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HDSO Digestion System > Metabolism -- Normal and Abnormal Carb Metabolism > Flashcards

Metabolism -- Normal and Abnormal Carb Metabolism Flashcards

1
Q

∆G(ATP hyd)

A

-7.3 Kcal/mol

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2
Q

Define catabolism

A

Conversion of energy-yielding nutrients into energy-poor end products (larger to smaller molecules, basically)

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3
Q

Define anabolism

A

Conversion of precursor molecules into complex molecules (smaller to larger, basically)

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4
Q

Components of lactose

A

Galactase - glucose

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5
Q

Components of maltose

A

Glucose - glucose

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6
Q

Components of sucrose

A

Glucose - fructose

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7
Q

Where do disaccharides get digested into monosaccharides?

A

In gut

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8
Q

Where do monosaccharides become transformed and phosphorylated for further metabolism?

A

In liver

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9
Q

Phosphorylated product of glucose

A

Glucose-6-P

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10
Q

Phosphorylated product of fructose

A

Fructose-1-P

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11
Q

Phosphorylated product of galactose

A

Glucose-1-P

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12
Q

Metabolic fates of glucose-6-P

A

Can either:

  1. Enter glycolysis
  2. Convert into glucose-1-P for conversion into glycogen
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13
Q

Metabolic fate of fructose-1-P

A

Glycolysis

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14
Q

Metabolic fate of glucose-1-P

A

Glycogen

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15
Q

Define lactose intolerance

A

Deficiency in gene expression for lactase (as we age), causing gut flora to use the lactose instead, creating acid and CO2 in gut –> bloating, cramping and diarrhea

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16
Q

Disaccharide intolerance of Inuits

A

Sucrose intolerance (10%)

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17
Q

Define type I diabetes mellitus

A

Autoimmune destruction of insulin-producing beta cells of the pancreas

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18
Q

Define type II diabetes mellitus

A

Insulin is not sensed is later under produced (“insulin resistance” and deficiency – strongly linked with obesity

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19
Q

Consequence of diabetes mellitus

A

Glucose and fat homeostasis are deregulated –> hyperglycemia and a very large number of serious health risks

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20
Q

Location of GLUT-2

A

Liver, pancreas, kidney

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21
Q

Location of GLUT-4

A

Muscle and adipose tissue

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22
Q

What controls GLUT-4 availability?

A

Insulin

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23
Q

Input for glycolysis

A
  • 2 ATP
  • 1 glucose
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24
Q

Output of glycolysis

A
  • 4 ATP
  • 2 NADH
  • 2 pyruvate
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25
Q

Net profit from glycolysis

A
  • 2 ATP
  • 2 NADH
  • 2 pyruvate
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26
Q

What is required to make ATP out of NADH

A

Oxygen

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27
Q

Location of hexokinase

A

In tissues other than the liver and pancreas

28
Q

Hexokinase’s maximal speed and what this means

A

Moderate = tissues don’t take more glucose than they can use

29
Q

Location of glucokinase

A

Liver and pancreas

30
Q

Glucokinase use in liver

A

Soak up all the sugar from a meal (high maximal speed)

31
Q

Glucokinase use in pancreas

A

Sense glucose levels and control insulin release

32
Q

What regulated GK transcription in the liver?

A

+ = insulin

  • = glucagon
33
Q

3 glycolysis enzymes whose transcriptions are regulated by insulin and glucagon

A
  • Glucokinase
  • PFK-1
  • PK
34
Q

Drug target for type II diabetes and why

A

Glucokinase –> up-regulate activity (soak up more sugar and release more insulin)

35
Q

Condition associated with a single gene mutation in glucokinase

A

Maturity-Onset Diabetes of the Young (MODY)

36
Q

Consequence of mutating both genes of glucokinase

A

Permanent Neonatal Diabetes Mellitus (PNDM)

37
Q

3 consequences of aldolase B deficiency

A
  • Hypoglycemia
  • Secretion of all phosphate –> unable to synthesize ATP
  • Fructose bypasses regulation by glucokinase –> Hereditary fructose intolerance
38
Q

Define the Warburg effect?

A
  • Cancer cells use glucose faster –> lactate instead of acetyl CoA
  • Overexpression of hexokinase
  • Expression of special variant of pyruvate kinase
39
Q

Why can lactic acidosis occur?

A

Lack of oxygen, as seen in:

  • Myocardial infarction
  • Pulmonary embolism
  • Uncontrolled hemorrhage
  • Tumor microenvironment
  • Muscle overuse/exertion
40
Q

Enzyme to convert pyruvate to acetyl CoA

A

Pyruvate dehydrogenase

41
Q

2 ways that pyruvate dehydrogenase is regulated

A
  • Phosphorylation/dephosphorylation cycle
  • Product inhibition
42
Q

Vitamin required as a cofactor in PDH

A

Thiamine

43
Q

Consequence of thiamine deficiency

A

Lactic acidosis

44
Q

Consequence of PDH deficiency

A

Chronic lactic acidosis –> severe neurological defects –> usually lethal

45
Q

ETC complex that is NOT a proton pump

A

Complex II

46
Q

ETC complex that FADH2 enters

A

Complex II

47
Q

Effect of cyanide poisoning

A

Stops ETC by CN- binding Fe3+ in complex IV –> rapid cell death and DNS damage

48
Q

Effect of CO poisoning

A

Stop ETC by CO binding Fe2+ in complex IV

49
Q

Special property of brown fat

A

Contains proteins in mitochondria that form a channel to allow H+ back into the mitochondria without going through ATP synthase

50
Q

Enzyme to link glucose molecules together to form glycogen

A

Glycogen synthase

UDP-glucose + (glucose)n –> (glucose)n+1 + UDP

51
Q

Activator fro glycogen synthase

A

Insulin

52
Q

Inhibitor of glycogen synthase

A

Glucagon

53
Q

Purpose of liver in gllucose storage

A

For later supply of glucose to other tissues in times of fasting

54
Q

Purpose of muscle in glucose storage

A

Use as energy source during exercise

55
Q

Enzyme to remove one glucose link from glycogen

A

Glycogen phosphorylase

Glycogen chain + Pi –> Glucose 1-P

56
Q

Enzyme to convert glucose 6-P to Glucose

A

Glucose 6-phosphatase

57
Q

Fate of gllucose-6-P in muscle

A

Glycolysis directly

58
Q

Fate of glucose-6-phosphate in liver

A

Conversion into glucose by glucose-6-phosphatase for distribution to other tissues

59
Q

2 pathologies of glycogenolysis

A

McArdle Disease

Von Gierke Disease

60
Q

Enzyme affected bby McArdle disease

A

Glycogen phosphatase

61
Q

Enzyme affected by Von Gierke Disease

A

Glucose-6-Phosphatase

62
Q

3 irreversible reactions in glycolysis

A
  • Glucose –> Glucose-6-P
  • Fructose-6-P –> Fructose 1-6-bisP
  • PEP –> pyruvate
63
Q

4 enzymes to get around glycolysis’ irreversible steps in gluconeogenesis

A
  • Glucose-6-phosphatase
  • Fructose-1,6-bisphosphatase
  • Pyruvate carboxylase
  • PEPC
64
Q

AEnzyme most tightly regulated to differentiate between the bodies needs for gluconeogenesis vs. glycolysis

A

Fructose-1,6-bisphosphatase

65
Q

Activator of fructose-1,6-bisphosphatase

A

Glucagon

66
Q

INhibitor of fructose-1,6-bisphosphatase

A

Insulin

67
Q

Activator of pyruvate carboxylate

A

Acetyl-CoA

HDSO Digestion System (29 decks)

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