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COM SFM > Carbohydrate Metabolism > Flashcards

Carbohydrate Metabolism Flashcards

1
Q

What is the only type of fuel that RBCs use and brain uses when not starving

A

Glucose, via glycolysis

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2
Q

GLUT1 and GLUT2 transporter location/affinity

A

GLUT1- ubiquitous, but high expression in RBC/brain
High affinity
GLUT2- Liver, low affinity

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3
Q

GLUT3 and GLUT4 transporter location/affinity

A

GLUT3- neurons, high affinity
GLUT4- skeletal muscle, heart, adipose tissue- insulin dependent- stored in vesicles and transported to membrane when triggered by insulin

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4
Q

Glyceraldehyde-3-phosphate–> 1,3-BPG reaction is carried out by what enzyme and creates what side product

A

Carried out by G3P dehydrogenase and creates 2 NADH

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5
Q

1,3-BPG–>3PG is carried out by what enzyme and has what side product

A

Phosphoglycerate kinase and makes 2 ATP

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6
Q

PEP–>Pyruvate carried out by what enzyme and has what side product

A

Pyruvate kinase and makes 2 ATP

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7
Q

Which two reactions in the early phase of glycolysis require ATP

A

Glucose–>G6P

F6P–>F1,6-BP

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8
Q

Glucokinase vs hexokinase

A

Glucokinase is only located in liver/pancreas, has lower affinity, and is not affected by G6P concentration as much. Insulin induces its synthesis, glucagon inhibits

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9
Q

What is Tarui disease

A

Deficiency in PFK-1

Exercise induced muscle cramps/weakness

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10
Q

Most defects in glycolytic enzymes cause what, and why

A

Hemolytic anemia, because RBCs do not have mitochondria so they are affected the most

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11
Q

Type I diabetes

A

Insulin deficiency due to loss of pancreatic b cells

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12
Q

Type II diabetes

A

Insulin resistance that progresses to loss of b cell function

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13
Q

Clinical markers of hemolytic anemia

A

Elevated lactate dehydrogenase, unconjugated bilirubin

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14
Q

Fanconi-Bickel syndrome

A

Mutation in GLUT2 transporter in liver/pancreas, unable to take up glucose
-Fasting hypoglycemia

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15
Q

Activation/inhibition of pyruvate kinase is done by who, and is PK activated/inhibited by phosphorylation

A

Activation- F1,6BP, Insulin
Inhibition- ATP, Alanine, Glucagon
Inhibited by phosphorylation, which means insulin stimulates protein phosphatases

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16
Q

Gluconeogenesis occurs where

A

Liver, kidney, small intestine

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17
Q

First reaction in gluconeogenesis, reactants, products, enzyme

A

Pyruvate + ATP CO2–> OAA

Pyruvate carboxylase

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18
Q

What are activators and inhibitors of Fructose 1,6 biphosphatase

A

Activators- Cortisol and citrate

Inhibitors- AMP and F26BP

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19
Q

How is G6P transported where it needs to be for conversion to glucose, and where does it need to be?

A

Conversion occurs in ER

G6P transported into ER, Glucose and Phosphate transported out

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20
Q

What does the cori cycle do

A

Links lactate produced by glycolysis to gluconeogenesis in liver
-Prevents lactate accumulation, regenerates glucose

21
Q

F1,6BP deficiency

A

Hypoglycemia, lactic acidosis, ketosis

22
Q

Von gerke disease

A

Deficiency in glucose 6-phosphate

23
Q

Dietary source of Fructose is

A

Sucrose- cleaved by sucrase to give fructose and glucose

24
Q

Dietary source of Galactose is

A

Lactose- cleaved by lactase to give galactose and glucose

25
Q

Fructose uptake is mediated by what transporter

A

GLUT5

26
Q

Galactose uptake is mediated by what transporter

A

SGLT1

27
Q

Why is metabolism of fructose faster than glucose

A

Because it bypasses PFK1, the rate limiting step of glycolysis

28
Q

Which cells lack sorbitol dehydrogenase, and was is the result

A

Kidneys, retina, schwann cells. Sorbitol cannot be converted to fructose and accumulates, causing water to enter cell. Retinopathy, cataracts, peripheral neuropathy

