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Term 2: Metabolism > Unfed Metabolism > Flashcards

Unfed Metabolism Flashcards

1
Q

What are the phases of starvation? Include times for each stage.

A
  1. Early starvation = 4-24 hours after eating
  2. Intermediate Starvation = 24 hrs - 3days after eating
  3. Prolonged Starvation = 3 days - death
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2
Q

Where is glycogen stored?

A
  • liver

- muscle

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3
Q

What happens to glycogen stored in the liver during a fasting state?

A

-it is broken down and sent to the rest of the body, as the liver can use other substances for fuel

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4
Q

What happens to glycogen stored in the muscle during a fasted state?

A
  • it is broken down and used by that muscle

- muscle is selfish

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5
Q

How can protein be utilized as energy?

A
  • gluconeogenesis

- feed directly into citric acid cycle

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6
Q

What are the two rules of the fasted state?

A
  1. Make sure that glucose requiring tissues are fed (brain and erythrocytes) from energy stores.
  2. Make sure everything else gets fed from energy stores.
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7
Q

What can the brain use as energy?

A
  • Glucose (Preferred)

- Ketone bodies

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8
Q

What doe the erythrocytes use as energy?

A

-glucose only

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9
Q

What does the liver use for energy in the fasted state?

A

-fat

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10
Q

What do the muscles use for energy in the fasted state?

A

-fat

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11
Q

What is the byproduct of metabolism in blood cells?

A

-lactate

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12
Q

Does muscle react to glucagon levels?

A

-no, muscle is only insulin sensitive. Therefore it will respond to low insulin levels.

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13
Q

What enzyme degrades glycogen?

A
  • glycogen phosphorylase

- with the assistance of two debranching enzymes

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14
Q

What enzyme converts glucose 1-phosphate to glucose 6-phosphate in glycogenolysis?

A

-phosphoglucomutase

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15
Q

Why can’t muscle export its broken down glycogen?

A

-Glucose 6-phosphate needs to be hydrolyzed by glucose 6-phosphatase before it can be exported from cells. Muscle cells do not contain glucose 6-phosphatase.

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16
Q

What are the metabolite activators of glycogenolysis in the muscle and liver?

A

Muscle:

  • Ca2+
  • AMP

Liver:
-Ca2+

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17
Q

What are the metabolite inhibitors of glycogenolysis in the muscle and liver?

A

Muscle:

  • Glucose 6-phosphate
  • ATP

Liver:

  • Glucose 6-phosphate
  • ATP
  • Glucose
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18
Q

In muscle, why does Ca2+ activate Phosphorylase Kinase without it being phosphorylated?

A. – Ca2+ is a master second messenger and is superior to other mechanisms.

B. - Ca2+ levels increase during muscle exercise and signals a need for energy.

C. – Phosphorylation of Phosphorylase Kinase is not required for activation.

D. – Ca2+ acts independently through calmodulin- dependent mechanisms

A

B. Ca2+ levels increase during muscle exercise and signals a need for energy

C and D are also true, but B is best answer

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19
Q

How do gucagon and epinephrine stimulate glycogenolysis?

A
  • bind receptor and activate adenylate cyclase
  • increase cAMP
  • activate PKA signalling cascade which activates glycogen phosphorylase
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20
Q

What steps in gluconeogensis are done by separate enzymes than glycolysis?

A
  • Pyruvate–>Oxaloacetate–>PEP
  • Fructose 1,6-BP–>Fructose 6-P
  • Glucose 6-P–>Glucose
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21
Q

What enzymes catalyze the gluconeogenic reaction of pyruvate–>PEP?

A
  • Pyruvate carboxylase

- phosphoenol pyruvate carboxylase

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22
Q

What enzyme catalyzes the gluconeogenic reaction of fructose 1,6-BP to Fructose 6-P?

A

-Fructose 1,6-bisphosphatase

23
Q

What enzyme catalyzes the gluconeogenic reaction of glucose 6-P to Glucose?

A
  • Glucose 6-phosphatase

- only exists in liver and kidneys

24
Q

What are the regulators of the conversion of pyruvate to PEP in gluconeogenesis?

A

Activators:
-acetyl CoA (pyruvate carboxylase)

Inhibitors:
-ADP (pyruvate carboxylase & PEP carboxylase)

25
Q

Tell me about McCardle syndrome.

A

-deficiency in skeletal muscle glycogen phosphorylase, which leads to cramping, muscle weakness, and no lactate increase after exercise. There is a high concentration of glycogen in muscles, just can’t be broken down.

26
Q

Tell me about Pompe Disease.

A

-a lysosomal alpha 1,4-glucosidase deficiency. That means it’s a lysosomal storage disease with excessive glycogen in vacuoles. This causes cardiomegaly and early death from heart failure.

27
Q

Tell me about Cori Disease.

A

a deficiency in 4:4 transferase or 1:6 glucosidase (debranching enzymes) wich causes fasting hypoglycemia.

28
Q

Tell e about Von Gierke disease.

