Lipid Metabolism Flashcards
describe the various classes of lipids
1. Fatty acid derivatives
- Fatty acids – fuel molecules.
- Triacylglycerols (triglycerides) – fuel storage and insulation
- Phospholipids – components of membranes and plasma lipoprotein
2. Hydroxy-methyl-glutaric acid derivatives
- Cholesterol – membranes and steroid hormone synthesis
- Cholesterol esters – cholesterol storage
- Bile acids and salts – lipid digestion
3. Vitamins
AKED
what r the fat soluble vitamins?
AKED
what r ketone bodies?
water soluble fuel molecules produced by liver from fatty acids during periods of low food intake (fasting) or starvation.
Ketone bodies are important fuel molecules that can be used by all tissues containing mitochondria including the central nervous system.
why should there also be dietry restriction if u r giving advice for an obese person
Fatty deposits r high energy stores, theyre very difficult to lose
where does fatty oxidation take place?
in mitochondria
when triglycerides break down, and yield glycerol that goes to liver, what does this glycerol do? where do what about the fatty acids?
in non fasting>>goes to make TAG
fasting>> goes through glycolysis to make pyruvate
FFA= goes to liver via albumin and enters FA B-oxidation.
effects of glucagon and insulin in fat mobilisation
glucagon= stimulates Insulin=inhibits
explain how, when and why ketone bodies are formed
they spare glucose in early starvation/diabetes.
r produced from acetyl-CoA in the mitochondrial matrix of hepatocytes when carbs r so scarce that energy must be obtained from breaking down FFA. (which will become acetyl coa> HMGca> Acetoacetate and so on))
The kidney can also produce ketone bodies under extreme conditions but at a much lower level than liver.
describe the central role of acetyl~CoA in metabolism
important intermediate in lipid biosynthesis.
main convergence point in catabolic pathways.
how is fatty acid transported into the mitochondria for b-oxidation
carnatine shuttle
what r the 3 ketone bodies produced in the body?
acetoacetate, acetone, B-hydroxybutyrate
describe how fatty acids r activated, where does this occur?
by linking to COENZYME A, in cytoplasm
**LOW EXTRACELLULAR GLUCOSE RESULTS IN FATTY ACID RELEASE AS AN ALTERNATIVE FUEL
yas
r lipids more reduced or more oxidised than carbs? what does this mean?
more REDUCED, meaning they have a higher energy content, they therefore release more energy when oxidised.
what is the typical daily energy requirement of a 70kg man?
11.000 kilojoules
stage 1 of metabolism of triacylglycerol
(hint: in SI)
hydrolised by pancreatic lipase in SI, a complex that requires bile salts & protein factor called Colipase
in fatty acid catabolism, which enzyme facilitates the activation of FA by linking coenzyme-A
Explain the process of fatty acid catabolism starting its release from adipose tissue into the liver.
Coenzyme A is derived from vitamin ____
fatty acyl CoA synthase
1) its gunna be activated by linking w/ co-enzyme A outside the mitochondria
2) Transported across the inner mitochondrial membrane using a carnitine shuttle
3) cycles through sequence of oxidative reactions, with C2 removed each cycle
B5!
what would inhibit the carnation shuttle?
Malonyl-CoA
during B-oxidation of FA, how many carbons r removed per cycle?
2 carbons
explain the pathway which glycerol can re-enter glycolysis
after phophorylation into glycerol phosphate &conversion to DHAP,
glycerol can now enter glycolysis
which enzyme converts glycerol to glycerol phosphate?
Glycerol kinase
in which organ r ketone bodies synthesised?
liver
products of b-oxidation
- acetyl coA–> enters kreb cycle
- NADH & FADH2–>goes to ETC
a patient was given Disulfiram and drank alcohol that day, he turned up with ‘hangover symptoms” what is disulfuram and how does it work & why did it cause a hangover?
treatment of chronic alcohol
inhibits enzyme aldehyde dehydrogenease
Acetate is NOT made when patient drank alchohol, aceytlaldehyde accumalated in blood causing hangover
