L36 - Cell Signalling: Insulin

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balance for adrenalin

Last updated 6:26 AM on 6/2/26
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9 Terms

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Insulin Signalling

uses:

Enzyme-coupled Receptors = binding of signal molecule turns on receptors enzyme domain

→ contains receptor tyrosine kinases (RTKs) : phosphorylate the receptors own tyrosines when signal binds → phosphorylates target proteins too

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Insulin Signalling: Purpose

  1. makes digestive enzyme for gut

  2. releases glucagon proteins when blood [glucose] is low

via: alpha islet cells

mech: alpha cells release glucagon → signals liver cell to release glucose into blood

  1. releases insulin proteins when blood [glucose] is high

via: beta islet cells

mech: beta islet cells release insulin → signals fat/muscle cells to uptake glucose from blood

note: fat & muscle cells display insulin receptors → import glucose

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which cells have the most glucagon receptors?

liver cells

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Insulin Signalling: Activation

  1. insulin is released via regulated exocytosis

  2. insulin binds to insulin receptors (homodimers) on fat/muscle cells

  3. insulin receptors phosphorylate itself → results in phosphorylation of target proteins → activated

active target protein: responses

  1. GLUT to plasma membrane

  2. increased glycogen synthesis (store glucose)

  3. decreased glycogen breakdown

<ol><li><p>insulin is released via regulated exocytosis </p><img src="https://assets.knowt.com/user-attachments/c724dfc7-e466-4f0e-9579-6977a0e524a1.png" data-width="25%" data-align="center"></li><li><p>insulin binds to insulin receptors<em> (homodimers)</em> on fat/muscle cells</p></li><li><p>insulin receptors phosphorylate itself → results in phosphorylation of target proteins → activated </p></li></ol><p></p><p></p><p>active target protein: responses </p><ol><li><p>GLUT to plasma membrane</p></li><li><p>increased glycogen synthesis (store glucose)</p></li><li><p>decreased glycogen breakdown </p></li></ol><p></p>
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Insulin Signalling: Responses

  1. import glucose (brings GLUT out to plasma memb for glucose to enter cell)

via: kinase cascade

  1. store glucose

via: activation of glycogen synthase + inhibits glycogen breakdown

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Insulin Signalling: Deactivation

  1. remove insulin

  2. dephosphorylate target cells (via phosphates)

  3. pinocytosis brings GLUTs back into cell from plasma membrane

→ thus, glucose cant enter cell

<ol><li><p>remove insulin </p></li><li><p>dephosphorylate target cells (via phosphates)</p></li><li><p>pinocytosis brings GLUTs back into cell from plasma membrane </p></li></ol><p>→ thus, glucose cant enter cell </p><p></p>
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<p>Insulin Signalling: Medical Significance </p>

Insulin Signalling: Medical Significance

Diabetes Mellitus = inability to regulate blood glucose → high blood sugar

→ Type 1 = WBCs kill insulin producing beta islet cells

→ Type 2 = fat cells have fewer insulin receptors → CANT take in more glucose

  • from overeating

  • can use kidney cell SGLT to treat : acts as inhibitor to stop reuptake of glucose by kidneys → pee out extra glucose

treatments:

  • insulin

  • monitor blood glucose

  • healthy diet

<p>Diabetes Mellitus = inability to regulate blood glucose → high blood sugar</p><p><strong>→ Type 1 = WBCs kill insulin producing beta islet cells </strong></p><p></p><p>→ Type 2 = fat cells have fewer insulin receptors → CANT take in more glucose</p><ul><li><p>from overeating</p></li><li><p>can use kidney cell SGLT to treat : acts as inhibitor to stop reuptake of glucose by kidneys → pee out extra glucose </p><img src="https://assets.knowt.com/user-attachments/7b53e90a-887e-471a-881c-d6e0c012bf44.png" data-width="25%" data-align="center"></li></ul><p></p><p></p><p>treatments:</p><ul><li><p>insulin</p></li><li><p>monitor blood glucose</p></li><li><p>healthy diet </p></li></ul><p></p>
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Edmonton protocol to treat DM 1

  • take beta islets from donor → inject into liver instead of pancreas so WBCs cant kill them

<ul><li><p>take beta islets from donor → inject into liver instead of pancreas so WBCs cant kill them </p></li></ul><p></p>
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<p>Examinable Content </p>

Examinable Content