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Endocrine > The Endocrine Pancreas > Flashcards

The Endocrine Pancreas Flashcards

1
Q

Energy intake is determined by the balance of activity in which two hypothalamic centres?

A 
Feeding centre (promotes feelings of hunger + drive to eat)
Satiety centre (supresses feeding centre + promotes feeling of fullness)
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2
Q

What is the glucostatic theory?

A

Food intake is determined by blood glucose

As BG increases, drive to eat decreases

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3
Q

What is the lipostatic theory?

A

Food intake is determined by fat stores, as fat stores increase, drive to eat decreases

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4
Q

What hormone is implicated in the lipostatic theory?

A

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

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5
Q

Body energy =?

A

Energy intake - energy output

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6
Q

What are the 3 categories of energy output?

A

Cellular work
Mechanical work
Heat loss

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7
Q

What is cellular work?

A

Transporting molecules across membranes, growth and repair, storage of energy etc.

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8
Q

What is mechanical work?

A

Movement (on large scale or intracellularly)

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9
Q

What % of energy output does heat loss contribute?

A

50%

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10
Q

Define metabolism

A

Integration of all biochemical reactions in the body

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11
Q

What 3 things does the metabolism involve?

A

Extracting energy from nutrients
Storing that energy
Utilising that energy for work

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12
Q

What are anabolic pathways?

A

BUILD UP

Net effect is to synthesise large molecules from smaller ones, usually for storage

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13
Q

What are catabolic pathways?

A

BREAKDOWN

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

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14
Q

What state do we enter after we eat and what does this involve?

A

We enter an absorptive state, whereby ingested nutrients supply the energy needs of the body + excess is stored, this is an anabolic phase

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15
Q

What state do we enter between meals + overnight and what does this involve?

A

Nutrients in the plasma decreases and we enter a post-absorptive state, where we rely on body stores to provide energy
This is a catabolic phase

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16
Q

What can cells use for energy?

A

Carbs, fat, protein (expect brain which can only use glucose or ketones)

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17
Q

How do we maintain BG during times of not eating?

A

Breaking down glycogen into glucose (glycogenolysis) or making glucose from amino acids (gluconeogenesis)

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18
Q

Which two hormones keep blood glucose in a tight range?

A

Insulin

Glucagon

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19
Q

Where are the endocrine hormones produced in the pancreas?

A

Islets of Langerhans

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20
Q

How many Islets of Langerhan are in the pancreas?

A

1-2mil

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21
Q

What are the two types of cells present in Islets?

A

Alpha - produce glucagon
Beta - produce insulin
Delta - produce somatostatin
F cells - produce pancreatic polypeptide

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22
Q

What happens when insulin predominates over glucagon?

A

Blood glucose decreases as glucose taken up by cells

Increased glycogen production, fat synthesis and protein synthesis

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23
Q

What happens when glucagon predominates over insulin?

A

Glucose released into plasma from stores (BG increases)

Increased glycogenolysis, gluconeogenesis, ketogenesis

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24
Q

What kind of hormone is insulin?

A

Peptide

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25
Q

What is the role of insulin?

A

Stimulates glucose uptake by cells

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26
Q

How is insulin made?

A

Synthesised as large preprohormone, preproinsulin, which is converted into proinsulin in the ER

This is packaged into granules, within these proinsulin is cleaved to give insulin and C peptide

Insulin is stored until B cell is activated and secretion occurs

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27
Q

What occurs during the absorptive state?

A

Glucose, amino acids, fatty acids enter the blood via GIT

Glucose (mainly) + AA stimulate insulin secretion

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28
Q

Which hormone dominates the absorptive state?

A

Insulin

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29
Q

What is excess glucose stored as?

A

Glycogen in liver + muscle or TAGs in liver + adipose tissue

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30
Q

What are amino acids used to make? What are excess converted into?

A

Proteins

Excess converted into fat

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31
Q

What are fatty acids stored as?

A

Triglycerides in adipose tissue and liver

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32
Q

Describe the mechanism of control of insulin secretion by blood glucose concentration

A

B-cells have a specific K+ channel that is sensitive to [ATP] inside the cell (KATP channel)

If glucose is abundant it enters the cell via GLUT transporters and metabolism increases, so intracellular [ATP] increases causing KAPT to close, so intracellular [K+] increases –> depolarisation of the cell

Voltage caged Ca2+ channels open + trigger insulin vesicle exocytosis into the circulation

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33
Q

Explain why when [BG] is low, insulin is not released by B cells

A

When [BG] is low, [ATP] is low, so KATP channels are ions flow out removing the +ve charge from the cell + hyperpolarising it, so voltage gated Ca2+ channels remain closed + insulin is not secreted

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34
Q

What is the 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

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35
Q

How does insulin stimulate increased glucose uptake by binding to insulin sensitive tissues?

A

Stimulates the mobilisation of specific glucose transporters, GLUT4, which reside in the cytoplasm of unstimulated muscle + adipose cells

When stimulated GLUT4 migrates to cell membrane + is able to transport glucose into the cell

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36
Q

What happens to GLUT4 receptors when insulin levels drop?

A

GLUT4 transporters return to the cytoplasmic pool

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37
Q

Which tissues are insulin sensitive? What does this mean

A

Adipose and muscle tissue are insulin sensitive (i.e. they require insulin to take glucose into their cells)

Most types of tissue do not require insulin to take up glucose

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38
Q

How do other tissues take up glucose?

