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ENDOCRINE > 3a. Pancreas (Insulin) > Flashcards

3a. Pancreas (Insulin) Flashcards

1
Q

Body energy =

A

energy intake - energy output

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2
Q

what do the feeding centres do

A

promote feelings of hunger and the drive to eat

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3
Q

what do the satiety centres do

A

promote feelings of fullness by suppressing the feeding centres

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4
Q

what is the glucostatic theory of energy intake

A

food intake is determined by blood glucose: as [BG] increases, the drive to eat decreases (- Feeding Centre; + Satiety centre)

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5
Q

what is the lipostatic theory of energy intake

A

food intake is determined by fat stores: as fat stores increase, the drive to eat decreases (- feeding centre; + Satiety Centre).

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6
Q

what is Leptin

A

Leptin is a peptide hormone released by fat stores which depresses feeding activity

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7
Q

what are the three categories of energy output

A
  1. cellular work - transporting molecules across membranes, growth/repair, storage of energy, etc
  2. mechanical work - movement (either large scale with muscles or intracellularly)
  3. heat loss - associated with cellular and mechanical, accounts for half of energy output
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8
Q

define metabolism

A

the integration of all biochemical reactions in the body

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9
Q

what are the three elements of metabolism

A
  1. extracting energy from nutrients in food
  2. storing that energy
  3. utilising that energy for work
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10
Q

what are anabolic pathways

A

build up pathways - net effect is synthesis of large molecules from smaller ones, usually for storage purposes

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11
Q

what are catabolic pathways

A

break down pathways - net effect is degradation of large molecules into smaller ones, usually releasing energy for work

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12
Q

what is the absorptive state

A

the state we enter after eating where ingested nutrients supply the energy needs of the body and excess is stored - ANABOLIC PHASE

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13
Q

what is the post-absorptive state (i.e. fasted state)

A

the state we enter between meals and overnight when the pool of nutrients in the plasma decreases and we rely on body stores to provide energy - CATABOLIC PHASE

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14
Q

what chemical dominates the anabolic phase

A

insulin

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15
Q

what chemical dominates the catabolic phase

A

glucagon

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16
Q

what do most cells in the body use for energy

A

fats, carbohydrates or protein

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17
Q

why must we maintain blood glucose concentration

A

because the brain is an obligatory glucose utiliser i.e. can only use glucose for energy - so even if no new carbohydrate is gained by the body [BG] has to be maintained.

(but brain can later use ketone production in starvation)

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18
Q

How is blood glucose concentration maintained (in broad terms)

A

by synthesising glucose from glycogen (glycogenolysis) or from amino acids (gluconeogenesis)

19
Q

what is the normal range of blood glucose concentration

A

~5mmoles

4.2-6.3mM) (80-120mg/dl

20
Q

what [BG] constitutes hypoglycaemia

A

<3mM

21
Q

what percentage of the pancreas has endocrine function

A

1%

22
Q

where are the pancreases endocrine hormones produced

A

islets of langerhans - small areas of specialised cells

23
Q

what are the 4 types of islet cells and what do they produce

A
  1. alpha cells - glucagon
  2. beta cells - insulin
  3. delta cells - somatostatin
  4. F cells - pancreatic polypeptide
24
Q

What is the purpose of insulin and how does it do this

A

decreases blood glucose concentration

  • increases glucose oxidation
  • increases glycogen synthesis
  • increases fat synthesis
  • increases protein synthesis
25
Q

briefly describe the synthesis of insulin

A

synthesised as a large preprohormone (preproinsulin) - converted to proinsulin the the ER - asked as granules into secretory vesicles - within vesicle proinsulin is cleaved to give insulin and C-peptide - insulin stored in this form until the beta cell is activated and secretion occurs

26
Q

what stimulates insulin secretion

A

MAINLY [BG] - but both blood glucose concentration and amino acid concentration

27
Q

where is excess glucose stored

A

liver/muscle - as glycogen

28
Q

what are amino acids used to make

A

new proteins with excess converted to fat

29
Q

where are fatty acids stored

A

liver/adipose tissue - as triacylglycerols (TAG)

