Hormones Flashcards

0
Q

Name the four classes of hormonal signaling? Describe their general function.

A

Endocrine - released into blood, effects distant cells exocrine- released into duct for delivery to surface paracrine - released into interstitial space affecting neighboring cells autocrine - product affects releasing cells

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1
Q

What cell type releases insulin?

A

Beta cells

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2
Q

Describe the structure of insulin? How many chains? What types of bonds link those chains? Describe the different types of tertiary structures? What is Zincs role?

A
  • Insulin is composed of 2 primary amino acid chains - the alpha chain and the beta chain.
  • These chains are linked by disulfide bonds.
  • The alpha and beta chains form a monomer of insulin.
  • Two monomers form a dimer of insulin.
  • Two dimers form a hexamer of insulin.
  • Zinc holds the insulin molecules in the hexamer form.
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3
Q

Describe the mechanism by which insulin is released?

A
  1. Glucose enters the beta cell.
  2. This triggers glycolysis and ATP increases
  3. ATP sensitive K+channel is inhibited causing a buildup of charged potassium in cell
  4. This depolarizes the cell and triggers the opening of a voltage gated calcium channel.
  5. Calcium enters cell and insulin vesicles are released via exocytosis.
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4
Q

What contributes to the release of insulin?

A

High blood, GLP-1, GIP, and autonomic nervous system.

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5
Q

What does insulin stimulate?

A

Uptake of glucose in the cell, glycogen synthesis, uptake of amino acids by cells, glycerol synthesis, glycolysis in cell.

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6
Q

How do Catecholamines (Epinephrine) effect the muscles, liver, and adipose tissue?

A
  • Liver - make glucose for muscles NOW
    • Glycogenolysis
    • Gluconeogenesis
  • Muscles - Move NOW
    • Glycolysis
    • Glycogenolysis
    • Triglyceride utilization
  • Adipose Tissue - make glucose for Muslces
    • Lipolysis
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7
Q

What does insulin inhibit?

A
  • Protein catabolism
  • lipolysis
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8
Q

What does glucagon stimulate?

A
  • Gluconeogenesis
  • glycogenolysis
  • mobilization of fatty acids from adipose
  • hepatic lipase
  • Ketogenesis
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9
Q

What does somatostatin’s function

A

Inhibits release of insulin and glucagon

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10
Q

What stimulates the release of glucagon?

A

Low blood sugar, high protein meals, amino acids, cortisol, stress, epinephrine, sympathetic nervous system. It is constantly secreted.

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11
Q

What inhibits release of glucagon?

A
  • Glucose
  • insulin
  • GLP-1,
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12
Q

Describe the Synthesis of Insulin from gene to final hexameric form?

A
  1. Transcription of gene (chromosome 11) into mRNA & translation of mRNA on ribosome
  2. Initial translation of signal sequence and binding to rough ER.
  3. Synthesis of preproinsulin in lumen of ER.
  4. Signal sequence is cleaved & disulfide bonds form–>proinsulin
  5. Proinsulin in packaged and relasesd from ER to Golgi
  6. The C-chain is removed in the Golgi and new vesicles are formed–>insulin
  7. Mature insulin is packaged into a final hexameric structure with Zince and a C-chain remenants.
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13
Q

What is GLP-1?

Where is it produced?

What does it activate?

What does it inhibit?

A

GLP-1, or Glucagon-like peptide-1, is an incretin that aids glucose metabolism. It is produced in L-Cells (ileum and colon).

  • Activate
    • Increases release of insulin
    • Increases Beta cell proliferation
  • Inhibit
    • Glucagon
    • Gastric Empyting
    • Appetite
    • Beta Cell apoptosis
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14
Q

What is GIP?

What does it Activate?

What does it inhibit?

A

GIP, or glucose-dependant insulintropic peptide, is an incretin that aids in glucose metabolism. It is produced in K-cells in the jejunum.

  • Activates
    • Insulin release
    • Beta cell proliferation
    • lipogensis (build fatty acids)
  • Inhibits
    • Beta cell apoptosis
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15
Q

What is the effect of GLP-1 and GIP in people with diabetes?

A

GLP-1 levels are decreased in Type 2, but patients do respond to the effects of GLP-1. (GLP-1 thearpy is a potential option)

GIP levels are not decreased, but patients resist the effects.

16
Q

Why are the challenges with GLP-1 therpy for diabetics?

A

GLP-1 is rapidly degraded by the body. DPP-4 enzyme degrades GLP-1.

Half-life is less than 2 minutes

17
Q

What are 2 types of potential GLP-1 therapies?

A
  1. Those that mimic GLP-1 and bind to beta cells, but not to the DPP-4 enzyme that degrades it.
  2. Those that enhance GLP-1 and/or inhibit DPP-4 enzyme.
18
Q

What are the 4 main insulin counter regulatory hormones?

A
  1. Glucagon
  2. Catecholamines (epinephrine, adreniline)
  3. Cortisol
  4. Growth Hormones
19
Q

What is the effect of Counter Regulatory Horomones (CRH) in diabetics or people with repeated hypoglycemia?

A

CRH effects are lost or blunted. This leads to increased chances of hypoglycemia.

20
Q

What stimulates the release of GLP-1 and GIP?

A

Food ingestion

21
Q

What is the difference between Glucocorticoids and Catecholamines?

A

Catecholamines are a “fight or flight” response and glucorticoids are used under periods of stress to prepare for “fight or flight”

22
Q

What effects to Glucocorticoids have on Muscles, Liver, and Adipose Tissue?

A
  • Liver - Make and Store Glucose
    • increase gluconeogenesis
    • Glycogen Synthesis
  • Muscles - Make Glucose for liver
    • Degarde protein for gluconeogenesis
  • Adipose - Make glucose for liver
    • Lipolysis