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.
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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
How r lipids stored and where
TAG in adipose tossue
TAGs are hydrophobic and therefore stored in an anhydrous form in specialised tissue – adipose tissue
****Increased acetyl-CoA from alcohol oxidation would lead to an increase in__________
in the synthesis of fatty acids and ketone bodies.
Which reactive oxygen species is produced when molecular oxygen (O2) gains an electron?
Superoxide is produced by adding an electron to molecular oxygen.
Superoxide is also an important source of other reactive oxygen species such as hydrogen peroxide and hydroxyl radicals
Reactive oxygen species (ROS) damage to proteins can result in protein glycosylation. (TRUE or FASE?)
Glycosylation is a normal post-translational modification to some proteins not a consequence of oxidative damage.
Oxidative damage to proteins by free radicals includes hydroxylated adducts, di-tyrosine dimers, inappropriate disulphide bond formation and the formation of ring open species.
Name two sources of free radicals (oxidants) inside cells (i.e. endogenous sources)?
- The ETC is a major source of free radicals since electrons can occasionally accidently escape the chain and react with dissolved O2 to form superoxide.
- peroxidase enzymes, nitric oxide synthase (nitric oxide is a free radical) lipooxygenases, NADPH oxidase enzyme (used in “respiratory burst”), Xanthine oxidase and Monoamine oxidase.
Which enzyme is involved in protecting cells from oxidative damage by converting superoxide to H2O2 and O2
Superoxide dismutase (SOD).
Which enzyme protects cells from oxidative damage by converting H2O2 into H2O and O2
Catalase
why is paternal utilisation of glucose is reduced during the second half of pregnancy?
‘Decreased maternal utilisation of glucose’
paternal utilisation of glucose is reduced during the second half of pregnancy by switching tissues to the use of FFA.
This conserves glucose for the maternal brain and for supply the the fetus for growth.
Which class of hormone does adrenaline fall under?
amine
Which hormonal change would occur during the course of a marathon run?
rise in GLUCAGON would stimulates gluconeogenesis by activating PEPCK and fructose 1,6 bisphosphatase
What would the presence of Howell-Jolly bodies in circulating red blood cells be a sign of?
damaged spleen
just a recap Glyerol metabolism
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Functions of Acetyl Coa
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______________is an important polyunsatrutaed fatty acid as it is the starting point for the synthesis of eicosanids, which r a family of signalling molecules like Prostaglandins!
Arachadoinic acid
which hormone stimulates/ inhibits lipolysis?
adreniline, glucagon, GH, cortisol, thyroxine,
Insulin inhibits!
the process by which fatty acids are released as energy is called __________
B- oxidation!
which cells in our body cannot undergo B-oxidation & why?
RBC’s> cuz they dont have mitchondria
cell of CNS> bc they FFA cannot cross blood brain barrier!
Explain how tissues obtain the lipids they need from lipoproteins.
TAG’s are obtained from chylomicrons and VLDLs by the lipoprotein lipase present in the capillary bed of the tissue. This hydrolyses TAG to fatty acids and glycerol. The fatty acids are taken up by tissues and re-esterified to TAG using glycerol phosphate derived from glucose metabolism.
Cholesterol is obtained from LDLs by receptor mediated endocytosis. The LDL particles bind to LDL receptors on the surface of target cells. The receptor with its bound LDL is taken into the cell by endocytosis. The endosome is attacked by lysosomal enzymes releasing free cholesterol in the cell and destroying the receptor protein. The cholesterol is converted to cholesterol esters for storage. When the cell has enough cholesterol, cholesterol inhibits the synthesis of new LDL receptors and the uptake of cholesterol is reduced