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2ND YEAR SYSTEMS: Diabetes and Endocrinology > Endocrine pancreas 1+2 > Flashcards

Endocrine pancreas 1+2 Flashcards

1
Q

The balance of activity in which 2 hypothalamic centres determines energy (food) intake? and how is it controlled?

A

Feeding centre - promotes feelings of hunger and drive to eat

Satiety centre - promotes feelings of fullness by suppressing the Feeding centre

In both - activity is controlled by a complex balance of neural and chemical signals as well as the presence of nutrients in plasma

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2
Q

What is the glucostatic theory

A

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

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3
Q

What is the lipostatic theory?

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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4
Q

What is leptin?

A

A peptide hormone released by fat stores which depresses feeding activity

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5
Q

How does obesity result?

A

imbalance in energy balance - too much input not enough output

rare for it to come about due to metabolic problem

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6
Q

What are the 3 categories of energy output?

A

Cellular work - transporting molecules across membranes; growth and repair; storage of energy (eg. fat, glycogen, ATP synthesis)

Mechanical work - movement, either on large scale using muscle or intracellularly (voluntary – posture etc and involuntary – cellular level etc)

Heat loss - associated with cellular and mechanical work accounts for half our energy output

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7
Q

What is the only part of energy output that can be regulated?

A

The mechanical work doen by skeletal muscle

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8
Q

What are the 3 elements of metabolism

A

Extracting energy from nutrients in food

Storing that energy

Utilising that energy for work

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9
Q

Why is it important to maintain blood glucose concentration?

A

We need sufficient levels of glucose in the blood to meet the brain’s requirements

The brain gets first dibs on any glucose in the blood (it will take it to the detriment of any other tissues in the body) – needs it to function properly

hypoglycaemia can lead to coma and death

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10
Q

What is glycogenolysis?

A

synthesising glucose from glycogen (stored in muscle)

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11
Q

What is gluconeogenesis?

A

Synthesising glucose from amino acids

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12
Q

Normal blood glucose range

A

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

remember 5 mmoles as this is pretty much normal

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13
Q

What normally happens if blood glucose levels become too low?

A

Brain only has access to [BG]

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14
Q

Overflow due to problem with glucose metabolism can cause what?

A

overflow of glucose into urine

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15
Q

What is lipogenesis?

A

excess glucose moves into fat stores

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16
Q

What is lipogenesis? what is stimulated by

A

excess glucose moves into fat stores

stimulated by insulin binding to receptor on fat cell

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17
Q

What is glucagon responsible for?

A

Increasing blood glucose levels - peptide hormone produced by alpha cells of the pancreatic islet cells

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18
Q

What is insulin responsible for?

A

Decreasing blood glucose levels

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19
Q

What does the pancreas release through ducts to support digestion?

A

enzymes

NaHCO3

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20
Q

Only 1% of the pancreas has endocrine function. Where are it’s hormones produced?

A

In the Islets of Langerhans

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21
Q

What are the 4 types of Islet cells?

A

alpha cells produce GLUCAGON

beta cells produce INSULIN

delta cells produce SOMATOSTATIN

F cells produce pancreatic polypeptide (function not really known, may help control of nutrient absorption from GIT.)

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22
Q

In what ways does insulin reduce [BG]? (4)

A

Increases glucose oxidation

Increases Glycogen synthesis

Increases fat synthesis

Increases protein synthesis

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23
Q

In what ways does glucagon increase [BG]? (3)

A

Increases Glycogenolysis

Increases Gluconeogenesis

Increases Ketogenesis

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24
Q

What happens during the absorptive state?

A

Glucose, amino acids and fatty acids enter the blood from the GI tract

Both stimulate insulin secretion but the major stimulus is [BG]

25
Q

What is the only hormone that lowers [BG]?

A

Insulin

26
Q

What is glucose stored as in liver and adipose tissue

A

Triacylglycerols

27
Q

What is glucose stored as in liver and muscle

A

glycogen

28
Q

What is the mechanism by which [BG] controls insulin secretion

A

High [BG]

Metabolism increases

ATP increases

K-ATP channels (specific to pancreatic B cells) close

cell depolarises and calcium channels open

Ca2+ entry acts as an intracellular signal

Ca2+ signal triggers exocytosis and insulin is secreted

29
Q

What happens to close Ca2+ voltage gated channels and stop insulin secretion?

