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MBChB - Y2 - Endocrine > The Endocrine Pancreas 1 and 2 > Flashcards

The Endocrine Pancreas 1 and 2 Flashcards

1
Q

What are the two centres that are responsible for regulating how much food we take in?

A

Feeding centre (hunger)

Satiety centre (fullness, by suppressing the hunger centre)

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2
Q

What controls the feeding centre and the satiety centre?

A

Controlled by a complex balance of neural and chemical signals as well as the presence of nutrients in plasma.

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3
Q

What is meant by the glucostatic theory?

A

As blood glucose concentration increases the drive to eat decreases

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4
Q

What is meant by the lipostatic theory?

A

As fat stores increase the drive to eat decreases

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5
Q

What is the role of leptin?

A

A peptide hormone released by fat stores which depresses feeding activity

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6
Q

What are the three 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 (skeletal muscle is the only portion of energy output that we can regulate voluntarily)

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

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7
Q

What is meant by metabolism?

A

The integration of all biochemical reactions in the body

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8
Q

What are the three elements of metabolism?

A

Extracting energy from nutrients in food

Storing that energy

Utilising that energy for work

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9
Q

What are anabolic pathways?

A

Build Up. Net effect is synthesis of large molecules from smaller ones, usually for storage purposes.

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10
Q

What are catabolic pathways?

A

Break Down. Net effect is degradation of large molecules into smaller ones, releasing energy for work.

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11
Q

Describe the absorptive state we enter after having a meal

A

Ingested nutrients supply the energy needs of the body and excess is stored

ANABOLIC PHASE

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12
Q

Describe the fasted state or post - absorptive state

A

The pool of nutrients in the plasma decreases and we enter a post-absorptive state where we rely on body stores to provide energy

CATABOLIC PHASE

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13
Q

What can the brain use as a supply of energy?

A

Glucose or Ketones

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14
Q

How is blood glucose maintained?

A

By synthesising glucose from the glycogen (glycogenolysis) or amino acids (gluconeogenesis)

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15
Q

Why is glucose detected in the urine of those with diabetes?

A

Glucose cannot be taken up by cells

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16
Q

What is the normal range of blood glucose?

A

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

Roughly around 5 mmoles

Regulated by insulin and glucagon

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17
Q

What are the different portions of the pancreas that are related to hormone production?

A

99% of the pancreas operates as an exocrine gland (enzymes and NaHCO3 via the ducts into the alimentary canal to support digestion)

1% - endocrine function (islets of langerhans)

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18
Q

What are the four types of islet cell and what do they produce?

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 the GIT)

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19
Q

What hormone predominates in a fed state vs a fasted state?

A

Fed state: Insulin dominates

Fasted state: Glucagon dominates

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20
Q

How does insulin affect glucose oxidation, glycogen synthesis, fat synthesis and protein synthesis?

A

All increase

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21
Q

How does glucagon affect glycogenolysis, gluconeogenesis and ketogenesis?

A

All increase

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22
Q

What is the precursor of insulin?

A

Preproinsulin

Which is then converted to proinsulin in the ER.

Proinsulin is then packaged as granules in secretory vesicles. Within the granules the proinsulin is cleaved again to give insulin and C-peptide. Insulin is stored in this form until the b cell is activated and secretion occurs.

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23
Q

What stimulates insulin secretion (from pancreatic B cells)?

A

Both glucose and aa’s stimulate insulin secretion but the major stimulus is blood glucose concentration.

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24
Q

Which hormone dominates the absorptive state?

A

Insulin dominates the absorptive state. Only hormone which lowers [BG].

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25
Q

What happens to excess glucose that is not used by cells during the absorptive state?

A

Any excess is stored as glycogen in liver and muscle, and as triacylglycerols (TAG) in liver and adipose tissue

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26
Q

What happens to excess amino acids?

A

Amino acids are used mainly to make new proteins with excess being converted to fat. Also form an energy source.

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27
Q

Where are fatty acids stored?

A

Fatty acids are stored in the form of triglycerides in adipose tissue and liver.

