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Z- Endocrinology > The endocrine pancreas > Flashcards

The endocrine pancreas Flashcards

1
Q

what is metabolism?

A

Refers to all chemical reactions that occur within cells of the body

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2
Q

what is fuel metabolism (intermediary metabolism)?

A

Refers to reactions involving catabolism, anabolism and transformation of protein, carbohydrate (CHO) and fat

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3
Q

what hormones are fuel metabolism regulated by?

A

Insulin, glucagon, adrenaline, cortisol and growth hormone

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4
Q

what regulates metabolic rate?

A

thyroid hormone

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5
Q

what is glucose stored as?

A

glycogen

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6
Q

what are endocrine glands made of?

A

islets of langerhans

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7
Q

what 4 major types of secretory cells do islets contain?

A

1) Alpha cells (glucagon)
2) Beta cells (insulin, proinsulin, C peptide and amylin)
3) Delta cells (somatostatin)
4) F cells (pancreatic polypetide )

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8
Q

what are the most abundant cells in the islet?

A

beta cells

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9
Q

where are beta cells located in the islet?

A

in the centre of the islet

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10
Q

what cells sit at the periphery of the islet?

A

alpha and delta cells

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11
Q

how do cells within the islet communicate?

A

gap and tight junction

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12
Q

what do the cells in islets receive external input from?

A

Both branches of the autonomic nervous system

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13
Q

what do beta cells do?

A

synthesise and secrete insulin

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14
Q

what is the structure of mature insulin?

A

2 peptide chains (A and B chains) joined by disulfide linkages.
The mature insulin molecule has a total of 51 AA:
21 on the A chain + 30 on the B chain

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15
Q

what does the secretory vesicle release into the blood when glucose stimulates the beta cell?

A

insulin
proinsulin
C peptide

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16
Q

what is the role of insulin during fasting and feeding?

A

integrates body fuel metabolism

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17
Q

Describe the events of insulin during fasting (post-absorptive period)

A

The beta cell secretes less insulin:
Lipids are mobilised from adipose tissue
Amino acids (AAs) are mobilised from muscle and other tissues
Lipids and AAs provide fuel for oxidation and act as pre-cursors for hepatic ketogenesis and gluconeogenesis, respectively

18
Q

Describe the events of insulin during feeding (absorptive period)

A

The beta cell secretes more insulin:
Catabolism of endogenous fuel stores is inhibited
CHO, lipid and AA uptake by specific insulin-sensitive tissues is stimulated
(Insulin directs tissues to replenish fuel reserves that were used during periods of fasting)

19
Q

what are the overall function of insulin?

A

Insulin maintains the [glucose]*blood within narrow limits

Helps provide the CNS with a constant supply of glucose for fuel to maintain cortical function

20
Q

what are symptoms of hypoglycaemia?

A

confusion, seizures, coma

21
Q

what are symptoms of hyperglycemia?

A

characteristic of the diabetic state: osmotic diuresis –> severe dehydration, hypotension and vascular collapse

22
Q

what are glucose levels in an healthy individual?

A
  • After an overnight fast: 4-5 mM

- Rises after a meal: does not exceed 10 mM

23
Q

what do modest increases in plasma [glucose] provoke?

A

increase in insulin secretion and hence plasma insulin

24
Q

why is insulin levels after glucose injected by IV much lower than that of insulin after glucose after oral digestion?

A
  • 3 peptides : CCK, GLP-1 and GIP enhance insulin secretion

- all 3 are released in the GI tract in response to feeding

25
Q

Describe the metabolism of glucose by the beta cell trigger insulin secretion.

A
  • Glucose is taken up by pancreatic beta cells facilaitated by GLUT 2 – then undergoes glycolyiss
  • Leads to increase in intraceullar ATP
  • This closes ATP sensitive channels (potassium)-prevents loss of potassium ions from the cells – positive charge in cell

-Causes depolarisationm of membrane potential which
opens voltage dependant calcium channels , increase in interceullar calcium

-stimulates exocyotsis of the vesicles to release the insulin into the ECF and eventusally in the blood

26
Q

what are the roles of the autonomic nervous system in insulin secretion?