30
Q

what are K ATP channels

A

specialised K+ ion channels that are sensitive to the [ATP] within the cell - found in beta cells

31
Q

How do K ATP channels work when there are high blood glucose levels

A
  1. High glucose levels in blood
  2. glucose enters into cell via transport proteins (GLUT 2)
  3. Metabolism increases
  4. ATP increases
  5. K ATP channels close
  6. [K+] rise within cell
  7. cell depolarises and opens Ca channels
  8. Ca2+ entry acts as an intracellular signal
  9. Ca2+ signal triggers exocytosis and insulin is secreted
32
Q

How do K ATP channels work when there are low blood glucose levels

A
  1. When [BG] is low,
  2. [ATP] is low
  3. K ATP channels open so K+ ions flow out
  4. removes +ve charge from the cell and hyperpolarises it
  5. voltage-gated Ca2+ channels remain closed
  6. insulin is not secreted.
33
Q

what are the only insulin sensitive tissues

A

muscle and adipose - ie require insulin to take up glucose

all other tissues do not require insulin for glucose uptake

34
Q

What is the primary action of insulin

A

binds to tyrosine kinase receptors on cell membrane of insulin sensitive tissues - increases glucose uptake by these tissues

35
Q

How does insulin increase glucose uptake by cells

A

binds to receptor - cause signal transduction cascade - stimulates specific glucose transporter GLUT4 (found in the cytoplasm) - GLUT 4 exocytoses to cell membrane - glucose is transported through membrane here

Once stimulation by insulin stops – vesicles endocytose back into cell

36
Q

In non-insulin sensitive tissues how does glucose uptake occur

A

via insulin-independent GLUT transporters

GLUT 1 and 3 - basal glucose uptake in many tissues e.g. brain, kidney, RBC

GLUT 2 - beta cells of pancreas and liver

37
Q

How does glucose enter into the liver hepatocytes

A

GLUT 2 transporters take up glucose which enters down concentration gradient

38
Q

How does insulin enhance glucose movement into hepatocytes despite GLUT 2 being insulin independent

A

alters concentration gradient:

  1. Insulin cases signal cascades
  2. cause hexokinase to convert glucose into glucose-6-phosphate
  3. this keeps glucose concentration low
  4. therefore movement of glucose into the cell is favoured

(when low insulin the liver synthesises glucose via glycogenolysis and gluconeogenesis, inc. glucose concentration in the cell, gradient changes to favour glucose movement out of cell)

39
Q

How can insulin cause serious arrhythmias

A

by promoting K+ ion entry into cells stimulating Na+/K+ ATPase

40
Q

summarise the effects of insulin

A
  1. Glucose entry
  2. Glycogen stored in muscle and liver
  3. Amino acid uptake
  4. Protein synthesis
  5. Increased fat synthesis – produce glycerol
  6. Inhibits gluconeogenesis
  7. Stimulation of K+ uptake by stimulating Na+/K+ ATPase
41
Q

5 stimuli that increase insulin release

A
  1. HIGH [BG]
  2. increases plasma [amino acid]
  3. glucagon
  4. vagal nerve activity
  5. other (incretin) hormones controlling GI secretion and motility (e.g. gastrin, secretin, CCK, GLP-1, GIP)
42
Q

4 stimuli that inhibit insulin release

A
  1. LOW [BG]
  2. Somatostatin (GHIH from pancreas and hypothalamus)
  3. Sympathetic alpha2 effects
  4. stress eg hypoxia
43
Q

Why is the insulin response to IV glucose load less than the equivalent oral glucose load

A

IV glucose = increased insulin by direct effect of increased glucose on beta cells

BUT

Oral glucose = increased insulin by direct effect on beta cells AND vagal stimulation of beta cells PLUS incretin effects

ENDOCRINE (13 decks)

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