The Peripheral Endocrine Glands Lecture 8 - hormones secreted by pancreas Flashcards

(46 cards)

1
Q
A
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2
Q

Beta cells

A
  • 60%
  • site of insulin synthesis and secretion
  • located centrally in islets
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3
Q

Alpha cells

A
  • 25%
  • produce glucagon
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4
Q

delta cells

A
  • 10%
  • pancreatic site of somatostatin synthesis
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5
Q

F cells

A
  • 1%
  • least common islet cells
  • secrete pancreatic polypeptide (PP)
  • reduce appetite and food intake
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6
Q

Connective tissue, blood vessels and nerves

A
  • 4%
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7
Q

Epsilon cells:

A

secrete Ghrelin

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8
Q

Somatostatin is produced by

A
  • delta-cells in pancreas
  • hypothalamus (aka GHIH) – inhibits secretion of GH
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9
Q

Somatostatin
Stimulus for secretion:

A

increased blood sugar and blood amino acids during absorption of a meal

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10
Q

Somatostatin functions:

A

decrease digestion and absorption of nutrients
Prevents excessive plasma levels of nutrients
Presence of somatostatin - decrease secretion of insulin, glucagon, and somatostatin itself

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11
Q

Insulin:

A

Decreases blood glucose, fatty acids & amino acids – promotes their storage

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12
Q

During absorptive state:

A

(just after a meal)
- Most NB time for insulin
- insulin promotes cellular uptake of blood glucose, fatty acids & amino acids and their conversion into glycogen, triglycerides and protein

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13
Q

Insulin exerts its effects through:

A
  • increased activity of glycogen synthase (glucose –> glycogen)
    = glycogenesis
  • decreased activity of hormone sensitive lipase
    (triglycerides –> free fatty acids and glycerol)
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14
Q
A
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15
Q

Circulating glucose concentrations are determined by:

A
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16
Q

Action of insulin on blood glucose levels and storage of carbohydrates

A

insulin:
- Facilitates glucose transport into most cells
- increases glycogenesis (glucose –> glycogen) in skeletal muscle and liver

decrease glycogenolysis (glycogen –> glucose)
decrease hepatic glucose output by decreasing gluconeogenesis (amino acids –> glucose)

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17
Q

Glucose transport into cells

A
  • Transport between blood and cells – plasma membrane carrier, glucose transporter (GLUT)
  • 14 forms
  • Passive facilitated diffusion across plasma membrane
  • Inside cell glucose is P to glucose-6-phosphate –> glucose is trapped inside the cell, also keeps [ ] of plain glucose inside cell low – gradient favouring facilitated diffusion of glucose into cell
  • Family members of GLUT family performs different functions
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18
Q

GLUT-1:

A

transport glucose across blood-brain barrier

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19
Q

GLUT-2:

A

transfer glucose that has entered the kidney and intestinal cells into adjacent bloodstream by means of sodium and glucose co-transporter.

20
Q

GLUT-3:

A

transport glucose into neurons

21
Q

GLUT-4:

A

abundant in tissues that account for the bulk of glucose uptake in the absorptive state – skeletal muscle & adipose tissue

22
Q

GLUT-4 is the only glucose transporter that responds to insulin
- Why?

A
  • these organs are responsible for highest uptake of glucose for storage, thus must respond to insulin
  • No insulin, no GLUT-4 in plasma membrane
  • Intracellular vesicles contain GLUT-4
  • When insulin binds to receptor (phosphorylated tyrosine kinase) on surface membrane of target cell, vesicles moves to plasma membrane, fuse with it and inserting GLUT-4 on membrane
  • Decrease in insulin – glucose transporters are retrieved from membrane by endocytosis, returned to intracellular pool
23
Q

Brain, working muscles and liver _______ depend on insulin for glucose uptake

24
Q

Brain, working muscles and liver DO NOT depend on insulin for glucose uptake
Brain:

A

requires constant supply of glucose – freely permeable to glucose at all times – GLUT-1 & GLUT-3