A

When [BG] is low, [ATP] is low so KATP channels are open

K+ ions flow out removing +ve charge from the cell and hyperpolarizing it, so that voltage-gated Ca2+ channels remain closed and insulin is not secreted

30
Q

Primary action of insulin

A

Binds to tyrosine kinase receptors on the cell membrane of insulin-sensitive tissues to increase glucose uptake by these tissues.

In muscle and adipose tissue, insulin stimulates the recruitment of GLUT4 transporter to the membrane

Glucose can then be transported into the cell

when insulin stimulation stops then GLUT 4 transporters return to cytoplasm pool

the glucose taken up by cells is primarily used for energy

31
Q

Which are the only types of tissue that are insulin dependent?

A

Muscle and fat (takes up large proportion of body mass - so actually a lot of the body is dependent on insulin)

not all tissues require insulin to take up glucose - instead its via GLUT transporters

32
Q

Functions of GLUT1, GLUT2 and GLUT3

A

GLUT1 + GLUT2 - Basal glucose uptake in many tissues eg brain, kidney and red blood cells.

GLUT 3 - B cells of pancreas and liver

33
Q

Liver and glucose uptake

A

liver is not insulin dependent

takes up glucose via GLUT 2 transporters (insulin independent)

Glucose enters down conc gradient

although insulin has no direct effect on the liver, glucose transport into hepatocytes is affected by insulin status

34
Q

How does insulin status indirectly affect glucose transport into hepatocytes?

A

after eating, insulin promotes intracellular glucose metabolism so lowering the [glucose]IC

this creates a concentration gradient favouring glucose movement into the cells

35
Q

How does the liver release glucose in fasted state (post-absorptive)?

A

The liver synthesises glucose via glycogenolysis and gluconeogenesis (stimulated by glucagon)

this increases [glucose]ic creating a gradient favouring glucose movement out of the cells into the blood.

36
Q

Additional actions of insulin - activation of multiple signal transduction pathways associated with the insulin receptor

A

Increases glycogen synthesis in muscle and liver. Stimulates glycogen synthase and inhibits glycogen phosphorylase.

Increases amino acid uptake into muscle, promoting protein synthesis.

Increases protein synthesis and inhibits proteolysis

Increases triacylglycerol synthesis in adipocytes and liver i.e. stimulates lipogenesis and inhibits lipolysis.

Inhibits the enzymes of gluconeogenesis in the liver

Has a permissive effect on Growth hormone

Promotes K+ ion entry into cells by stimulating Na+/K+ ATPase. Very important clinically.*** Diabetes – lose K+ entry? - hyperkalaemia

37
Q

Half life of insulin

A

5 minutes

38
Q

Where is insulin degraded principally

A

In the liver and the kidneys

39
Q

What happens once insulin action is complete?

A

Insulin-bound receptors are internalised by endocytosis and destroyed by insulin protease, some recycled.

40
Q

Stimuli that increase insulin release (5)

A

Increased [BG]

Increased [amino acids]plasma

Glucagon - insulin takes up glucose which is created by gluconeogenesis which is stimulated by glucagon

vagal nerve activity

Other hormones controlling GI secretion and motility

41
Q

Stimuli which inhibit insulin release

A

low [BG]

Somatostatin GHIH

Sympathetic alpha 2 effects

stress - hypoxia

42
Q

Vagal activity

A

Vagal activity stimulates release of major GI hormones, and also stimulates insulin release

therefore meaning that the insulin response to an IV glucose load is less than the equivalent amount of glucose administered orally (goes through gut)

43
Q

Half life of glucagon

A

5-10 mins in plasma

degraded mainly by liver

44
Q

What is involved in the glucose counter-regulatory control system

A

Glucagon

Epinephrine

Cortisol

Growth hormone

45
Q

When is glucagon most active?

A

Post-absorptive state (between meals/at night)

46
Q

What are glucagon receptors like?