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28
Q

What causes the release of insulin from cells?

A

Glucose is abundant and enters the cells through GLUT transport proteins

ATP increases ATP concentration and the KATP channel closes (KATP specific potassium ion channel that is sensitive to ATP in the beta cells of the pancreas).

Intracellular potassium concentration rises, cell depolarises and voltage dependant calcium channels open and trigger insulin vesicle exocytosis into the circulation.

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29
Q

Sumary of KATP

A

Why the channels remain closed

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30
Q

Which tissues are described as insulin sensitive?

A

Muscle and adipose tissue

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31
Q

What does insulin bind to?

A

Binds to tyrosine kinase receptors on the cell membrane of insulin - sensitive tissues

(increases glucose uptake by the tissues)

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32
Q

What is the effect of insulin on GLUT-4?

A

Insulin stimulates the mobilization of specific glucose transporters, GLUT-4, which reside in the cytoplasm of unstimulated muscle and adipose cells.

When stimulated by insulin GLUT4 migrates to the membrane and is then able to transport glucose into the cell. When insulin stimulation stops, the GLUT-4 transporters return to the cytoplasmic pool.

The glucose taken up by cells is primarily used for energy.

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33
Q

What portion of the bpdy is dependant on insulin for the uptake of glucose?

A

Just muscle and fat are insulin sensitive

Muscle (40% BW)

Fat (20-25% BW)

In other tissues glucose uptake is via other GLUT-transporters, which are NOT insulin-dependent.

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34
Q

Where do you find GLUT1,2,3 ?

A

GLUT-1 Basal glucose uptake in many tissues eg brain, kidney and red blood cells.

GLUT-2 b-cells of pancreas and liver

GLUT-3 Similar

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35
Q

How does glucose enter the liver?

A

GLUT - 2 transporters down the concentration gradient

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

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36
Q

How does insulin affect hepatocytes in the fed state?

A

Insulin activates signal cascade which in turn activates hexokinase, an enzmy that converts Glucose to glucose-6-phosphate which means that instracellular levels of glucose concentration remain low - maintaining the diffusion gradient. Favouring the movement of glucose into the cells

37
Q

How is the gradient of glucose between hepatocytes and the blood created in the fasted state?

A

Liver synthesises glucose by glycogenolysis and gluconeogenesis

Favours movement of glucose out of the cell

38
Q

What are the additional anabolic effects of insulin?

A

a) Increases glycogen synthesis in muscle and liver. Stimulates glycogen synthase and inhibits glycogen phosphorylase.
b) Increases amino acid uptake into muscle, promoting protein synthesis.
c) Increases protein synthesis and inhibits proteolysis
d) Increases triacylglycerol synthesis in adipocytes and liver i.e. stimulates lipogenesis and inhibits lipolysis.
e) Inhibits the enzymes of gluconeogenesis in the liver

39
Q

What is the effect of insulin on growth hormone?

A

Has a permissive effect on Growth Hormone

40
Q

What is the effect of insulin on potassium?

A

Promotes K+ ion entry into cells by stimulating Na+/K+ ATPase. Very important clinically.***

41
Q

LOOK

A
42
Q

What is responsible for the degradation of insulin?

A

Insulin has a half-life of » 5 minutes and is degraded principally in the liver and kidneys.

43
Q

Once insulin action is complete what happens to the insulin bound receptors?

A

Once insulin action is complete insulin-bound receptors are internalised by endocytosis and destroyed by insulin protease, some recycled.

44
Q

Summary

A
45
Q

What increases insulin release in the body?

A

Increased [BG]*****

  1. Increased [amino acids]plasma
  2. Glucagon (insulin required to take up glucose created via gluconeogenesis stimulated by glucagon)
  3. Other (incretin) hormones controlling GI secretion and motility eg gastrin, secretin, CCK, GLP-1, GIP. Released by ileum and jejunem in response to nutrients. Early insulin release prevents glucose surge when absorption occurs.
  4. Vagal nerve activity (see next slide)
46
Q

What inhibits insulin release?