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Brain, working muscles and liver DO NOT depend on insulin for glucose uptake Skeletal muscle
depend on insulin ONLY at rest for glucose uptake Muscle contraction triggers insertion of GLUT-4 on plasma membrane
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Brain, working muscles and liver DO NOT depend on insulin for glucose uptake Liver
does not depend on insulin for glucose uptake; does not use GLUT-4 Insulin enhance the metabolism of glucose by liver through P glucose to glucose-6-phosphate
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Action of insulin on FAT
- increase fatty acids into adipose tissue - increase glucose into adipose tissue through GLUT-4 recruitment - Promotes chemical reactions that use glucose and fatty acids derivates for triglyceride synthesis - decreases lipolysis (fat breakdown) THUS: favouring removal of fatty acids and glucose from blood, promotes their storage as triglycerides
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Actions of insulin on PROTEIN
- increase active transport of amino acids from blood into muscle and other tissue – provides building blocks for protein synthesis - increase rate of amino acid incorporation into protein – stimulating cell’s protein-synthesizing machinery - Inhibits protein degradation THUS: protein anabolic effect – essential for normal growth (permissive to GH).
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Glucose stimulates insulin secretion through excitation-secretion coupling process NB
Must be able to draw and explain! - high levels of glucose are detected by the beta cells of the pancreas - these beta cells then take up the glucose via the GLUT-2 transporter - this will increase the intracellular glucose levels - this glucose is then phosphorylated to form G6P - it will then be oxidised and ATP will be formed - ATP responsible for closure of ATP sensitive potassium channels - this results in an increase in intracellular potassium levels, which causes depolarization of the membrane of the cell - this then opens up the voltage-gated calcium channels and calcium will enter the cells - high levels of calcium in the cells will be responsible for the exocytosis of the vesicles which are filled with insulin
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inputs for insulin secretion:
- high blood glucose levels - increase in blood amino acid level - induces insulin secretion in the same way as glucose - by generating ATP, which leads to excitation-excretion coupling - gastrointestinal hormones (incretins) incretins - consist of GIP (Glucose-dependent insulinotropic peptide) and GLP (glucose-like peptide) the secretion of these hormones will notify the Beta cells (stimulated by food intake)
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Most common of all endocrine disorders
Diabetes Mellitus
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Diabetes Mellitus Prominent features:
elevated blood glucose levels Urine acquires sweetness from excess blood glucose that spills into urine
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Type I diabetes
Characterized by lack of insulin secretion
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Type II diabetes
Characterized by normal or even increased insulin secretion but reduced sensitivity of insulin’s target cells
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https://www.youtube.com/watch?v=JAjZv41iUJU
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3 P’s of Diabetes
- polydipsia: extreme thirst - polyuria: frequent urination - polyphagia: hunger
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NB diagram!!
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Diabetic person can lose consciousness and die from:
diabetic ketoacidotic coma due to insulin deficiency (deep laboured breathing and fruity breath) acute hypoglycemia caused by insulin shock
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Insulin excess hypoglycemia is caused by:
In diabetic patient when too much insulin is injected – insulin shock Consequences: - More glucose than necessary is driven into insulin-dependent cells > decrease blood glucose, brain starves, depressed brain function, unconsciousness, death. Treatment: Immediately eat or drink something sugary
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Insulin excess: hypoglycemia
Reactive hypoglycemia is caused by: B-cell tumours: secreting increased insulin B-cells: over-responsive to glucose Consequences: tremor, fatique, sleepiness, inability to concentrate (non-specific) Treatment: limit sugar and carbohydrate intake
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What will be the metabolic effects in a diabetic persons under stress conditions?
- look at metabolic effect of cortisol and epinephrine (stress hormones) - both these hormones increase blood glucose levels - diabetic person already has elevated blood glucose levels, which is now further aggravated by these stress hormones - must inject a little bit higher level of insulin to regulate blood glucose levels
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NB: Study this summary of the metabolic effects of the different hormones and the control of secretion