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Physiology section 3 > Metabolism > Flashcards

Metabolism Flashcards

1
Q

Liver prefers to use:

A
  • fatty acids
  • glucose
  • amino acids
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2
Q

Adipose Tissues prefer to use:

A

fatty acids

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3
Q

Skeletal Muscle prefers to use:

A
  • fatty acids at rest

- glucose on exertion

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4
Q

Heart Muscle prefers to use:

A

Fatty acids

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5
Q

Brain prefers to use:

A
  • Glucose in fed state

- Ketone bodies under starvation

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6
Q

Dry calories in carbohydrates

A

4 kcal/g

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7
Q

Dry calories in proteins

A

4 kcal/g

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8
Q

Dry calories in fat

A

9 kcal/g

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9
Q

Glycogenolysis

A

Breakdown of glycogen to glucose

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10
Q

Glycolysis

A

single glucose into 2 pyruvate, 2 molecules of NADH, 2 ATP and 2 H20

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11
Q

Gluconeogenesis

A

generation of glucose from non-carbohydrates

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12
Q

Glycogenesis

A

Formation of glycogen from glucose

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13
Q

Insulin does what?

A
  • promotes glycolysis and Pentose Phosphate pathways
  • promotes glycogen formation
  • inhibits gluconeogenesis in liver
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14
Q

Where can Hexokinase and Glucokinase be found?

A
  • hexokinase = all cells

- glucokinase = pancreas & liver

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15
Q

What inhibits Hexokinase?

A

Glucose 6 phosphate

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16
Q

What inhibits Glucokinase?

A

Fructose 6 phosphate

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17
Q

What increases Glucokinase activity?

A

Glucose

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18
Q

What are their Km values? Which one can be saturated?

A
  • Glucokinase = Km 20
  • Hexokinase = Km 5
  • Hexokinase can be saturated
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19
Q

Pyruvate Carboxylase genetic deficiency

A
  • increase in Alanine, Lactate, and Pyruvate blood levels

- Diagnosis = developmental delays, recurrent seizures, and metabolic acidosis

20
Q

Pyruvate dehydrogenase complex

A
  • requires vitamins (Thiamine, Riboflavin, and Niacin

- Not regulated by glucagon or epinephrine

21
Q

Lactate dehydrogenase (LDH) Deficiency

A
  • unable to convert Pyruvate to Lactate
  • NAD+ becomes limiting during exercise
  • glyceraldehyde dehydrogenase flux reaction is inhibited
22
Q

NAD+ levels are regenerated through what pathways?

A
  • LDH
  • Malate Aspartate shuttle
  • Glycerol Phosphate shuttle
23
Q

Galactosemia

A

Small Group problem

24
Q

Glucose 6 Phosphate Dehydrogenase

A

Place holder

25
Q

Fine Control of Citric Acid Cycle (CAC)

A
  • high ADP & Ca2+ stimulate CAC

- high ATP, GTP, and NADH inhibit CAC

26
Q

Pyruvate dehydrogenase deficiency

A
  • common form caused by mutation in E1 alpha gene, inherited in X-linked manner
  • Other forms autosomal recessive
  • results in increased Alanine, Lactate, and Pyruvate blood levels
  • chronic lactic acidosis
  • treated with thiamine, carnitine, lipoic acids
27
Q

Pyruvate Carboxylase deficiency

A
  • accumulation of pyruvate, lactic acid, and alanine

- failure to thrive, developmental delays, recurrent seizures, and metabolic acidosis

28
Q

Glucose 6 Phosphatase deficiency

A
  • autosomal recessive metabolic disease
  • glycogen storage disease
  • GSD type I or von Gierke disease
  • poor tolerance to fasting, growth retardation, hepatomegaly
29
Q

Effects of Ethanol

A
  • Ethanol metabolism can cause hypoglycemia
  • Ethanol dehydrogenase increases NADH to NAD+ ratio
  • high NADH opposes gluconeogenesis
  • high NADH converts pyruvate to lactate, oxaloacetate to malate (which removes substrates from glycogenic pool)
30
Q

What is ideal fasting glucose level?

A

60 - 100 mg/mL

31
Q

First step of Gluconeogenesis (with pyruvate)

A
  • Pyruvate is converted to oxaloacetate by Pyruvate Carboxylase
  • then from Oxaloacetate to Phosphoenolpyruvate (PEP) by PEP Carboxykinase
  • Biotin and bicarbonate required (with ATP)
32
Q

What is the major source of ATP from an overnight fast?

A

oxidation of fatty acids

33
Q

What is the rate-limiting enzyme in fatty acid biosynthesis?

-What product does it form?

A

Acetyl-coA Carboxylase

-Malonyl-coA

34
Q

What are you likely to find increased levels of in the blood when fasting?

A
  • increased free fatty acids

- increased levels of ketone bodies

35
Q

What catalyzes the reaction from Fatty Acyl-coA to Acetyl-coA

A

(CPT-1)

Carnitine palmotyltransferase - 1

36
Q

What can Fatty Acids be estrified to form?

A
  • Triaglycerols

- Cholesterol Ester

37
Q

What two substrates are triacylglycerols broken down to form?

A
  • Fatty Acids

- Glycerol

38
Q

What enzyme catalyzes the conversion of triacylglycerols to fatty acids?
-What stimulates its activity?

A

HSTL

-epinephrine

39
Q

What inhibits CPT - 1 ?

A

Malonyl-coA

40
Q

Increased Malonyl-coA results in?

A
  • less fatty acid oxidation

- inhibition of CPT - 1

41
Q

What does an increase in acetyl-coA carboxylase do to ketone bodies?

A

lowers ketone body production

42
Q

Effect of excess cholesterol on HMG coA reductase

A

inhibits it

43
Q

Effect of excess cholesterol on ACAT

A

increases it

44
Q

Effect of excess cholesterol on 7 alpha hydroxylase

A

increases it

45
Q

What medication inhibits HMG-coA reductase?

A

Statins

Physiology section 3 (18 decks)

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