Biochem: insulin and Glucagon Flashcards

1
Q

Enzyme that cleaves the pro-insulin hormone into biologically active insulin and peptide C.

A

Convertase

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2
Q

Type of glucose transporter on pancreatic beta cells.

A

GLUT 2

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3
Q

Describe the steps involved with insulin secretion.

A
  1. Glucose enters pancreatic beta cells
  2. Glucose is metabolized into ATP which closes potassium ion channels
  3. The membrane is depolarized and opens calcium ion channels
  4. Calcium ions signal fusion and exocytosis of vesicles containing insulin and peptide C
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4
Q

Which glucose transporter is Insulin-Sensitive and where is it located?

A

GLUT 4

Located on muscle and fat cells

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5
Q

When insulin binds its receptor, what effects does activation of the Ras gene have? Two things.

A
  1. Activates MAP kinase pathways for growth and division

2. Signals dephosphorylation of Glycogen synthase to activate it for glycogen formation

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6
Q

When insulin binds its receptor, what effect does the activation of PKB have?

A

Signals GLUT 4 transporters to move to the cell membrane.

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7
Q

Generally describe how insulin signaling affects the FOX01 transcription factor and the resulting effects.
(6 effects)

A

Insulin binds the insulin receptor which leads to phosphorylation of PI3K, which phosphorylates AKT which phosphorylates FOX01.

Phosphorylation of FOX01 allows it to be degrades by proteasomes and all its actions are stopped.

Effects of Insulin causing degredation of FOX01
(Most effects are on hepatocytes)
1. Increased Lipogenesis
2. Increased Glycolysis
3. Decreased VLDL production (however a phenomenon occurs with hyperinsuinemia which causes increased VLDL production)
4. Decreased gluconeogenesis
5, Decreased glycogenolysis
6. Increased survival and proliferation of pancreatic beta cells

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8
Q

Generally describe how insulin signaling affects AMPK enzyme and the resulting effects.

A
Insulin binds the insulin receptor phosphorylating PI3K which phosphorylates AKT which inactivates AMPK.  AMPK stimulates catabolic energy pathways and inhibits anabolic energy pathways.  These actions are inhibited with insulin.
Effects of insulin binding to inactivate AMPK:
1. Increased protein synthesis
2. Decreased glycolysis
3. Increased gluconeogenesis
4. Increased cholesterol synthesis
5. Increased TG synthesis
6. Increased fatty acid synthesis
7. Decreased fatty acid oxidation
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9
Q

What action does Metformin have on AMPK and why is it used?

A

Activates AMPK. Used in diabetes mellitus primarily to reverse hyperglycemia. This is achieved because metformin activates glycolysis and inhibits gluconeogenesis which rapidly depletes blood glucose.

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10
Q

Signaling pathway used by glucagon.

A

Gs

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11
Q

Effects of glucagon-like peptides on the brain and stomach.

A

Brain: appetite suppression
Stomach: inhibits gastric acid secretion and emptying (which also helps inhibit appetite)

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12
Q

Hormone secreted by delta cells in the pancreas.

A

Somatostatin

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13
Q

Functions of the 28AA prosomatostatin and the 14AA Somatostatin.

A

The 28AA is usually the final product of preprosomatostatin (it is not further cleaved into the 14AA somatostatin product) secreted by the hypothalamus. Its main action is on the ant. pit. to inhibit GH release.

The 14AA is secreted by the delta cells in the pancreas and acts on the alpha cells to inhibit glucagon release.

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14
Q

What environmental factors are associated with Type 1 Diabetes Mellitus (DM)?

A

Viruses: mumps, rubella, measles

Toxins: CN, rat poison

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15
Q

Mechanism of Type 2 DM.

A

Insulin insensitivity.
-mechanism not understood. Visceral adiposity, adipokines, and inflammation to due visceral fat release are all thought to contribute.

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16
Q

Most common defect leading to MODY.

A

Maturity Onset of Diabetes in the Young

  • mutation in beta cell glucokinase
  • patients unable to “trap” glucose in beta cells leading to low insulin secretion