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REVISION BIOCHEM > Carb Metabolism > Flashcards

Carb Metabolism Flashcards

1
Q

Glut, speed and insulin dependent

A 
Glut 1- RBC
2- Kidney, Liver, Pancreas - fastest
3- Brain
4- Heart, Muscle, Adipose Tissue - insulin dependent
5- Intestine
SGLUT1- Intestine mainly & Kidney
2- Kidney only
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2
Q

what can you get glycerol 3 phosphate from?

glycerol 3 phosphate is used in

A

synthesis of TAG

From DHAB

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3
Q

site of glycolysis

A

cytosol of all cells

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4
Q

arsenide and iodoacetate inhibits

fluoride inhbiits

A

glyceraldehyde 3 phosphate DH

enolase

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5
Q

deficiency of PK results in

A

hemolytic anemia (no glycolysis=no RBCs)

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6
Q

feeding and fasting has no effect on

A

hexokinase

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7
Q

affinity and KM

hexokinase vs glucose

A

hexo- high affinity low KM

gluco- opposite

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8
Q

PFK 1 is activated and inhibited by

A

activated by: Insulin, AMP, Fructose 2,6 bis p, fructose 6p

inhibited by: glucagon, ATP, Citrate

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9
Q

PK is activated and inhibited by

A

activated by insulin-PEP

inhibited by: glucagon and ATP

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10
Q

effect of fatty acid oxidation on glycolysis

A

fatty acid oxidation produces:

ATP: inhibits
Citrate: inhibits
Acetyl CoA –> inhibits PDH and activates PC

so FA oxidation inhibits glycolysis and activates gluconeogenesis

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11
Q

sources of pyruvate

fates of pyruvate

A

glycolysis, glycerol, alanine, lactate, malate

fates: oxaloacetate, acetyl coA, alanine, lactate

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12
Q

PDH Regulation

A

inhibited by product of reaction (acetyl coA & NADH & ATP)

activated by substrates (NAD, Pyruvate, ADP) and calcium

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13
Q

PDH in adipose tissue regulation

A

insulin increases its activity so it can form acetyl coA for lipogenesis
fasting decreases its activity

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14
Q

lactic acidosis causes and effects

A

deficiency in PDH, TPP or arsenic poison. can’t convert pyruvate to acetyl coA so its get converted to lactic acid. this is fetal and leads to brain damage

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15
Q

sources and fates of oxaloacetate

A

source: pyruvate, citrate, malate(krebbs), aspartate (transamination)
fate: citrate, 2PEP (by PEPCK), malate, aspartate

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16
Q

acetyl CoA activates

A

Pyruvate carboxylase

17
Q

PC hormonal regulation

A

PC Is important in gluconeogenesis.
anti insulin -> induce
insulin - repress

18
Q

energy yield in presence of O2

A

glycolysis - 7 ATP
Each pyruvate (2) - 2.5 ATP (by PDH)
Oxidation of acetyl coA (2)- 10 ATP

Total: 32 ATP one glucose molecule

19
Q

site of gluconeogenesis

A

cytosol of liver and kidney except PC (in mitochondria)

20
Q

reversal of PK and shuttle

A

by PC and PEPCK
pyruvate -> oxaloacetate (mitochondria) by PC
Oxaloacetate -> malate (malate DH)
Malate-> Malate shuttle to cytosol -> Oxaloacetate by Malate DH
Oxaloacetate -> 2 PEP by PEPCK
shuttle - dicarboxylitic acid shuttle

21
Q

reversal of PFK1

A

by fructose 1,6 bisphosphatase

22
Q

reversal of glucokinase

A

glucose 6 phosphatase

23
Q

ATP and NADH required for gluconeogenesis

A 
6 ATP (2 for PC, 2 for PEPCK, 2 for reversal of PG kinase)
2 NADH+H for reversal of glyceraldehyde 3 PDH
24
Q

cori cycle and importance

A

lactate is formed in RBCs or muscles.
lactate goes to blood then liver
in liger, it is converted to glucose by gluconeogenesis then goes back to RBCs or muscle for energy

it prevents loss of lactate as waste product

25
Q

glucose alanine cycle

A

pyruvate is converted to alanine (transamination) and alanine is converted back to pyruvate in liver then pyruvate becomes glucose by gluconeogenesis and goes back to muscle and RBCs.

26
Q

proteins and amino acids are main source of energy after

A

18 hours due to depletion of liver glycogen

27
Q

how does glycerol get glucose

A

glycerol goes to glycerol 3 phosphate which can become DHAB (intermediate of glycolysis)

28
Q

odd chain FA to glucose; co enzymes needed

A

last 3 carbon becomes propionyl coA then malonyl then succinyl coA by the help of B12

29
Q

fatty acids can’t pass

A

blood brain barrier

30
Q

fructose 1,6 bisphosphatase deficiency symptoms and treatment

A

hypoglycemia because no gluconeogenesis
lactic acidosis because no Cori cycle = because no gluconeogenesis
ketosis = due to increase in FA oxidation

treatment:
avoid prolonged fasting and fructose and sucrose food

REVISION BIOCHEM (11 decks)

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