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protein control in cellular regulation > lipid metabolism > Flashcards

lipid metabolism Flashcards

1
Q

what are the general properties of lipids?

A

hydrophobic molecules that are structurally diverse and insoluble in water. they are more reduced than carbohydrates

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2
Q

what are the general properties of cholesterol?

A

has OH group, and regulates membrane fluidity. is the starting point for many reactions

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3
Q

what are ketone bodies formed from?

A

acetyl-CoA

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4
Q

where do lipids come from?

A

dietary sources, which are stored. some can also be synthesised

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5
Q

how are lipids transported?

A

in complex with proteins. on the interior, insoluble compounds are packaged away. on the exterior, there are phospholipids, free cholesterol and apolipoproteins

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6
Q

what is the role of apolipoproteins?

A

direct lipids to the appropriate place

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7
Q

what are chylomicrons?

A

small fat globules composed of protein and lipid. found in the blood and lymphatic fluid. used for transport of dietary lipids to tissues

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8
Q

what is apoCII?

A

an apolipoprotein that activates lipoprotein lipase, which hydrolyses TAGs that line the luminal wall of tissues

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9
Q

what are VLDLs composed of?

A

TAGs and cholesterol

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10
Q

what is the role of VLDLs?

A

carry newly synthesised lipids made in the liver around the body

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11
Q

what is apoB-100?

A

an apolipoprotein that allows uptake of lipid into the cells via LDL receptor

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12
Q

what happens when LDL receptors bind LDL?

A

the LDL receptor is internalised, recycled and the lipoprotein is degraded in endosomes

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13
Q

what is the role of HDL?

A

transports cholesterol and cholesterol esters back to the liver. activated by apoA

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14
Q

how are dietary lipids processed for uptake into intestinal mucosal cells?

A

FFAs and monoacylglycerols are very hydrophobic and require emulsification to micelles before they can be broken down by lipase into smaller FFAs

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15
Q

where are bile salts secreted from? what is the precursor for glycocholate?

A

gallbladder

cholesterol

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16
Q

how is lipid processing in the small intestine regulated?

A

endocrine cells secrete CCK or secretin. CCK slows gastric motility and stimulates the release of bile. secretin stimulates pancreatic secretions

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17
Q

where does synthesis of chylomicrons begin?

A

in the ER of intestinal epithelial cells

18
Q

how are chylomicrons formed?

A

apoE and apoCII are added from HDL in lymph and blood to form mature chylomicrons. they enter the blood stream and are transported to target tissues

19
Q

how are chylomicrons metabolised?

A

lipoprotein lipase hydrolyses TAGs -> glycerol +FFAs. apoCII acts as a cofactor

20
Q

where are fatty acids synthesised?

A

cytoplasm of the liver and adipose tissue

21
Q

what does acetyl-CoA carboxylase do?

A

adds carbonate group to CoA in the first step of fatty acid biosynthesis.

22
Q

what occurs in each step of fatty acid synthesis?

A

2 carbons are added on via acetyl-CoA, using 2NADPH

23
Q

how is acetyl-CoA carboxylase regulated?

A

the enzyme can exist in an active or inactive (phosphorylated) form. when energy is low, the enzyme is phosphorylated by AMP-activated protein kinase, insulin acts in the opposite way via phosphatase activity, promoted in the fed state

24
Q

what is a feedback inhibitor of acetyl-CoA carboxylase?

A

Palmitoylation-CoA - this is the endpoint of the pathway

25
Q

where is acetyl-CoA for fatty acid synthesis sourced from?

A

carbohydrate - excess carbohydrate is converted to acetyl-CoA via glycolysis
protein - excess protein is converted to acetyl-CoA via pyruvate dehydrogenase

26
Q

how are fats stored?

A

as triacylglycerol in adipose tissue

27
Q

how is fat mobilisation triggered?

A

in fasted conditions, a GPCR is activated, which activates PKA and adipose triglyceride lipase, this breaks TAGs into diacylglycerols. PKA also stimulates hormone sensitive lipase, which converts diacylglycerol into monoacylglycerol

28
Q

how is fat mobilisation by ATGL indirectly activated?

A

perilipin is phosphorylated, and interacts with AGTL, activating it.

29
Q

what does MAG lipase do?

A

breaks monoacylglycerols down to release fatty acids and glycerol into the blood

30
Q

what is the effect of insulin on fat mobilisation?

A

activates phosphatase, inactivates perilipin. this reduces the mobilisation of TAGs

31
Q

what is beta oxidation? where does it occur?

A

an oxidative process that releases a large amount of energy, it occurs in the matrix of the mitochondria

32
Q

what is produced and removed in each cycle of B-oxidation?

A

C2 removed

1 acetyl-CoA, 1NADH and 1FADH2 produced in each cycle

33
Q

how is fatty acyl-CoA transported into the mitochondria during B-oxidation?

A

via carnitine acyl shuttle in a process where the acyl group is removed before transport then a CoA group is added again inside

34
Q

when is an increase in fatty acid oxidation required?

A

when there is an increase in demand for ATP which cannot be met by an increase in glucose oxidation, or to provide an alternative fuel to glucose during starvation, during stress, or to provide an alternative fuel to glucose during trauma

35
Q

how is B-oxidation reciprocally regulated?

A

if acetyl-CoA carboxylase is fully active, it adds extra carbon to acetyl-CoA, producing malonyl-CoA. as the concentration of malonyl-CoA increases, the carnitine transport system becomes inactivated. when the concentration of malonyl-CoA decreases, rate of FA oxidation increases

36
Q

when are ketone bodies used?

A

formed from acetyl-CoA when fat breakdown predominates, e.g. during fasting or diabetes

37
Q

why do ketone bodies cause Ketoacidosis?

A

when in a prolonged fasted state, ketone bodies are secreted into the blood and taken to other tissues. they had acidic side chains, which cause the pH of the blood to drop

38
Q

what are the steps of cholesterol biosynthesis?

A

1- three acetate condense to form a Mevalonate
2- Mevalonate converts to phosphorylated 5C isoprene
3- six isoprenes polymerise to form a 30C linear squalene
4- squalene cyclises to form the four rings that are modified to form cholesterol

39
Q

what is the rate-limiting step for cholesterol biosynthesis?

A

formation of Mevalonate catalysed by HMG-CoA reductase

40
Q

what is simvastatin? how does it work?

A

a competitive inhibitor for HMG-CoA reductase
lowers endogenous production of cholesterol and causes the body to make more LDL receptors to promote the uptake of cholesterol

41
Q

how does sterol-dependent regulation of gene expression work?

A

when there is high [cholesterol/sterol], the sterol binds to SCAP, inducing an interaction with insulin induced gene protein. SREBP is tethered in the ER, and is subject to proteolytic cleavage, releasing sterol regulatory element, this causes transcriptional activation of HMG-CoA reductase

protein control in cellular regulation (10 decks)

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