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GI > Biochemistry > Flashcards

Biochemistry Flashcards

1
Q

What is glycogenesis?

A

synthesis of glycogen from glucose

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2
Q

what is glycogenolysis?

A

breakdown of glycogen to form glucose

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3
Q

what is gluconeogenesis?

A

de novo synthesis of glucose from metabolic precursors (lactate, amino acids, glycerol)

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4
Q

what is glycogen?

A

main storage form of glucose in liver and muscle cells.

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5
Q

what does liver glycogen do?

A

broken down between meals and released to maintain blood glucose levels for red blood cells and brain.

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6
Q

what does muscle glycogen do?

A

provides energy via glycolysis and the TCA during bursts of physical activity

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7
Q

what does a glycogen ‘primer’ covalently attach to?

A

a protein called glycogenin

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8
Q

what does glycogen synthase do?

A
  • synthesises glycogen from UDP-glucose
  • adds one glucose molecule to glycogen at a time
  • can only extend the chains of glycogen
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9
Q

what is the rate limiting enzyme of glycogensis?

A

glycogen synthase

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10
Q

what is glycogenolysis catalysed by?

A

glycogen phosphorylase

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11
Q

what is the rate limiting enzyme for glycogenolysis?

A

glycogen phosphorylase

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12
Q

where does lactate as a precursor for gluconeogenesis come from?

A

synthesised by skeletal muscle under anaerobic conditions

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13
Q

where does amino acids as a precursor for gluconeogenesis come from?

A

derived from muscle protein by proteolysis

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14
Q

where does glycerol as a precursor for gluconeogenesis come from?

A

derived from triglycerides by lipolysis in adipose tissue

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15
Q

what does gluconeogenesis require?

A

four unique liver enzymes.

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16
Q

what happens during the cori cycle?

A

blood transports lactate to liver, liver converts lactate back to glucose, glucose is released into blood stream.

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17
Q

when is lactate formed?

A

in fast-twitch muscle under conditions of heavy exercise

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18
Q

what do high levels of AMP or ADP mean?

A

low energy

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19
Q

what do high levels of ATP mean?

A

high energy

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20
Q

what do high/low levels of fructose 2,6-bisphosphate mean?

A

high in fed state

low in starved state

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21
Q

what do high levels of citrate, alanine, acetyl-CoA mean?

A

high when intermediates or building blocks abundant

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22
Q

what are glycogen storage diseases?

A

group of diseases with increased glycogen deposits in liver or muscle or both

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23
Q

what does increased fat intake without appropriate energy expenditure lead to?

A
  • increase in number of adipocytes

- more fat in adipocytes

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24
Q

what does control of energy balance depend on?

A
  • genetically linked factors e.g. protein messengers regulating appetite
  • environmental factors e.g. food abundance, fashionable foods
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25
Q

what can a deficiency in essential fatty acids lead to?

A

membrane disorders, increased skin permeability and mitochondrial damage

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26
Q

what are the fat soluble vitamins?

A

vitamins A,D,E and K

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27
Q

what are triglycerides?

A

main energy storage form in adipose tissue

28
Q

what is the structure of triglycerides?

A

consist of glycerol and 3 fatty acids

29
Q

what does aliphatic mean?

A

no rings

30
Q

what are the main natural fatty acids?

A

palmitic acid, stearic acid and oleic acid

31
Q

what lowers melting point?

A

double bonds

32
Q

what are the main products of fat absorption?

A

glycerol, fatty aids and monoglycerides

33
Q

what is lipolysis?

A

breakdown of lipids

34
Q

what has to happen to fatty acids before they can be oxidised to generate energy?

A

they have to be converted to CoA derivatives

35
Q

how much energy does fatty acid oxidation require?

A

2 ATP

36
Q

where does fatty acid oxidation occur?

A

cytoplasm

37
Q

what is the carnitine shuttle?

A

in the cytoplasm, fatty acids are transferred from acyl-CoA to carnitine.
net result - acyl-CoA located in mitochondrial matrix

38
Q

what does acyl-carnitine transporter in inner membrane do?

A

faciliates antiport of acyl-carnitine into the mitochondria and carnitine out

39
Q

where does beta oxidation occur?

A

mitochondrial matrix

40
Q

how many steps in beta oxidation?

A

four

41
Q

what are the products of each cycle of beta oxidation?

A

1 acetyl-CoA
1 FADH2
1 NADH + H+
1 fatty acyl-CoA, shortened by 2 carbon atoms

42
Q

what is glycerol broken down by/to?

A

activated to glycerol-3-phosphate by glycerol kinase

43
Q

what is glycerol dehydrogenated to?

A

dihydroxyacetone phosphate

44
Q

what are ketones formed from?

A

acetyl-CoA from beta oxidation

45
Q

where are ketones important?

A

energy metabolism for heart muscle and renal cortex

46
Q

what is the precursor of all new fatty acids called?

A

malonyl-CoA

47
Q

what happens to amino acids which are not used as building blocks?

A

they are degraded

48
Q

what is the major site of amino acid degradation?

A

liver

49
Q

what does amino acid breakdown produce?

A

ammonia and ammonium ions

50
Q

what amino acid product is toxic at high concentrations?

A

ammonium ions

51
Q

what are the major nitrogen-containing excretory molecule?

A

Urea, uric acid, creatinine and ammonium ions.

52
Q

where is urea formed?

A

liver

53
Q

what are the three steps in the synthesis of urea?

A

transamination, de-amination and urea (or ornithine) cycle

54
Q

what enzyme moves the amino group from alpha-amino acids to alpha-keta acids during transamination?

A

aminotransferases usually alpha-ketoglutarate

55
Q

During transamination what are the major carriers of nitrogen in the blood to liver?

A

alanine and glutamine

56
Q

How is alanine made during transamination?

A

amino group of glutamate is transferred to pyruvate, giving alanine

57
Q

How is glutamine made during transamination?

A

glutamine synthase adds NH4+ to glutamate giving glutamine

58
Q

where does deamination/urea cycle happen?

A

in the liver

59
Q

what happens during deamination/urea cycle?

A

amino group of glutamate is converted to free ammonium ion and then urea is synthesised in a complex series of reactions

60
Q

What are ketogenic amino acids degraded to?

A

acetyl-CoA or acetoacetyl-CoA, can give rise to ketone bodies or fatty acids

61
Q

what are glucogenic amino acids degraded to?

A

degraded to pyruvate or TCA cycle intermediates, can be converted into phosphoenolpyruvate and then into glucose

62
Q

what happens during alcaptonuria?

A

degradation of phenylalanine and tyrosine is blocked

63
Q

what is maple syrup urine disease?

A

degradation of phenylalaine and tyrosine is blocked, urine smells like maple syrup, mental and physical retardation and prevented by appropriate diet

64
Q

what is phenylketonuria?

A

phenylalanine accumulates in all body fluids, leads to severe mental retardation if untreated, as therapy must go as low phenylalanine diet

65
Q

what happens during a defect in a urea cycle enzyme?

A
  • accumulation of urea cycle intermediates
  • glutamine levels increase in the circulation
  • alpha-ketoglurarate is no longer regenerated
  • alpha- ketoglurarate levels become too low to fix more free ammonium ion
66
Q

how do you treat urea cycle disorders?

A

treatment with low-protein diet, drugs which remove nitrogen

GI (10 decks)

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