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endocrine system 1 > Endocrine Pancreas > Flashcards

Endocrine Pancreas Flashcards

1
Q

<p>What is energy intake determined by?</p>

A

Balance of activity in 2 hypothalamic centres

  1. feeding centre
  2. satiety centre
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2
Q

<p>What does the feeding centre promote?</p>

A

<p>Promotes feelings of hunger and drive to eat</p>

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3
Q

<p>What does the satiety centre promote?</p>

A

<p>Promotes feelings of fullness by suppressing the feeding centre
insulin sensitive</p>

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4
Q

<p>How is activity in the feeding and satiety centres controlled?</p>

A

<p>A complex balance of neural and chemical signals as well as the presence of nutrients in plasma</p>

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5
Q

<p>Glucostatic theory</p>

A

<p>Food intake is determined by blood glucoseas [BG] increases, the drive to eat decreases (- Feeding Centre; + Satiety centre)</p>

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6
Q

<p>Lipostatic theory</p>

A

<p>Food intake is determined by fat stores</p>

<p>as fat stores increase, the drive to eat decreases</p>

<p>(- feeding centre; + satiety centre)</p>

<p>leptin (peptide hormone) released by fat stores depress feeding activity</p>

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7
Q

<p>What are the 3 categories of energy output?</p>

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

heat loss

  • associated with cellular and mechanical work
  • accounts for half our energy output
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8
Q

<p>What is the only part of our energy output we can regulate voluntarily?</p>

A

<p>Mechanical work done by skeletal muscle</p>

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9
Q

<p>Metabolism</p>

A

<p>Integration of all biochemical reactions in the body</p>

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10
Q

<p>What are the 3 elements of metabolism?</p>

A

<p>- Extracting energy from nutrients in food</p>

<p>- Storing that energy</p>

<p>- Utilising that energy for work</p>

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11
Q

<p>Anabolic pathways</p>

A
  • build up
  • net effect is synthesis of large molecules from smaller ones
  • usually for storage purposes
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12
Q

<p>Catabolic pathways</p>

A
  • break down
  • net effect is degradation of large molecules into smaller ones
  • releasing energy for work
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13
Q

<p>What state do we enter after eating?</p>

A 
absorptive state (anabolic phase)
- ingested nutrients supply the energy needs of the body and excess is stored
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14
Q

<p>What state do we enter between meals and overnight?</p>

A

post-absorptive state/fasted state (catabolic phase)

- rely on body stores to provide energy

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15
Q

<p>What is meant by the brain being an obligatory glucose utiliser?</p>

A

<p>Most cells can use fats, carbohydrates or protein for energy but the brain can only use glucose</p>

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16
Q

<p>What affect does the brain have on the post-absorptive state?</p>

A

MUST maintain blood glucose concentration [BG] sufficient to meet the brain’s requirements.

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17
Q

<p>Why does hypoglycaemia occur?</p>

A

<p>failure to maintain [BG] sufficient to meet the brain's requirements</p>

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18
Q

<p>How is BG maintained?</p>

A

<p>Synthesising glucose from glycogen (glycogenolysis) or amino acids (gluconeogenesis)</p>

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19
Q

<p>Why does BG rise in diabetes?</p>

A

<p>In diabetes, glucose cannot be taken up by cells so BG rises and glucose is detected in the urine</p>

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20
Q

<p>What is the only structure to have access to BG when it falls below normal range?</p>

A

<p>Brain</p>

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21
Q

<p>What is the normal range of [BG]?</p>

A

<p>4.2-6.3 mM</p>

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22
Q

<p>When does hypoglycaemia occur?</p>

A

<p>[BG] <3mM</p>

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23
Q

<p>What 2 key endocrine hormones maintain [BG]?</p>

A

<p>-Insulin-Glucagon</p>

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24
Q

<p>What does 99% of the pancreas produce?</p>

A

NaHCO3

- operates as an exocrine gland releasing via ducts into the alimentary canal to support digestion

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25

What produces the endocrine hormones of the pancreas?

Islets of Langerhans

26

What are the 4 types of Islets of Langerhans?

- alpha cells - beta cells - delta cells - f cells
27

What do the a cells produce?

Glucagon

28

What do the B cells produce?

Insulin

29

What do the delta cells produce?

Somatostatin

30

What do the F cells produce?

