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Personal PoM MBC > cell metabolism 2 > Flashcards

cell metabolism 2 Flashcards

1
Q

what are the five main classes of lipids?

A 
free fatty acids
triacyl glycerides
phospholipids
glycolipids
steroids
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2
Q

what is a saturated fatty acid?

A

no carbon-carbon double bonds

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3
Q

what is an unsaturated fatty acid?

A

has at least one c-c double bond

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4
Q

how are fatty acids stored?

A

often as triacylglycerols in cytoplasm

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5
Q

what does the ester bond between glycerol and fatty acid do?

A

neutralise carboxylic acid group and keeps Ph in cells unaffected

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6
Q

what are the 3 primary sources of fats?

A

diet
de novo synthesis (in liver)
storage deposits in adipose

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7
Q

what are bile salts produced from?

A

cholesterol

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8
Q

where are bile salts generated and then stored?

A

liver then gall bladder

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9
Q

what is the role of bile salts?

A

to emulsify fats in the intestine aiding their digestion and absorption and fat soluble vitamins A,D,E and K

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10
Q

what does a lack of bile salts cause?

A

steatorrhea(fatty stool) due to more fat passing through the gut

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11
Q

what are the features of bile salts?

A

hydrophobic and a hydrophilic face

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12
Q

what is orlistat?

A

treatment for obesity. an inhibitor of pancreatic lipase, which means less fat is absorbed
main side effects are abdominal pain, need to defecate, increased flatus and steatorrhea

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13
Q

how are lipids transported in plasma?

A

via lipoproteins

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14
Q

what is the source and role of chylomicrons CM?

A

intestines. dietary fat transport

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15
Q

what is the source and role of very low density lipoproteins VLDL?

A

liver. endogenous fat transport

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16
Q

what is the source and role of intermediate density lipoproteins IDL?

A

VLDL(very low density lipoproteins). LDL precursor

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17
Q

what is the source and role of low density lipoproteins LDL?

A

IDL(intermediate density lipoproteins). cholesterol transport

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18
Q

what is the source and role of high density lipoproteins HDL?

A

liver. reverse cholesterol transport

19
Q

what absorbs digested dietary products?

A

enterocytes that line the brush border of the small intestine

20
Q

what happens to the digested fatty acids before they enter chylomicrons?

A

triglycerides are resynthesized

21
Q

where are the apoproteins in the chylomicron from?

A

HDL

22
Q

describe the anatomy of a chylomicron?

A

single phospholipid layer with integrated apoproteins surrounding the triglycerides

23
Q

how are chylomicrons transported?

A

in lymphatics and then into blood (from lacteals to the thoracic duct and to the left subclavian vein)

24
Q

what is lipoprotein lipase?

A

its located on capillary endothelial cells lining many tissues including adipose, heart and skeletal. breaks open chylomicron by binding to apoproteins

25
Q

what happens after the chylomicron is broken?

A

fatty acids undergo beta-oxidation and the glycerol is returned to the liver for gluconeogenesis

26
Q

outline the life cycle of a chylomicron

A

nascent chylomicron(no apoproteins)——————————>chylomicron(apoproteins transferred from HDL)—————>release of fatty acids and glycerol—–>uptake of remnants via liver

27
Q

outline the anatomy of a lipoprotein

A

phospholipid monolayer containing cholesterol and apoproteins surrounding a core of cholesterol esters and triacylglycerols

28
Q

outline the formation of cholesterol esters

A

cholesterol + phosphatidylcholine(lecithin)———–> cholesterol ester + lysophosphatidylcholine
enzyme: lecithin:cholesterol acyltransferase(LCAT)
occurs in plasma

29
Q

outline the lifecycle of lipoproteins

A

VLDL releases free fatty acids and glycerol——->lipid-depleted remnant transfers proteins to form a HDL and IDL———> IDL gain cholesterol esters and become LDL—————–> LDL is up taken by macrophage or liver

30
Q

compare HDL and LDL in terms of cholesterol

A

HDL- ‘good cholesterol’- take cholesterol from peripheral tissues to the liver for use or disposal (lowers total serum cholesterol)
LDL- ‘bad cholesterol’- prolonged elevation of LDL leads to atherosclerosis(hardening of arteries) more than 40% of the weight is cholesterol esters

31
Q

how much energy to fatty acids produce compared to carbohydrates?

A

around double

32
Q

how much of the bodies needs comes from fatty acid oxidation?

A

around half not including the brain

33
Q

outline how acyl CoA species are formed (step 1 of beta oxidation)

A 
fatty acid(RCOOH) + ATP + HS-CoA----------> Acyl CoA + RCO-S-CoA + AMP + 2Pi
enzyme: Acyl CoA synthetase
34
Q

outline the carnitine shuttle (method of producing acyl CoA in the matrix)

A

cytoplasmic side
carnitine + acyl CoA ——–> CoA + acyl carnitine( travels across translocase(membrane bound carrier protein))
enzyme: carnitine acyltransferase I
matrix side
acyl carnitine + CoA ———> Acyl CoA + carnitine (travels across translocase)
enzyme: carnitine acyltransferase II)

35
Q

outline primary carnitine deficiency

A

autosomal recessive disorder
symptoms: encephalopathies( cardiomyopathies, muscle weakness and hypoglycaemia)
presents during infancy or early childhood
caused by mutations in SLC22A5 gene which encodes a carnitine transporter so reduces uptake of carnitine

36
Q

outline the beta-oxidation cycle

A

sequence of oxidation—>hydration—->oxidation—->thiolysis
produces one molecule of acetyl CoA and an acyl CoA species that is 2 carbons shorter than the original aswell as an FADH2 and NADH
this continues until a 4 carbon acyl CoA is formed which then produces 2 molecules of acetyl CoA

37
Q

what causes ketone body formation?

A

when fat breakdown is greater than carbohydrate
‘‘fat burns in the flame of the carbohydrate’’ acetyl CoA from beta oxidation can only enter TCA cycle if carbohydrate metabolism and beta oxidation are balanced

38
Q

what are the ketone bodies?

A

acetoacetate, acetone, D-3-hydroxybutyrate

39
Q

what enzymes are involved in lipogenesis?

A

acetyl CoA carboxylase and fatty acid synthase

40
Q

how are fatty acids formed?

A

by decarboxylative condensation reactions involving acetyl-CoA and malonyl-CoA

41
Q

what happens after each round of elongation(of the fatty acid)?

A

reduction and dehydration by sequential action of a ketoreductase(KR), dehydratase(DH) and enol reductase

42
Q

what is the growing fatty acyl group linked to?

A

acyl carrier protein(ACP)

43
Q

compare fatty acid synthesis and degradation

A

synthesis
cytoplasm-NADPH(reducing power)-ACP(carrier)
degradation
mitochondrial matrix-FAD/NAD+(reducing powers)-CoA(carrier)

44
Q

outline medium chain acyl-coenzyme A dehydrogenase deficiency(MCADD)

A

autosomal recessive (predominantly in Caucasians)
can be fatal (1/100 sudden infant death syndrome)
patient should never go without food for more than 10-12 hours should have high carb diet
patients with an illness resulting in appetite loss or severe vomiting can have IV glucose

Personal PoM MBC (8 decks)

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