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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
fxn of trehalase
cleaves trehalose found in mushrooms
26
fxn of lactase
cleaves lactose into glucose, galactose
27
after small intestine brush border complex cleavage, what happens to carbs?
Na and facilitative transporters bring carbs into enterocytes to be released in blood stream -> absorption by GLUT receptors
28
where are each of the GLUT receptors found?
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)
29
lactose intolerance
- pain, gas, nausea after eating lactose - caused by lack of lactase - lactose not absorbed produces H2/methane gas, diarrhea
30
diagnosis of lactose intolerance
done by measuring H2 gas on breath
31
additional undigestable sugars
- raffinose | - soluble fiber = pectin, gums
32
sucrose is?
glucose + fructose
33
maltose is?
glucose + glucose
34
lactose is?
glucose + galactose
35
four possible fates of G6P
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
36
fate of glycogen in muscle vs. liver
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
how is glycogen synthesis initiated?
on the protein glycogenin by autoglycosylation w/ UDP-glucose on Tyr
38
connections in glycogen
a-1,4 linkages and a-1,6 branches
39
purpose of branches in glycogen
allows for synthesis or degradation at multiple ends at once
40
steps of glycogen synthesis
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
what is the key biosynthetic substrate for glycogen?
UDP-glucose
42
function of branching enzyme
chains over 11 residues are hydrolyzed and attached via a-1,6 bonds to create branch site
43
what enzymes depend on PLP as a cofactor?
- glycogen phosphorylase | - transaminases
44
steps of glycogen degradation
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
what is the only B vitamin you can get toxicity from?
B6 - PLP - neuropathy
46
debranching enzyme
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
control of glycogen metabolism
insulin: - stimulates glycogen synthase - inhibits phosphorylase (phosphorylase b - less active) glucagon: - stimulates phosphorylase (phosphorylase a - more active) - inhibits glycogen synthase
48
what enzyme (de)phosphorylates phosphorylase?
phosphoprotein phosphatase and phosphorylase kinase
49
control of phosphoprotein phosphatase
+ insulin | - cAMP
50
which form of phosphorylase is more susceptible to regulation by small molecules?
phosphorylase b - allosteric interactions
51
is glycogen synthase active when phosphorylated or no?
active when no phosphorylation
52
is glycogen phosphorylase active when phosphorylated or no?
active when phosphorylated
53
effects of glucagon on liver and muscle
liver: inactivates glycogen synthase, activates glycogen phosphorylase muscle: no effect
54
how does AMP affect liver and muscle glycogen phosphorylase?
liver: no effect muscle: allosteric activator of glycogen phosphorylase
55
regulation of glycogen degradation
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
McArdle's disease
defective muscle glycogen phosphorylase - exercise induced cramps, muscle pain (young adult/ adult diagnosis)
57
von Gierke's disease
defective G6phosphatase (liver) - severe hypoglycemia; epinephrine secretion -> stimulates FA release -> increased VLDL made in liver (newborn diagnosis)
58
Herr's disease
defective liver glycogen phosphorylase
59
primary sources for glucose production from gluconeogenesis
- 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
primary site for gluconeogenesis
liver (small amount in kidney cortex)
61
which steps of gluconeogenesis are not the reverse of glycolysis?
1. G6phosphatase (GK) 2. F-1,6-bisphosphatase (PFK1) 3. pyruvate carboxylase + PEPCK (pyruvate kinase)
62
describe conversion of pyruvate back into PEP (where, cofactors, enzymes, energy)
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
how does FA oxidation affect gluconeogenesis?
FA oxidation -> increased acetyl coA, NADH -> activate pyruvate DH kinase -> inhibit pyruvate DH -> keeps pyruvate around for gluconeogenesis
64
control of G6phosphatase
+ cAMP + glucagon - insulin
65
control of F-1,6-bisphosphatase
+ cAMP + citrate - AMP - F2,6BP
66
control of PEPCK
+ cAMP
67
control of pyruvate carboxylase
+ acetyl coA + glucagon + steroids - ADP - insulin
68
Cori cycle
release of lactate by muscles -> converted by liver to glucose -> released in blood
69
Alanine cycle
release of Ala by muscle -> converted by liver to glucose -> released in blood
70
key products for PPP
- ribose: nt synthesis | - NADPH: FA synthesis, glutathione reduction, cholesterol/steroid hormone synthesis, p450 detox in liver
71
what is the only way for RBCs to make NADPH
PPP
72
oxidative phase of PPP
- generates 2 NADPH/ G6P - generates 1 ribulose-5P/ G6P - key enzyme: G6P DH
73
non-oxidative phase of PPP
- generates different sugars (ribose-5P!) - transaldolase: transfers 3C keto units - transketolase: transfers 2C keto units
74
which requires thiamine, transaldolase or transketolase?
transketolase
75
how can you diagnose B1 deficiency?
measure transketolase rxn: - in absence of B1, then in excess of B1 - if NOT deficient, shouldn't see much of a difference
76
what do transaldolase and transketolase use for their nucleophilic attack?
transaldolase: Lysine transketolase: TPP
77
G6P DH deficiency
- most common enzyme deficiency - relative resistance to malaria - most asymptomatic - hemolytic anemia
78
how does G6P DH deficiency affect RBCs?
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
where is dietary fructose metabolized? galactose?
both in liver
80
steps in fructose metabolism
1. fructose -> F1P (fructokinase) 2. F1P -> glyceraldehyde + DHAP (aldolase B) 3. Glyceraldehyde -> G3P (triose kinase) DHAP and G3P both feed into glycolysis
81
fructosuria
fructokinase deficiency
82
fructosemia
aldolase B deficiency -> hypoglycemia
83
aldolase isozymes
- only B can cleave F1P - only in liver, kidney, intestine | - muscle only has A
84
effect of aldolase B deficiency on aldolase A
aldolase B deficiency -> build up of F1P -> F1P inhibits aldolase A -> gluconeogenesis inhibited in liver
85
what is the rate limiting step of fructose metabolism?
aldolase B
86
what does F1P inhibit?
glycogenolysis (inhibits phosphorylase)
87
steps of galactose metabolism
1. galactose -> gal-1P (galactokinase) 2. gal-1P -> G1P (galactose-1P uridylyltransferase) 3. G1P -> glycogen or G6P for release into blood or glycolysis
88
what converts UDP galactose -> UDP glucose?
UDP-galactose-4-epimerase
89
galactosemia
galastose-1P uridylyltransferase deficiency - galactose in urine - cataracts, mental retardation (indirectly)

Biochem - Exam 2 (5 decks)

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