Pancreatic polypeptide ( function not really known, may help control of nutrient absorption)

31

How many islets are there scattered throughout the pancreas?

1-2 million each with a copious blood supply

32

What does control of BG depend on?

Balance between insulin and glucagon

33

What state does insulin dominate?

Fed state

34

What state does glucagon dominate?

Fasted state

35

What does an increase in insulin result in?

- Increased glucose oxidation

- Increased glycogen synthesis

- Increased fat synthesis

- Increased protein synthesis

36

What does an increase in glucagon result in?

- Increased glycogenolysis

- Increased gluconeogenesis

- Increased ketogenesis

37

What is insulin?

Peptide hormone produced by pancreatic B cells

38

What does insulin stimulate?

Glucose uptake by cells

39

How is insulin synthesised?

as a large preprohormone (preproinsulin) then converted to proinsulin in the ER
40

How does proinsulin become insulin?

proinsulin packaged as granules in secretory vesicles and cleaved to give insulin and C-peptide (stored in this form until the beta cell is activated and secretion occurs)
41

What enters the blood from the GIT during the absorptive state?

- glucose

- amino acids (aa)

- fatty acids

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

42

What is the only hormone which lowers BG?

Insulin

43

What happens to excess glucose during the absorptive state?

stored as glycogen in liver and muscle or triacylglycerols (TAG) in liver and adipose tissue
44

What are amino acids used to do?

to make new proteins converted to fat (in excess)

45

How are fatty acids stored?

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

46

What special channel do B cells possess?

KATP channel- specific type of K+ ion channel that is sensitive to the [ATP] within the cell

47

How does glucose enter cells when it is abundant?

glucose transport proteins (GLUT) and metabolism increases

48

Once glucose enters the cell and increases metabolism what happens?

- increases [ATP] within the cell causing the KATP channel to close - intracellular [K+ ] rises, depolarising the cell - voltage-dependent Ca2+ channels open and trigger insulin vesicle exocytosis into the circulation
49

How does low [BG] prevent insulin being secreted?

- [ATP] is low so KATP channels are open - K+ ions flow out removing +ve charge from the cell and hyperpolarizing it, - voltage-gated Ca2+ channels remain closed and insulin is not secreted
50

What is the primary action of insulin?

binds to tyrosine kinase receptors on the cell membrane of insulin-sensitive tissues (muscle and adipose tissue) to increase glucose uptake by these tissues
51

What does insulin stimulate with regards to GLUT4?

mobilization of GLUT-4 which reside in cytoplasm of muscle and adipose cells
52

What happens to GLUT4 after being stimulated by insulin?

GLUT4 migrates to the membrane and transports glucose into the cell

When insulin stimulation stops, the GLUT-4 transporters return to the cytoplasmic pool.

53

What is the glucose taken up by cells primarily used for?

used for energy.

54

What are the only insulin sensitive tissues?

Muscle and fat

55

What percentage of the body do muscle and fat make up?

-Muscle ~40%-Fat ~20-25%

56

How is glucose taken up in tissues other than muscle and fat?

 via GLUT-transporters which are not insulin-dependent

(GLUT-1, GLUT-2, GLUT-3)

57

What do GLUT 1,3 and 2 facilitate the movement of?

glucose GLUT-1: brain, kidney and red blood cells GLUT-2: beta cells of pancreas and liver GLUT-3: Similar to GLUT-1
58

How does the liver take up glucose?

GLUT 2 transporters which are insulin independent
59

How does glucose enter the liver?

Down a concentration gradient

60

In terms of glucose transport, what affect does insulin have on the liver?

no direct effect on the liver | glucose transport into hepatocytes is affected by insulin status
61

Why does the liver take up glucose in the fed state?

insulin activates hexokinase which lowers [glucose]ic creating a gradient favouring glucose movement into the cells
62

What does liver do in the fasted state?

synthesises glucose via glycogenolysis and gluconeogenesis | increasing [glucose]ic creating a gradient favouring glucose movement out of the cells into the blood
63

What anabolic actions does insulin have?

- increases glycogen synthesis in muscle and liver: stimulates glycogen synthase and inhibits glycogen phosphorylase - increases amino acid uptake: increases protein synthesis and inhibits proteolysis - increases triacylglycerol synthesis in adipocytes and liver: stimulates lipogenesis and inhibits lipolysis - inhibits the enzymes of gluconeogenesis in the liver
64

Other than its effect on glucose and its anabolic actions, what other 2 actions does insulin have on the body?