A

G protein coupled receptors linked to the adenylate cyclase/cAMP system - when activated phosphorylate specific liver enzymes

47
Q

What happens when specific liver enzymes are phosphorylated after glucagon binds

A

increased glycogenolysis

increased
gluconeogenesis (substrates: aa’s and glycerol (lipolysis))

formation of ketones from fatty acids (lipolysis)

48
Q

Stimuli that promote glucagon release

A

Low [BG] (<5mM)

high [amino acids] - prevent hypoglycaemia

Sympathetic innervation and epinephrine, B2 effect

Cortisol

Stress - exercise, infection

49
Q

Stimuli that inhibit glucagon release

A

BG

free fatty acids and ketones

Insulin

somatostatin

50
Q

Autonomic nervous system innervation of islet cells

A

generally…

increased parasympathetic activity (vagus) increases insulin and to a lesser extent increases glucagon, in association with the anticipatory phase of digestion.

increased sympathetic activation promotes glucose mobilisation which increases glucagon which increases epinephrine and inhibition of insulin - all appropriate for fight or flight response.

51
Q

Somatostatin (also known as growth hormone inhibiting hormone)

A

Somatostatin is a peptide hormone secreted by Delta cells of the pancreas

Main pancreatic action is to inhibit activity in the GI Tract.
It seems to slow down absorption of nutrients to prevent exaggerated peaks in plasma concentrations.

SS is NOT a counter-regulatory hormone in the control of blood glucose but it does strongly suppresses the release of both insulin and glucagon in a paracrine fashion.

52
Q

Effect of exercise on [BG]

A

The entry of glucose into skeletal muscle is increased during exercise, even in the absence of insulin.

Exercise also increases the sensitivity of muscle to insulin, and causes an insulin-independent increase in the number of GLUT-4 (on skeletal muscle) transporters incorporated into the muscle membrane.

regular exercise can produce prolonged increases in insulin sensitivity

critical in improving type 2 diabetes - – exercise lowers BG without requiring insulin

53
Q

Starvation

A

When nutrients are scarce, body relies on stores for energy – when adipose tissue is broken down fatty acids are released.

Free FA’s can be readily used by most tissues to produce energy and liver will convert excess to ketone bodies which provides an additional source for muscle and brain (in extreme cases)!

this serves to ‘spare protein’ as otherwise too much protein would be lost - very weakening, vulnerable to infection

54
Q

After a period of starvation what does the brain do

A

adapts to be able to use ketones as an energy source

55
Q

How does life- threatening acidocis come about in diabetes type 1

A

in poorly controlled insulin-dependent diabetes a lack of insulin depresses ketone body uptake (because insulin supports this uptake).

They build up rapidly in the plasma and because they are acidic create life threatening acidosis (ketoacidosis or ketosis) with plasma pH < 7.1. (normal = 7.4)

Death will occur within hours if untreated.

56
Q

Type 2 diabetes - non-insulin dependent diabetes mellitus

A

Peripheral tissues become insensitive to insulin = insulin resistance.

Muscle and fat no longer respond to normal levels of insulin. This is either due to an abnormal response of insulin receptors in these tissues or a reduction in their number.

B-cells remain intact and appear normal, there may even be hyperinsulinaemia.

90% of diabetic patients are of this type

57
Q

Glucose tolerance test

A

Patient ingests glucose load after fasting [BG] measured. [BG] will normally return to fasting levels within an hour, elevation after 2 hours is indicative of diabetes.

Does not distinguish Type I from II.

[BG] elevated in both Type I and Type II Diabetes for different reasons:

Type 1 - inadequate insulin release
Type 2 - inadequate tissue response

Hyperglycaemia (elevated [BG]) is the diagnostic criterion for diabetes - detected by GTT

58
Q

Glucose tolerance test

A

Patient ingests glucose load after fasting [BG] measured. [BG] will normally return to fasting levels within an hour, elevation after 2 hours is indicative of diabetes.

Does not distinguish Type I from II.

[BG] elevated in both Type I and Type II Diabetes for different reasons:

Type 1 - inadequate insulin release
Type 2 - inadequate tissue response

Hyperglycaemia (elevated [BG]) is the diagnostic criterion for diabetes - detected by GTT

59
Q

Diabetic complications (4)

A

Retinopathy
Neuropathy
Nephropathy
Cardiovascular Disease

2ND YEAR SYSTEMS: Diabetes and Endocrinology (21 decks)

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