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Biochem - Exam 2 > Carbohydrate Metabolism > Flashcards

Carbohydrate Metabolism Flashcards

1
Q

GI

A

indicator of how rapidly glucose levels rise

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2
Q

GI of glucose; fruit, veggies, milk; corn flakes, baked potatoes

A

glucose = 100
fruit, veggies, milk < 55
corn flakes, baked potatoes > 70

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3
Q

how is insulin produced?

A

pre-pro-hormone in B cells of islets of Langerhans

  • preproinsulin has N-term signal peptide
  • cleaved to form proinsulin
  • proinsulin cleaved into A and B chains
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4
Q

how does insulin respond to increased intracellular glucose?

A

increase in [ATP] in cells inhibits an ATP dependent K+ channel that depolarizes the cell, allowing extracellular Ca++ to enter -> insulin released from vesicles, binds receptors on muscle/adipose tissue, stimulates GLUT4 receptors

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5
Q

describe the insulin receptor

A

membrane bound, tyrosine kinase receptor

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6
Q

function of insulin

A
  • promotes fuel storage after meal
  • promotes growth
  • stimulates protein, glycogen, TG synthesis
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7
Q

function of glucagon

A
  • mobilizes fuel

- maintains blood glucose during fasting

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8
Q

how is glucagon produced?

A

peptide hormone produced in pre-pro form in a cells of pancreas

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9
Q

what directly suppresses release of glucagon?

A

glucose and insulin

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10
Q

describe the glucagon receptor

A

activates a G-protein, an ATP cyclase, and a cAMP dependent kinase

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11
Q

function of epinephrine in metabolism

A

mobilizes fuel during acute stress

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12
Q

action of epinephrine

A

activates glycogen phosphorylase to release glucose but does not stimulate gluconeogenesis

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13
Q

epinephrine in muscle vs. liver

A

muscle: activates a G protein and an adenylate cyclase to activate protein kinase A (similar to glucagon)
liver: binds a-agonist receptor signals through IP3 and Ca++ to activate multiple kinases

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14
Q

function of cortisol on metabolism

A

(glucocorticoid) alters long-term metabolism

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15
Q

action of cortisol

A
  • binds an intracellular receptor and moves to the nucleus where it controls gene transcription
  • stimulates gluconeogenesis and FA release from adipose - influences long-term fuel mobilization
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16
Q

C-peptide of insulin

A

internal peptide cleaved from insulin - measurement can determine endogenous vs. exogenous insulin

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17
Q

what drugs can help stimulate insulin release in patients w/ functional B cells (T2DM)?

A

sulfonylureas (glipizide, glyburide) - close K+ channels and stimulate Ca++ influx -> stimulate insulin release

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18
Q

when does insulin peak after a high carb meal?

A

45 min

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19
Q

fxn of salivary amylase

A

digests starch to maltose, trisaccharides, dextrins

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20
Q

dextrins

A

4-9 glucosyl units

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21
Q

fxn of stomach acid

A

inactivates salivary amylase

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22
Q

what carb digestion occurs in duodenum?

A
  • neutralization of acid

- alpha-amylase from pancreas forms more maltose, di-trisaccharides, dextrins

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23
Q

what carb digestion occurs in small intestine brush border complexes?

A
  • glucoamylase
  • sucrase-isomaltase
  • trehalase
  • lactase
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24
Q

fxn of glucoamylase

A

cleaves a-1,4-glycosidic bonds

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25
Q

fxn of trehalase

A

cleaves trehalose found in mushrooms

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26
Q

fxn of lactase

A

cleaves lactose into glucose, galactose

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27
Q

after small intestine brush border complex cleavage, what happens to carbs?

A

Na and facilitative transporters bring carbs into enterocytes to be released in blood stream -> absorption by GLUT receptors

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28
Q

where are each of the GLUT receptors found?

A

GLUT1: RBC, brain endothelial cells (high affinity)
GLUT2: pancreas, liver (low affinity)
GLUT3: neurons
GLUT4: fat, muscle, heart (insulin induced)
GLUT5: testis (actually for fructose)

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29
Q

lactose intolerance

A
  • pain, gas, nausea after eating lactose
  • caused by lack of lactase
  • lactose not absorbed produces H2/methane gas, diarrhea
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30
Q

diagnosis of lactose intolerance

A

done by measuring H2 gas on breath

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31
Q

additional undigestable sugars

A
  • raffinose

- soluble fiber = pectin, gums

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32
Q

sucrose is?

