Integrating the Metabolic Response to Starvation Flashcards

1
Q

What are the principal organs of gluconeogensis?

A

LIVER and KIDNEY!

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2
Q

What is difference between anabolic and catabolic phase?

A
Anabolic= fed! Storing nutrients
Catabolic = fasting, using nutrients
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3
Q

How does Glucose stimulate it’s own storage?

A

It enhances net glycogen and fatty acid synthesis!

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4
Q

What inhibits? and activates AMPK?!

A

Low ATP will activate 5-AMP which activates AMPK and high ATP inhibits AMPK.

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5
Q

What does happens when AMPK is activated?

A

It increases ATP generation: SO you have increased fatty acid oxidation and increase cellular glucose uptake

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6
Q

When would AMPK be inhibited?

A

When you have high ATP. SO you have decreased ATP utilization. So you have decreased fatty acid and sterol synthesis and decreased cell division

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7
Q

What happens when blood glucose levels rise?

A

Insulin is secreted and glucagon & epinephrine is suppressed!

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8
Q

What does GLP-1 do?

A

It is made in the small intestine after a carbohydrate rich meal. Stimulates the beta cell to release insulin.

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9
Q

When Glucagon secreted?

A

Released by the alpha cells, it is triggered by falling blood glucose. Insulin usually suppresses the alpha cell so when insulin levels fall, this releases that inhibition. Epinephrine is also released during low glucose levels and this stimulates glucagon release.

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10
Q

Insulin is synthesized in ___ cells as a preprohormone. What do the pre and pro sequences do?

A

Beta cells.

Pre (N-terminal) sequence directs the nascent polypeptide chain from the ribosomes into the cisternae of the ER where the pre is replaced with the pro sequence (C-peptide). The pro sequence directs proper folding of insulin.

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11
Q

What does cAMP Phosphodiesterase (PDE) do?

A

It breaks down cAMP

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12
Q

How does insulin begin to work?

A

First it activates tyrosine kinase. This leads to autophosphorylation of the receptor and to tyrosine phosphorylation of key intracellular proteins (docking proteins IRS-1, IRS-2).

Phosphorylated versions of these docking proteins recruit other important proteins that contain SH2 domains and initiate “downstream” signaling events that involve action of serine/threonine-directed protein kinases (regulates Akt)

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13
Q

What does Insulin do to PDE? What would this favor?

A

It leads to the phosphorylation of cAMP phosphodiesterase, causing its activation.

These actions would favor glycogen storage, inhibit gluconeogenesis and inhibit lipolysis (favoring TG storage) and ketogenesis

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14
Q

What does GLUT-4 do? What happens when Insulin levels fall?

A

Insulin during anabolism promotes glucose uptake into muscle and adipose tissue using GLUT-4. When insulin concentrations fall, glucose entry into these tissues is diminished and glucose is rerouted to tissues where glucose uptake is NOT dependent on insulin’s actions (brain, RBC)

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