insulin and glucose Flashcards

1
Q

describe insulin processing

A
  • formation of insulin from proinsulin precursor assures that A and B chain are always present in equal amounts
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2
Q

describe familial hyperproinsulinemia

A
  • defects in insulin processing due to mutations in insulin gene
  • high proinsulin levels in the blood
  • normal glucose metabolism
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3
Q

describe the EVENTS FOLLOWING INSULIN BINDING TO RECEPTOR

A
  1. Autophosphorylation of Beta subunits (Tyr)
  2. Phosphorylation stimulates tyrosine kinase activity of the receptor
  3. IRS1 (insulin receptor substrate 1) is phosphorylated
  4. Most of the insulin effects require Ser/Thr phosphorylation

Paradox: receptor activation leads to phosphorylation of signaling proteins and dephosphorylation of metabolic enzymes

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4
Q

describe effects of insulin

A
  1. Insluin binding to receptor results in:
    1. endocytosis of insulin-receptor complex
    2. translocation of glucose transporter
    3. Beta-subunit tyrosine kinase activation
  • Results in:
    • increase foramtion of glycogen
    • increased uptake of glucose
    • increased utilization of glucose
    • decreased foramtion of glucose from glycogen, fat and protein

** DECREASED BLOOD GLUCOSE LEVELS***

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5
Q

describe gestational diabetes

A
  • INsulin sensitivity of the mother decreases to provide glucose to the fetus
  • In gestation diabetes mellitus (GDM) is characterized by DECREASED INSULIN SENSITIVITY and inadequate secretion
  • decreased insulin receptor kinase activity in GDM
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6
Q

describe the biochem of glucagon

A
  • glucagon ins a peptide hormone which is synthesized in a manner similar to insulin
    • synthesized in the ALPHA-CELLS of the pancreatic islets
    • Pre-pro-glucagon is proteolytically processed toyeild glucagon
    • in contrast to insulin, glucagon does not contain disulfide bridges
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7
Q

describe the effects on liver of insulin vs glucagon

A

Insulin

–> activates glycogen synthetase

–> stimulates glycolysis and ATP generation

–> no effect on glucose uptake

Glucagon

–> inactivates glycogen synthetase

–> activates glycogen phosphorylase

–> activates glucose-6-phosphatase

–> activates gluconeogenesis

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8
Q

describe the effects on muscle of insulin vs glucagon

A

Insulin

–> stimulates glucose uptake

–> stimulates glyoclysis and ATP generation

–> increase muscle glyogen and creatine phosphate levels

Glucagon

–> no effect, because there are no glucagon receptors

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9
Q

describe the effects on adipose tissue of insulin vs glucagon

A

INsulin

–> stimulates glucose uptake

–> promotes glycolysis

–> inhibits lipases

Glucagon

–> no effects, because there are no glucagon receptors

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10
Q

what stimulates insule and glucagon release

A
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11
Q

describe somatostatin

A
  • somatostatin is a cyclic peptide
  • synthesized in the Delta-cells of the pancreatic islets, but also in other organs (hypothalamus)
  • Synthesized as pre-pro-somatostatin
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12
Q

describe actions of somatostatin

A
  • Many effects throughout the body
  • in pancreas, inhibits the synthesis of both insulin and glucagon
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13
Q

describe the degradation of peptide hormoens

A
  • Half-life of insulin is 3-5 mins
    • degraded by receptor-mediated endocytosis
    • degradation take place mainly in liver
    • 50% of circualting insulin is cleared at the first passage through the liver
  • half life of glucagon is 6-7 minutes
    • degradation takes place in liver and kidney endosomes
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