A

glucose + fructose

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33
Q

maltose is?

A

glucose + glucose

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34
Q

lactose is?

A

glucose + galactose

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35
Q

four possible fates of G6P

A
  1. PPP -> ribose + NADPH
  2. back into glucose to help w/ serum levels
  3. made into glycogen
  4. glycolysis to pyruvate for either TCA or lactate
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36
Q

fate of glycogen in muscle vs. liver

A

muscle: store of glucose for during anaerobic exercise (not released to blood)
liver: degraded and released to blood to increase serum glucose levels during fasting

37
Q

how is glycogen synthesis initiated?

A

on the protein glycogenin by autoglycosylation w/ UDP-glucose on Tyr

38
Q

connections in glycogen

A

a-1,4 linkages and a-1,6 branches

39
Q

purpose of branches in glycogen

A

allows for synthesis or degradation at multiple ends at once

40
Q

steps of glycogen synthesis

A
  1. GK/HK traps glucose in cell by phosphorylation
  2. phosphoglucomutase takes G6P -> G1P
  3. G1P-uridylyltransferase activates G1P w/ UTP
  4. glycogen synthase adds UDP-glucose to non-reducing end of growing glycogen molecule
41
Q

what is the key biosynthetic substrate for glycogen?

A

UDP-glucose

42
Q

function of branching enzyme

A

chains over 11 residues are hydrolyzed and attached via a-1,6 bonds to create branch site

43
Q

what enzymes depend on PLP as a cofactor?

A
  • glycogen phosphorylase

- transaminases

44
Q

steps of glycogen degradation

A
  1. glycogen phosphorylase releases G1P from glycogen
  2. phosphoglucomutase converts G1P -> G6P
  3. in liver: G6phosphatase forms glucose -> blood
    in muscle: PFK-1 forms pyruvate w/ glycolysis
45
Q

what is the only B vitamin you can get toxicity from?

A

B6 - PLP - neuropathy

46
Q

debranching enzyme

A

has transferase and hydrolysis activity:

  1. transfers 3 of 4 last units of branch from a-1,6 to a-1,4
  2. last glucose hydrolyzed (released as glucose, not G1P)
47
Q

control of glycogen metabolism

A

insulin:
- stimulates glycogen synthase
- inhibits phosphorylase (phosphorylase b - less active)

glucagon:
- stimulates phosphorylase (phosphorylase a - more active)
- inhibits glycogen synthase

48
Q

what enzyme (de)phosphorylates phosphorylase?

A

phosphoprotein phosphatase and phosphorylase kinase

49
Q

control of phosphoprotein phosphatase

A

+ insulin

- cAMP

50
Q

which form of phosphorylase is more susceptible to regulation by small molecules?

A

phosphorylase b - allosteric interactions

51
Q

is glycogen synthase active when phosphorylated or no?

A

active when no phosphorylation

52
Q

is glycogen phosphorylase active when phosphorylated or no?

A

active when phosphorylated

53
Q

effects of glucagon on liver and muscle

A

liver: inactivates glycogen synthase, activates glycogen phosphorylase
muscle: no effect

54
Q

how does AMP affect liver and muscle glycogen phosphorylase?

A

liver: no effect
muscle: allosteric activator of glycogen phosphorylase

55
Q

regulation of glycogen degradation

A

glucagon binds -> adenylate cyclase makes cAMP -> activates protein kinase A -> activates phosphorylase kinase/inhibits glycogen synthase -> phosphorylase kinase switches phosphorylase b to a -> phosphorylase a removes G1P from glycogen

56
Q

McArdle’s disease

A

defective muscle glycogen phosphorylase - exercise induced cramps, muscle pain (young adult/ adult diagnosis)

57
Q

von Gierke’s disease

A

defective G6phosphatase (liver) - severe hypoglycemia; epinephrine secretion -> stimulates FA release -> increased VLDL made in liver (newborn diagnosis)

58
Q

Herr’s disease

A

defective liver glycogen phosphorylase

59
Q

primary sources for glucose production from gluconeogenesis

A
  • lactate (lactate DH turns into pyruvate)
  • alanine (ALT turns into pyruvate)
  • glycerol (glycerol kinase turns into glycerol-3-P, glycerol-3-P DH turns into DHAP)
60
Q

primary site for gluconeogenesis

A

liver (small amount in kidney cortex)

61
Q

which steps of gluconeogenesis are not the reverse of glycolysis?