- permissive effect on Growth Hormone

- promotes K+ ion entry into cells by stimulating Na+/K+ ATPase. (very important clinically)

65

Why are the additional actions of glucose possible?

activation of multiple signal transduction pathways associated with the Insulin Receptor
66

What is the half-life of insulin?

~5 minutes

degraded principally in liver and kidneys

67

What happens once insulin action is complete?

insulin-bound receptors internalised by endocytosis and destroyed by insulin protease (some recycled)
68

Give examples of stimuli which increase insulin release.

- increased [BG] - increased [amino acids]plasma - glucagon (insulin required to take up glucose created via gluconeogenesis stimulated by glucagon) - incretin hormones controlling GI secretion and motility (gastrin, secretin, CCK, GLP-1, GIP) - vagal nerve activity
69

Give examples of stimuli which inhibit insulin release?

- Low [BG]

- Somatostatin (GHIH)

- Sympathetic a2 effects

- Stress eg hypoxia

70

Why is the insulin response to an IV glucose load less than that of an equivalent oral load?

oral load increases insulin by direct effect on B cells and vagal stimulation on B cells (plus incretin effects)
71

What is glucagon?

peptide hormone produced by a-cells of the pancreatic islet cells
72

What is the primary purpose of glucagon?

to raise blood glucose

It is a glucose-mobilizing hormone, acting mainly on the liver

73

What is the half-life of glucagon?

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

74

When is glucagon most active?

Post-absorptive state

75

What hormones make up the glucose counter-regulatory control system?

- Epinephrine

- Cortisol

- GH

- Glucagon

76

What are the glucagon receptors?

G-protein coupled receptors linked to the adenylate cyclase/cAMP system
77

What do the glucagon receptors do when activated?

phosphorylate specific liver enzymes

78

What does phosphorylation of specific liver enzymes by glucagon receptors result in?

- Increase glycogenolysis

- Increase gluconeogenesis (substrates: aa’s and glycerol (lipolysis))

- Formation of ketones from fatty acids (lipolysis)

79

What is the net result of activation of glucagon receptors?

Elevated [BG]

80

Describe the rate of secretion of glucagon?

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.

81

What do amino acids in the plasma stimulate the release of?

 release of both insulin and glucagon.

82

Why is important for amino acids to stimulate both insulin and glucagon?

insulin stimulating effects of amino acids result in very low [BG] and is counteracted by glucose mobilizing effects of glucagon

83

What can other tissues use as energy sources instead of glucose?

FFAs and ketones to produce energy

84

Why is there glucose sparing for obligatory glucose users in the post-absorptive state?

lower insulin levels mean a large mass of tissue (muscle and fat) cannot readily access glucose
85

Give examples of stimuli that promote glucagon release?

- Low [BG]

- High [amino acids]: prevents hypoglycaemia following insulin release

- Sympathetic innervation and epinephrine, B2 effect

- Cortisol

- Stress e.g. exercise, infection

86

Give examples of stimuli that inhibit glucagon release?

- Glucose

- Free fatty acids (FFA) and ketones

- Insulin (fails in diabetes so glucagon levels rise despite high [BG)

- Somatostatin

87

What effects does the parasympathetic system have on insulin and glucagon release?

- increase in insulin

- increase in glucagon (to a lesser extent)

 in association with the anticipatory phase of digestion.

88

What effect does the sympathetic system have on insulin and glucagon?

- increased glucagon (promotes glucose mobilization)

- increased epinephrine

- inhibition of insulin

89

What is somatostatin?

a peptide hormone secreted by D-cells of the pancreas (and hypothalamus aka GHIH)
90

What is the main pancreatic action of somatostatin?

Inhibit activity in the GIT

91

What is the function of SS in inhibiting the GIT?

slow down absorption of nutrients to prevent exaggerated peaks in plasma concentrations

92

Why may synthetic somatostatin be used clinically?

to help patients with life-threatening diarrhoea associated with gut or pancreatic tumours

93

What do patients with SS secreting tumours often develop?

symptoms of diabetes which disappear when the tumour is removed.