A
  1. Low [BG]
  2. Somatostatin (GHIH)
  3. Sympathetic a2 effects
  4. Stress e.g. hypoxia
47
Q

Why does glucose quantity A evoke a larger insulin response when given orally than intravenously?

A

Vagal activity stimulates release of major GI hormones, and also stimulates insulin release, therefore meaning that the insulin response to an intravenous glucose load is less than the equivalent amount of glucose administered orally

IV - increase in insulin as a result of increase in gluclose in beta cells

Orally - Increase in glucose in beta cells, vagal stimlation of beta cells and incretin effects (hormones that control GI secretion and motility)

48
Q

What is the primary purpose of glucagon?

A

Primary purpose is to raise blood glucose. It is a glucose-mobilizing hormone, acting mainly on the liver.

49
Q

What is the half life of glucagon?

A

Plasma half-life 5-10mins, degraded mainly by liver.

50
Q

What hormones are part of the insulin counter-regulatory control system?

A

Glucagon, epinephrine, cortisol and growth hormone

51
Q

What bidy state is glucagon most active?

A

Most active in the post absorptive state

52
Q

What are the receptors for glucagon?

A

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

53
Q

What is the result of the phosphorylated liver enzymes as a result of glucagon?

A
  1. increased glycogenolysis
  2. increased gluconeogenesis (substrates: aa’s and glycerol (lipolysis))
  3. formation of ketones from fatty acids (lipolysis)

All these processes occur in the liver

NET RESULT IS ELEVATED BG concentration

54
Q

Describe the release of glucagon?

A

Glucagon release is relatively constant although secretion increases dramatically when [BG] < 5.6mM

(normal [BG] 4.2-6.3mM). Nevertheless the ratio to insulin is more significant than actual concentration

55
Q

Why are both glucagon and insulin released after consumption of amino acids?

A

If it were not for the effect of aas on glucagon then the insulin-stimulating effects of aas would result in very low [BG]. This is counteracted by the glucose mobilizing effects of glucagon and so [BG] is maintained.

56
Q

How is there glucose sparing for obligatory glucose users?

A

In the post-absorptive state, lower insulin levels mean a large mass of tissue, i.e. muscle and fat, cannot readily access glucose

57
Q

What are the stimuli that promote glucagon release?

A
  1. Low [BG]
  2. High [amino acids] . Prevents hypoglycaemia following insulin release in response to aa.
  3. sympathetic innervation and epinephrine, b2 effect
  4. cortisol
  5. stress e.g. exercise, infection
58
Q

What stimuli inhibit the release of glucagon?

A
  1. glucose
  2. free fatty acids (FFA) and ketones
  3. insulin (fails in diabetes so glucagon levels rise despite high [BG] )
  4. somatostatin
59
Q

What is the ANS innervation of islet cells?

A

Parasympathetic: Vagus - Increase in insulin and slightly increases glucagon (in association with th anticipatory phase of digestion)

Sympathetic: Increase in glucagon, increase in epinephrine and inhibition of insulin

60
Q

Summary

A

My Liver Gives Ian Lovely Presents

Muscle glycogenolysis = 1

Liver glycogenolysis = 2

Gluconeogenesis = 3

Inhibition of glucose uptake = 4

Lipolysis = 5

Protein catabolism = 6

Glucagon = 2,3

Epinephrine = 1,2,3,5

Cortisol = 3,4,5,6

Growth hormone = 3,4,5

61
Q

What produces somatostatin?

A

Peptide hormone, secreted by D-cells of the pancreas (and hypothalamus aka GHIH).

62
Q

What is the function of somatostatin?

A

Inhibit activity of the GI tract

Slow down absorption of nutrients and prevents exaggerated peaks in plasma conecentrations

63
Q

What is synthetic SS used for?

A

(Synthetic SS may be used clinically to help patients with life-threatening diarrhoea associated with gut or pancreatic tumours).

64
Q

What is the effect of SS on glucagon and insulin?