29
Q

What is the result of high fructose diet

A

Fructose derived G3P and DHAP are processed to pyruvate and acetyl CoA in unregulated fashion. Excess Acetyl CoA is converted to fatty acids which accumulate in liver and cause fatty liver

30
Q

Galactosemia cause and effects

A

Deficiency in galactose-1-P uridyl transferase

-Cataracts, enlarged liver, mental retardation

31
Q

Oxidative phase of PPP is best for which cellular need

A

Nucleotide synthesis in rapidly dividing cells

32
Q

Non oxidative phase of PPP is best for which cellular need

A

NADPH production- non oxidative products are channeled into gluconeogenesis for re-entry into PPP

33
Q

What is the rate limiting enzyme in PPP, what happens if it is deficient

A

G6P Dehydrogenase- if deficient, hemolytic anemia presents when NADPH need is elevated

34
Q

Glycogen is stored where

A

In liver, muscles mainly

35
Q

What is the rate limiting enzyme in glycogenesis, and what does it do

A

Glycogen synthase- catalyzes transfer of glucose from UDP-glucose to non reducing end of glycogen

36
Q

What is the name of the branching enzyme in glycogenesis

A

Glucosyl (4:6) transferase

37
Q

What is the rate limiting step in glycogenolysis

A

Cleavage of glucose residue as glucose-1-phosphate by glycogen phosphorylase

38
Q

What is the name of the debranching enzyme

A

Transferase (4:4) transfers last 3/4 glucose residues to end of main glycogen chain, then a-1,6-glucosidase cleaves 1 remaining glucose

39
Q

Differential outcome of Glucose-1-phosphate in liver and muscle

A

Liver can directly convert G1P into glucose. Muscle cells lack the necessary enzymes and must use it for energy via glycolysis/TCA cycle

40
Q

Glycogen synthase vs glycogen phosphorylase - is each activated or deactivated by phosphorylation?

A

Glycogen synthase- inhibited by phosphorylation

Glycogen phosphorylase- activated

41
Q

During fed state, will glycogen synthase and phosphorylase be phosphorylated or not?

A

They will be dephosphorylated during fed state to promote glycogenesis

42
Q

What signals muscle cells to break down glycogen

A

High AMP, epinephrine, Ca2+

Glucagon DOES NOT act on muscle

43
Q

GSD 0

A

Deficiency in glycogen synthase

-Must eat frequently, hypoglycemic when fasting, muscle cramps due to lack of glycogen

44
Q

GSD1/Von gierke

A

Deficiency in glucose-6-phosphatase
Inefficient release of free glucose into bloodstream by liver following gluconeogenesis/glycogenolysis
-Fasting hypoglycemia, lactic acidosis, hepatomegaly

45
Q

GSD II/Pompe disease

A

Deficiency in acid maltase aka a-glucosidase
Impairs lysosomal glycogenolysis resulting in accumulation of glycogen in lysosomes
Disrupts normal function of liver/muscle cells

46
Q

GSD III/Cori disease

A

Defective a-1,6-glucosidase debranching enzyme

-Patients have glycogen molecules with large number of short branches. Light hypoglycemia/hepatomegaly

47
Q

GSD IV/Andersen

A

Defective glucosyl 4:6 transferase

-Long chain glycogen with fewer branches, hepatosplenomegaly, death by 5yrs

48
Q

GSD V/Mcardle disease

A

Defective muscle glycogen phosphorylase

Unable to supply muscles with enough glucose, can’t break down glycogen. Reduce exercise

49
Q

GSD VI/Hers disease

A

Defective liver glycogen phosphorylase

Hepatomegaly, low blood glucose

COM SFM (31 decks)

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