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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
Tell me about McCardle syndrome.
-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
Tell me about Pompe Disease.
-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
Tell me about Cori Disease.
a deficiency in 4:4 transferase or 1:6 glucosidase (debranching enzymes) wich causes fasting hypoglycemia.
28
Tell e about Von Gierke disease.
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
What hormones stimulate breakdown of triglycerides in adipose tissue?
- high concentration of glucagon (except in humans) and epinephrine - low concentration of insulin
30
What enzyme controls triglyceride breakdown in adipose tissue?
Hormone sensitive lipase
31
How does a decline in insulin levels increase triglyceride breakdown in the adipose tissue?
- 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
Describe the mechanism in which epinephrine increases TAG breakdown.
- epinephrine binds receptor, activating adenylyl cyclase - Adenylyl cyclase makes cAMP, which activates PKA - PKA phosphorylates hormone sensitive lipase, activating it
33
Why are fatty acids repackaged into VLDLs after being transported to the liver on albumin?
-VLDLs increase the efficiency of transporting fatty acids to tissues in need when compared to albumin
34
How does fatty acyl-CoA enter the mitochondria?
- Fatty acyl CoA diffuses passively into intermembrane space | - Then binds carnities and crosses inner mitochondrial membrane via the carnitine shuttle
35
What inhibits the carnitine shuttle?
- Malonyl CoA | - makes sense because malonyl CoA is a main precursor for FA synthesis
36
What happens to the last 3 carbon molecule of FA beta oxidation if the fatty acid is an odd-chain lenght?
- 3C product is propionyl-CoA - This is converted to succinyl CoA by biotin and B12 - Succinyl CoA then enters the TCA cycle
37
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)
C. Hormone Sensitive Lipase
38
Resting muscle prefers which energy store during fasting? A. Glucose B. FAs C. Glucose and FAs D. ketone bodies and glucose E. Triglycerides
B. Fatty Acids
39
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
E. Most except blood and liver
40
Which tissue(s) utilize Gln from protein degradation for energy? A. Brain B. Brain and blood C. Kidney and intestine D. Blood E. Muscle
C. Kidney and intestine
41
What amino acids are proteins converted to in the fasted state to be used as energy? Which are the main organ destinations?
- Alanine (Liver) | - Glutamine (intestine and kidney)
42
What are the byproducts of the use of Glutaminein the small intestine, and where are they sent?
- Lactate and Alanine | - sent to liver to be converted to glucose
43
As what metabolite does alanine enter the energy pathway?
pyruvate
44
As what metabolite does glutamine enter the energy pathway?
``` Alpha ketoglutarate (via glutamate) to contribute to TCA cycle ```
45
What is the function of the Alanine cycle?
-moves amino groups from the muscle to the liver for excretion as urea
46
What happens to the alanine used to transport nitrogen in the alanine cycle?
-it is deaminated and converted to glucose via gluconeogenesis
47
What causes pheynylketonurea? How is it treated?
- deficiency in phenylalanine hydroxylase - leads to accumulation of phenylalanine, and a scarcity of tyrosine -treatmentn is protein restricted diet, with ingestion of tyrosine
48
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
B. Glycogenolysis and gluconeogenesis
49
What is the largest energy store in the body during starvation? A. glycogen B. protein C. ketone bodies D. fat
D. Fat
50
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
E) Serum albumin and VLDL
51
What are the general high energy state signal metabolites in muscle??
ATP NADH Citrate AcCoA Glucose 6-Phosphate Phosphocreatine
52
What are the general low energy state signal metabolites in muscle?
-AMP ADP Pi NAD+ NH4+ Fructose 2,6-bisphosphate Ca2+
53
What substrate inhibits the carnitine shuttle?
-Malonyl CoA

Term 2: Metabolism (5 decks)

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