Carb Metabolism

Question 1

Glut, speed and insulin dependent

Answer 1

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

Question 2

what can you get glycerol 3 phosphate from?

glycerol 3 phosphate is used in

Answer 2

synthesis of TAG

From DHAB

Question 3

site of glycolysis

Answer 3

cytosol of all cells

Question 4

arsenide and iodoacetate inhibits

fluoride inhbiits

Answer 4

glyceraldehyde 3 phosphate DH

enolase

Question 5

deficiency of PK results in

Answer 5

hemolytic anemia (no glycolysis=no RBCs)

Question 6

feeding and fasting has no effect on

Answer 6

hexokinase

Question 7

affinity and KM

hexokinase vs glucose

Answer 7

hexo- high affinity low KM

gluco- opposite

Question 8

PFK 1 is activated and inhibited by

Answer 8

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

inhibited by: glucagon, ATP, Citrate

Question 9

PK is activated and inhibited by

Answer 9

activated by insulin-PEP

inhibited by: glucagon and ATP

Question 10

effect of fatty acid oxidation on glycolysis

Answer 10

fatty acid oxidation produces:

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

so FA oxidation inhibits glycolysis and activates gluconeogenesis

Question 11

sources of pyruvate

fates of pyruvate

Answer 11

glycolysis, glycerol, alanine, lactate, malate

fates: oxaloacetate, acetyl coA, alanine, lactate

Question 12

PDH Regulation

Answer 12

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

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

Question 13

PDH in adipose tissue regulation

Answer 13

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

Question 14

lactic acidosis causes and effects

Answer 14

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

Question 15

sources and fates of oxaloacetate

Answer 15

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

Question 16

acetyl CoA activates

Answer 16

Pyruvate carboxylase

Question 17

PC hormonal regulation

Answer 17

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

Question 18

energy yield in presence of O2

Answer 18

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

Total: 32 ATP one glucose molecule

Question 19

site of gluconeogenesis

Answer 19

cytosol of liver and kidney except PC (in mitochondria)

Question 20

reversal of PK and shuttle

Answer 20

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

Question 21

reversal of PFK1

Answer 21

by fructose 1,6 bisphosphatase

Question 22

reversal of glucokinase

Answer 22

glucose 6 phosphatase

Question 23

ATP and NADH required for gluconeogenesis

Answer 23

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

Question 24

cori cycle and importance

Answer 24

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

Question 25

glucose alanine cycle

Answer 25

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.

Question 26

proteins and amino acids are main source of energy after

Answer 26

18 hours due to depletion of liver glycogen

Question 27

how does glycerol get glucose

Answer 27

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

Question 28

odd chain FA to glucose; co enzymes needed

Answer 28

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

Question 29

fatty acids can't pass

Answer 29

blood brain barrier

Question 30

fructose 1,6 bisphosphatase deficiency symptoms and treatment

Answer 30

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