A

results from a glucose 6 phosphatase deficiency. This leads to severe fasting hypoglycemia, a fatty liver, and increased glycogen storage. This disease is treated via infusions of glucose or starch.

29
Q

What hormones stimulate breakdown of triglycerides in adipose tissue?

A
  • high concentration of glucagon (except in humans) and epinephrine
  • low concentration of insulin
30
Q

What enzyme controls triglyceride breakdown in adipose tissue?

A

Hormone sensitive lipase

31
Q

How does a decline in insulin levels increase triglyceride breakdown in the adipose tissue?

A
  • Decreases the rate of phosphate removal from the active hormone-sensitive lipase
  • Decreases DHAP, wihch is the source of glycerol for the synthesis of triglycerides
32
Q

Describe the mechanism in which epinephrine increases TAG breakdown.

A
  • epinephrine binds receptor, activating adenylyl cyclase
  • Adenylyl cyclase makes cAMP, which activates PKA
  • PKA phosphorylates hormone sensitive lipase, activating it
33
Q

Why are fatty acids repackaged into VLDLs after being transported to the liver on albumin?

A

-VLDLs increase the efficiency of transporting fatty acids to tissues in need when compared to albumin

34
Q

How does fatty acyl-CoA enter the mitochondria?

A
  • Fatty acyl CoA diffuses passively into intermembrane space

- Then binds carnities and crosses inner mitochondrial membrane via the carnitine shuttle

35
Q

What inhibits the carnitine shuttle?

A
  • Malonyl CoA

- makes sense because malonyl CoA is a main precursor for FA synthesis

36
Q

What happens to the last 3 carbon molecule of FA beta oxidation if the fatty acid is an odd-chain lenght?

A
  • 3C product is propionyl-CoA
  • This is converted to succinyl CoA by biotin and B12
  • Succinyl CoA then enters the TCA cycle
37
Q

During Fasting FAs are mobilized by activation of which enzyme?

A. Glycogen phosphorylase

B. Lipoprotein lipase

C. Hormone Sensitive Lipase

D. Acetyl CoA Carboxylase (ACC)

E. Carnitine-palmitoyl transferase (CPT, carnitine shuttle)

A

C. Hormone Sensitive Lipase

38
Q

Resting muscle prefers which energy store during fasting?

A. Glucose

B. FAs

C. Glucose and FAs

D. ketone bodies and glucose

E. Triglycerides

A

B. Fatty Acids

39
Q

Which tissue(s) use ketone bodies as an energy source during starvation?

A. Brain

B. Brain and blood

C. Kidney and liver

D. Blood

E. Most except blood and liver

A

E. Most except blood and liver

40
Q

Which tissue(s) utilize Gln from protein degradation for energy?

A. Brain

B. Brain and blood

C. Kidney and intestine

D. Blood

E. Muscle

A

C. Kidney and intestine

41
Q

What amino acids are proteins converted to in the fasted state to be used as energy? Which are the main organ destinations?

A
  • Alanine (Liver)

- Glutamine (intestine and kidney)

42
Q

What are the byproducts of the use of Glutaminein the small intestine, and where are they sent?

A
  • Lactate and Alanine

- sent to liver to be converted to glucose

43
Q

As what metabolite does alanine enter the energy pathway?

A

pyruvate

44
Q

As what metabolite does glutamine enter the energy pathway?

A 
Alpha ketoglutarate (via glutamate)
to contribute to TCA cycle
45
Q

What is the function of the Alanine cycle?

A

-moves amino groups from the muscle to the liver for excretion as urea

46
Q

What happens to the alanine used to transport nitrogen in the alanine cycle?

A

-it is deaminated and converted to glucose via gluconeogenesis

47
Q

What causes pheynylketonurea? How is it treated?

A
  • deficiency in phenylalanine hydroxylase
  • leads to accumulation of phenylalanine, and a scarcity of tyrosine

-treatmentn is protein restricted diet, with ingestion of tyrosine

48
Q

What are the principal sources of circulating glucose during the first 24 hours after feeding?

A. glycogenolysis

B. glycogenolysis and gluconeogensis

C. fatty acids

D. intestinal absorption

E. protein degradation

A

B. Glycogenolysis and gluconeogenesis

49
Q

What is the largest energy store in the body during starvation?

A. glycogen

B. protein

C. ketone bodies

D. fat

A

D. Fat

50
Q

What carriers are used to transport energy from stored fat to other tissues?

A. TG

B. VLDL

C. Serum Albumin

D. Glycerol

E. Serum albumin and VLDL

A

E) Serum albumin and VLDL

51
Q

What are the general high energy state signal metabolites in muscle??

A

ATP

NADH

Citrate

AcCoA

Glucose 6-Phosphate

Phosphocreatine

52
Q

What are the general low energy state signal metabolites in muscle?

A

-AMP

ADP

Pi

NAD+

NH4+

Fructose 2,6-bisphosphate

Ca2+

53
Q

What substrate inhibits the carnitine shuttle?

A

-Malonyl CoA

Term 2: Metabolism (5 decks)

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