A
  1. G6phosphatase (GK)
  2. F-1,6-bisphosphatase (PFK1)
  3. pyruvate carboxylase + PEPCK (pyruvate kinase)
62
Q

describe conversion of pyruvate back into PEP (where, cofactors, enzymes, energy)

A

pyruvate -> OAA by pyruvate carboxylase

  • needs biotin
  • in mitochondria
  • uses ATP

OAA -> PEP by PEPCK

  • releases CO2
  • in cytoplasm
  • uses GTP

OAA must be turned into malate (malate DH) to go to cytoplasm

63
Q

how does FA oxidation affect gluconeogenesis?

A

FA oxidation -> increased acetyl coA, NADH -> activate pyruvate DH kinase -> inhibit pyruvate DH -> keeps pyruvate around for gluconeogenesis

64
Q

control of G6phosphatase

A

+ cAMP
+ glucagon

  • insulin
65
Q

control of F-1,6-bisphosphatase

A

+ cAMP
+ citrate

  • AMP
  • F2,6BP
66
Q

control of PEPCK

A

+ cAMP

67
Q

control of pyruvate carboxylase

A

+ acetyl coA
+ glucagon
+ steroids

  • ADP
  • insulin
68
Q

Cori cycle

A

release of lactate by muscles -> converted by liver to glucose -> released in blood

69
Q

Alanine cycle

A

release of Ala by muscle -> converted by liver to glucose -> released in blood

70
Q

key products for PPP

A
  • ribose: nt synthesis

- NADPH: FA synthesis, glutathione reduction, cholesterol/steroid hormone synthesis, p450 detox in liver

71
Q

what is the only way for RBCs to make NADPH

A

PPP

72
Q

oxidative phase of PPP

A
  • generates 2 NADPH/ G6P
  • generates 1 ribulose-5P/ G6P
  • key enzyme: G6P DH
73
Q

non-oxidative phase of PPP

A
  • generates different sugars (ribose-5P!)
  • transaldolase: transfers 3C keto units
  • transketolase: transfers 2C keto units
74
Q

which requires thiamine, transaldolase or transketolase?

A

transketolase

75
Q

how can you diagnose B1 deficiency?

A

measure transketolase rxn:

  • in absence of B1, then in excess of B1
  • if NOT deficient, shouldn’t see much of a difference
76
Q

what do transaldolase and transketolase use for their nucleophilic attack?

A

transaldolase: Lysine
transketolase: TPP

77
Q

G6P DH deficiency

A
  • most common enzyme deficiency
  • relative resistance to malaria
  • most asymptomatic - hemolytic anemia
78
Q

how does G6P DH deficiency affect RBCs?

A

generate more ROS -> more pressure to get rid of them -> increased GLT in reduced form -> need more NADPH to oxidize GLT, but don’t have it -> can’t keep up w/ ROS -> disulfides form b/w Hb’s -> Heinz bodies

79
Q

where is dietary fructose metabolized? galactose?

A

both in liver

80
Q

steps in fructose metabolism

A
  1. fructose -> F1P (fructokinase)
  2. F1P -> glyceraldehyde + DHAP (aldolase B)
  3. Glyceraldehyde -> G3P (triose kinase)

DHAP and G3P both feed into glycolysis

81
Q

fructosuria

A

fructokinase deficiency

82
Q

fructosemia

A

aldolase B deficiency -> hypoglycemia

83
Q

aldolase isozymes

A
  • only B can cleave F1P - only in liver, kidney, intestine

- muscle only has A

84
Q

effect of aldolase B deficiency on aldolase A

A

aldolase B deficiency -> build up of F1P -> F1P inhibits aldolase A -> gluconeogenesis inhibited in liver

85
Q

what is the rate limiting step of fructose metabolism?

A

aldolase B

86
Q

what does F1P inhibit?

A

glycogenolysis (inhibits phosphorylase)

87
Q

steps of galactose metabolism

A
  1. galactose -> gal-1P (galactokinase)
  2. gal-1P -> G1P (galactose-1P uridylyltransferase)
  3. G1P -> glycogen or G6P for release into blood or glycolysis
88
Q

what converts UDP galactose -> UDP glucose?

A

UDP-galactose-4-epimerase

89
Q

galactosemia

A

galastose-1P uridylyltransferase deficiency

  • galactose in urine
  • cataracts, mental retardation (indirectly)

Biochem - Exam 2 (5 decks)

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