A

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

65
Q

What is the result of a tumour of the pancreas which secretes too much somatostatin?

A

pancreatic SS-secreting tumours develop the symptoms of diabetes which disappear when the tumour is removed.

66
Q

Summary

A
67
Q

How is glucose absorption into the muscle maximised during excersize?

A

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

This effect persists for several hours after exercise and regular exercise can produce prolonged increases in insulin sensitivity.

68
Q

How is adipose tissue used by the body during periods of starvation?

A

Free fatty acids are released from adipose tissue

Most tissues can use FFAs as a source of energy

Liver converts excess FFAs into ketone bodies whih provide an additional source for the muscle and the brain

69
Q

What is the last store to be depleted in starvation?

A

‘Spare protein’

Broken down to provide gluconeogenic substrates

(loss of protein, very weakening)

70
Q

What is the cause of diabetes mellitus type 1

(IDDM)

A

Autoimmune destruction of the pancreatic b-cells destroys ability to produce insulin and seriously compromises patients ability to absorb glucose from the plasma. 10% of diabetic patients are insulin-dependent.

71
Q

What is the result of untreated type 1 diabetes?

A

Untreated type 1 diabetes leads to many complex changes in the body which ultimately cause starvation and death.

Without insulin the body becomes excessively wasted, develops ketoacidosis, coma and death

72
Q

How is type 1 diabetes managed?

A

Daily injections of insulin

Peptide hormones cannot be given orally

73
Q

The person who discovered insulin was

A

JJR Macleod, Aberdeen medical graduate and later Physiology Professor won Nobel Prize in 1923 for discovery of insulin with Canadian colleagues.

74
Q

Which tissues can use ketone bodies?

A

The muscle and the brain

75
Q

What is the consequence of lack of insulin during a period of starvation?

A

Depresses ketone body uptake

They build up in the plasma and create life threatening acidosis

Plasma pH less than 7.1

Death will occur within hours if left untreated

76
Q

What causes type 2 diabetes (NIDDM)?

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.

77
Q

What is the status of beta cells in NIDDM?

A

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

78
Q

What percentage of diabetic patients are NIDDM?

A

90% of diabetic patients are insulin-resistant (NIDDM)

79
Q

What is the aetiology of type 2 diabetes?

A

Typically associated with obesity

Usually appears >40yrs but age decreasing

High sugar and animal fat diet together with little exercise are major contributors

80
Q

What is the treatment of type 2 diabetes?

A

Pre-diabetic stage: Insulin sensitivty can be restored with exercise and dietary change

First line is hypoglycaemic drugs

(METFORMIN)

SULPHONYLUREAS (cannot be used to treat type 1 diabetes)

Eventually many type II patients end up taking insulin (very pharmacological doses) in order to prevent hyperglycaemia

81
Q

What is the effect of hypoglycaemic drugs?

A

Inhibits hepatic gluconeogenesis and antagonises action of glucagon

82
Q

What is the effect of sulphonylureas?

A

A class of drug that acts to close the KATP in beta cells and therefore stimulate calcium entry and insulin secretion

Cant be used for type 1 diabetes because it requires functioning beta cells

83
Q

Why is blood gloucose increased in both type 1 and type 2 diabetes?

A

Type 1 - inadequate insulin release

Type 2 - inadequate insulin response

84
Q

What is the diagnostic criteria for diabetes?

A

Elevated blood glucose

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.

85
Q

How do you convert mg/dl into mM/l?

A

Multiply by 10 to give mg/l

Moles equals mass divided by formula mass

Formula mass of glucose is 180

Divide the mg by 180 to give mM

86
Q

What are the dangers of hyperglycaemia?

A

glucose is a highly reactive molecule which can eventually produce long-term problems that may be very serious = diabetic complications

87
Q

What are diabetic complications

A

Retinopathy

Neuropathy

Nephropathy

Cardiovascular Disease

88
Q

Look at the changes associated in health in correlation to changes in glood glucose

A

MBChB - Y2 - Endocrine (25 decks)

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