerides
Not acidic
Synthesised from glycerol and 3 fatty acids
Lipoprotein lipase
Required to break down TG into 3 fatty acids and glycerol in the periphery
Cell surface linked enzyme in capillary walls
TG cannot go through cell membranes
Hepatic lipase
Required to beak down TG into 3 fatty acids and glycerol in the blood vessels of the liver
Cholesterol
Essential component of cell membranes, precursor of bile acids, steroid hormones and vitamin D
Sourced from diet or made in the liver
Cholesterol esters
Made from free cholesterol in the plasma by LCAT
Addition of long chain fatty acid to cholesterol
Steroids (6)
Cholesterol Cortisol Testosterone Aldosterone Oestrogen Progesterone
Acetyl Coenzyme A
Main energy production precursor
H2O added to break bond between acetyl group and Coenzyme A
Ketone bodies
3 soluble chemicals
Made from acetyl CoA during fasting
Last for 5 hours
Acetoacetic acid, beta-hydroxybutyric acid, acetone
Saturated fats
Less vulnerable to rancidity
More solid at room temperaure
Unsaturated fats
At least one double bond
More liquid at body temperature
Most naturally ocurring are cis so kink
4 lipid transport pathways
Exogenous: from gut to liver and periphery
Endogenous: from liver to periphery
Reverse cholesterol transport: from periphery to liver
Bile production: from liver into digestive tract
Exogenous pathway
From gut to liver and periphery
Lipids from diet packaged by small intestine into chylomicrons
Chylomicrons taken up by liver
Endogenous pathway
From liver to periphery (stored in adipose and muscle)
Lipid from liver packaged into VLDL
Reverse cholesterol transport
From periphery to liver
Occurs when lipid supplies in liver are being exhausted
HDL in blood indicated reverse path activity
Bile production
From liver into gut and gall bladder (bile released into cystic duct)
Cholesterol converted into bile acids (emulsifies fats)
Most bile acids reabsorbed by gut, returned to liver and recycled
Lipoprotein particles
Soluble and can carry lipids Vary in size depending on: - triglyceride content - cholesterol content - apolipoprotein content - stage in circulation through the body
Apolipoproteins
Proteins in LP particles that can hold lipids
Amphipathic
Lipid density
Protein is most dense
Cholesterol is middle density
Triglycerides are lowest density
Low density lipoprotein
Most dangerous lipoprotein
LDL content gets incorporated into atheromas
Left over after periphery absorbs endogenous TG from VLDL from liver
High density lipoprotein
The good lipoprotein
Reverse cholesterol transport
Appears when cholesterol is being used up
Very low density lipoprotein
Signifies risk of atheroma
Used to transport endogenous cholesterol and TG from liver to adipose and muscle
After TG removed by periphery from VLDL, leaves IDL
Intermediate density lipoprotein
Results from VLDL losing TG to periphery
IDL will become LDL
Sign of CV risk
Chylomicron
Not usually associated with CV risk
Normally high after fat containing meals
Carries lipids from gut to periphery for exogenous lipids
Insulin
Released by beta cells
Decrease blood glucose levels
Glucagon
Released by alpha cells
Increase blood glucose levels
Type 1 diabetes
No insulin is made
Type 2 diabetes
Insulin resistance
Relative insulin deficiency
Caused by obesity and genetic predisposition
Symptoms of type 2 diabetes
Excess thirst, frequent urination, constant hunger
Hypercholesterolaemia
High fasting levels of plasma cholesterol
Increased risk of arteriosclerosis
Due to combination of environmental and genetic factors
Statins
Drugs use to treat hypercholesterolaemia
- block endogenous cholesterol synthesis
- block HMG-CoA reductase (entry step into cholesterol synthesis)
e.g. simvastin
Simvastin
One of the most commonly prescribed drugs
Especially in men over 50
Prescribed for CAD prophylaxis
Metabolic syndrom
Group of risk factors that lead to increased risk for CAD, stroke, type 2 diabetes
- insulin resistnace
- central obesity
- high blood pressure
- high plasma cholesterol