94

Although SS is not a counter regulatory hormone, what effect does it have on both insulin and glucagon?

It strongly suppresses the release of both insulin and glucagon in a paracrine fashion

95

What does GHIH inhibit release of from the anterior pituitary?

GH

96

What is increased during exercise even in the absence of insulin?

Entry of glucose into skeletal muscle is increased

97

What effect does exercise have on [BG]?

increases the insulin sensitivity of muscle causes an insulin-independent increase in the number of GLUT-4 transporters incorporated into the muscle membrane
98

What can regular exercise produce?

prolonged increases in insulin sensitivity

99

How does glucose enter the cell in non-active muscle?

insulin binds to its receptor = (glucose transporters) GLUT4 migrates to the cell membrane allowing glucose to enter.

100

How does glucose enter the cell in active muscle?

GLUT4 transporters migrate to the membrane  | - exercise causes glucose uptake independently of insulin and increase in sensitivity of the muscle to insulin
101

What does the body rely on when nutrients are scarce?

Stores for energy

102

What happens to the brain after a period of starvation?

Brain adapts to be able to use ketones

103

How are stores used during starvation?

Adipose tissue is broken down and fatty acids are released

104

Why are spare FFAs converted to ketones and used by the brain in starvation?

FFA’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!

105

Diabetes mellitus

Loss of control of blood glucose levels

106

How does T1DM occur?

autoimmune destruction of the pancreatic B-cells destroys ability to produce insulin

compromises patients ability to absorb glucose from the plasma

10% of diabetic patients are insulin-dependent

107

What is another name for T1DM?

Insulin dependent diabetes mellitus (IDDM)

108

What can untreated T1DM lead to?

starvation and death
109

What do T1DM have an absolute need for?

Insulin

110

How does ketoacidosis occur in T1DM?

a lack of insulin depresses ketone body uptake.

build up rapidly in the plasma and because they are acidic create life threatening acidosis (ketoacidosis or ketosis)

with plasma pH < 7.1. Death will occur within hours if untreated.

111

How are ketones detectable?

In urine and produce distinctive acetone smell to breath

112

What is another name for T2DM?

Non-insulin dependent diabetes mellitus (NIDDM)

113

How does T2DM occur?

peripheral tissues become insensitive to insulin = insulin resistance

due to an abnormal response/reduction of insulin receptors

114

What may B cells be in T2DM?

Hyperinsulinaemia

115

What is T2DM typically associated with?

Obesity

116

When does T2DM usually occur?

>40 years

117

What is initial treatment of T2DM aimed at?

restore insulin sensitivity of tissues with exercise and dietary change

118

What treatment options are there for T2DM?

- Lifestyle changes

- Metformin

- Sulfonylureas

- Other oral hypoglycaemic drugs

- Insulin

119

What does metformin do?

Inhibits hepatic gluconeogenesis and antagonises action of glucagon

120

What do sulfonylureas do?

close the KATP in B cells and therefore stimulate Ca2+ entry and insulin secretion
121

Why is [BG] elevated in T1DM?

Inadequate insulin release increase [BG]

122

Why is [BG] elevated in T2DM?

Inadequate tissue response increase[BG]

123

What is the diagnostic criteria for diabetes?

Hyperglycaemia

124

What test is performed to diagnose diabete1s?

Oral glucose tolerance test

125

How is the OGTT carried out?

patient ingests glucose load after fasting and [BG] measured. elevation after 2 hours is indicative of diabetes ([BG] will normally return to fasting levels within an hour) (does not distinguish Type I from II)
126

What diabetic complications can occur?

- Retinopathy

- Neuropathy

- Nephropathy

- Cardiovascular disease

127

Who is hypoglycaemic a particular problem in?

Type 1 patients

128

What are the stages of hypoglycaemia?

- 4.6mM [BG]: Inhibition of insulin secretion

- 3.8mM [BG]: Glucagon, epinephrine and GH secretion

- 3.2mM [BG]: Cortisol secreted

- 2.8mm [BG]: Cognitive dysfunction

- 2.2mM [BG]: Lethargy

- 1.7mM [BG]: Coma

- 1.1mM [BG]: Convulsions

- 0.6mM [BG]: Permanent brain damage and death

129

What is leptin?

peptide hormone released by fat stores which depresses feeding activity

endocrine system 1 (25 decks)

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