A

Sympathetic stimulation inhibits insulin secretion

Parasympathetic stimulation stimulates insulin secretion (during feeding – cephalic phase)

27
Q

what happens during exercise?

A
  • suppresses insulin secretion

- Helps prevent excessive glucose uptake by muscle, which could lead to severe hypoglycemia (compromising the CNS)

28
Q

what are the 3 principal target tissues for insulin?

A
  1. liver (glucose stored as glycogen)
  2. skeletal muscle (glucose stored are glycogen)
  3. adipose tissue (stored as fat)
29
Q

what are the actions of insulin in the liver?

A

Promotes the synthesis of glycogen
Inhibits glycogenolysis
Inhibits gluconeogenesis (at high plasma [insulin])

Promotes the storage of fats as triglycerides and inhibits the oxidation of fatty acids (therefore insulin causes the liver to burn CHOs preferentially).

Stimulates the synthesis of protein and simultaneously reduces the degradation of protein within the liver

30
Q

what are the actions of insulin in skeletal muscle?

A

Stimulates glucose uptake via increased PM expression of GLUT4, an insulin-sensitive facilitative glucose transport protein (next slide)

Enhances conversion of glucose to glycogen

Increases glucose breakdown and oxidation (cells diminish fat utilisation, fatty acids stored as triglycerides)

Stimulates protein synthesis and slows protein degradation (preservation of protein mass)

31
Q

what effect does insulin have of GLUT 4 transporters?

A

Insulin stimulates glucose uptake by muscle and adipose tissue, leading to a reduction in blood glucose levels.
Insulin causes glucose transporter proteins (GLUT4) to be inserted in the plasma membrane from intracellular stores

32
Q

what else causes increased expression of GLUT 4 transporters?

A

when skeletal muscle cell contracts during exercise

33
Q

what are the actions of insulin in adipocytes?

A

Increases glucose uptake as a result of increased GLUT4 PM expression

Promotes the breakdown of glucose to metabolites that will eventually be used to synthesise triglycerides

Promotes the formation of triglycerides and inhibits hormone-sensitive triglyceride lipase (HSL)

Induces synthesis of lipoprotein lipase (LPL) which is exported from the cell to the e/c surface of endothelial cells.
Here LPL can act on triglycerides in the blood, cleaving them to FFAs and glycerol. FFAs can then enter the adipocytes to form triglycerides

34
Q

what is the main difference between type 1 and type 2 diabetes mellitus?

A

for type 1 there is little/no secretion of insulin but in type 2 there is a defect insulin sensitivity

35
Q

what are the effects of severe diabetes mellitus?

A

Plasma [Glucose] very high after a meal

Glucose appears in urine (glycosuria)
Osmotic diuresis, dehydration and consequently, thirst.

The inability of cells to utilise glucose causes a compensatory increase in lipolysis to generate fatty acids as an energy source.

Metabolism of fatty acids generates acetyl CoA.
Liver unable to process extra acetyl CoA thro’ citric acid cycle, ketone bodies formed

These lower blood pH (metabolic acidosis) initiating compensatory hyperventilation (“acid drop” breath)

36
Q

when do pancreatic alpha cells secrete glucagon?

A

in response to ingested protein (AAs)

37
Q

what is glucagon’s target tissue and what action does it take?

A

Liver-
Glucagon regulates hepatic CHO and lipid metabolism
Glucagon stimulates glycogenolysis, gluconeogenesis and ketogenesis

38
Q

what effect does glycagon have on cardiac, skeletal muscle and adipose tissue?

A
  • Glucagon also acts on cardiac and skeletal muscle to stimulate glycogenolysis
  • Glucagon stimulates lipolysis in adipose tissue
39
Q

what type of hormone is glucagon?

A

catabolic

40
Q

what does glucagon prevent after a protein-rich meal?

A

hypoglycaemia

41
Q

where is somatostatin secreted from?

A
  • the delta cells of the pancreatic Islets
  • D cells of the GI tract
  • Hypothalamus (suppresses the release of growth hormone)
  • Several other sites in the CNS
42
Q

what is the role of somatostatin?

A

inhibits the secretion of growth hormone, insulin, glucagon, gastrin and TSH

Z- Endocrinology (9 decks)

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