A

They have other GLUT transporters which are not insulin dependent (GLUT1 to GLUT3)

39
Q

Why is insulin so significant despite the fact it is only required for the uptake of glucose into two types of tissue?

A

These tissues constitute 60-65% of body weight, so a large proportion of the body is dependent on insulin for glucose uptake

40
Q

What are the actions of GLUT1 and 3?

A

Basal glucose uptake in many tissues, e.g. brain, kidney, red blood cells

41
Q

Where are GLUT2 receptors found?

A

B cells of pancreas and liver

42
Q

How does the liver take up glucose?

A

Via GLUT2 transporters (NON-insulin dependent)
Glucose enters down its concentration gradient

NB: glucose transport into hepatocytes is affected by insulin status

43
Q

How does the liver alter the concentration gradient to allow more glucose to move into hepatocytes when [BG] is high?

A

Insulin activates hexokinase (which converts glucose into glucose-6-phosphate to keep [glucose]ic low and ensures a gradient favouring glucose movement into cells)

44
Q

How does the liver create a concentration gradient to allow more glucose to leave the cell when [BG] is low?

A

Liver synthesises glucose via glycogenolysis + gluconeogenesis, increasing [glucose]ic, creating a gradient favouring glucose movement out of cells into the blood

45
Q

What additional effects does insulin have in the muscle and liver?

A

Increases glycogen synthesis

Stimulates glycogen synthase + inhibits glycogen phosphorylase

46
Q

What specific action does insulin have in the muscle?

A

Increases AA uptake, promoting protein synthesis

Also inhibits proteolysis

47
Q

What additional effect does insulin have in adipocytes + the liver?

A

Stimulates lipogenesis + inhibits lipolysis

48
Q

How does insulin affect gluconeogenesis in the liver?

A

Inhibits all the enzymes of gluconeogenesis

49
Q

How does insulin affect growth hormone?

A

Permissive effect on growth hormone

50
Q

How does insulin affect blood potassium?

A

Lowers blood potassium, as it promotes K ion entry into cells by stimulating Na/K ATPase

51
Q

Where is insulin degraded?

A

Liver and kidneys

52
Q

What happens to the insulin receptor after insulin has bound to it and had its effect?

A

Insulin bound receptors are internalised by endocytosis + destroyed by insulin protease

53
Q

Which stimuli increase insulin release?

A
  1. Increased [BG]
  2. Increased [blood AA]
  3. Glucagon
  4. Incretin hormones controlling GI secretion + motility
  5. Vagal nerve activity
54
Q

Why does glucagon cause insulin release?

A

Insulin req. to take up glucose created via gluconeogenesis stimulated by glucagon

55
Q

What are examples of incretin hormones which stimulate insulin release?

A

Gastrin, secretin, CCK, GLP-1, GIP

56
Q

What are incretin hormones?

A

Hormones released by the ileum + jejunum in response to nutrients to prevent glucose surge when absorption occurs

57
Q

What stimuli inhibit insulin release?

A
  1. Low [BG]
  2. Somatostatin
  3. Sympathetic a2 effects
  4. Stress, e.g. hypoxia
58
Q

Why is less insulin released from an IV load compared to an oral load of the same amount of glucose?

A

Oral loading leads to insulin production by direct effect of increased [BG] on beta cells, and vagal stimulation and incretin effects

59
Q

What is the primary purpose of glucagon?

A

Raised [BG]

60
Q

Where does glucagon mostly act?

A

The liver

61
Q

Where is glucagon degraded?

A

Liver

62
Q

When is glucagon most active?

A

In the post absorptive state

63
Q

What hormones are in the glucose counter-regulatory control system?

A

Glucagon
Epinephrine
Cortisol
GH

64
Q

What kind of receptors are glucagon receptors?

A

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

65
Q

What does stimulation of glucagon receptors lead to?

A

Increased glycogenolysis
Increased gluconeogenesis
Formation of ketones from fatty acids (lipolysis)
==> Increased [BG]

66
Q

Give examples of substrates for gluconeogenesis

A

AA, glycerol

67
Q

What are the only two substrates the brain can use for energy?

A

Ketones, glucose

But remember it is an obligatory glucose user

68
Q

What is more significant that measuring glucagon concentration?

A

Determining its ratio to insulin

69
Q

High levels of amino acid in the plasma have what effect on glucagon levels?

A

Cause increased glucagon levels (same as insulin), this is an adaption to adjust for composition of a meal very high in protein

70
Q

What would happen if you ate a really high protein/low carb meal and glucagon didn’t rise?

A

AAs –> inc. insulin –> reduced [BG], this would lead to a very low [BG], if glucagon wasn’t stimulated to increase [BG]

71
Q

What stimuli promote glucagon release?

A
  1. Low [BG]
  2. High [blood AA]
  3. Sympathetic innervation and epinephrine, b2 effect
  4. Cortisol
  5. Stress, e.g. exercise, infection
72
Q

What stimuli inhibit glucagon release?

A
  1. Glucose
  2. FFA + ketones
  3. Insulin
  4. Somatostatin
73
Q

How does parasympathetic activity (vagus) affect insulin secretion in the islet cells?

A

Leads to increased insulin production + to a lesser extent increased glucagon in anticipatory phase of digestion

74
Q

How does sympathetic activity affect insulin secretion in the islet cells?

A

Promotes glucose mobilisation –> increased glucagon, epinephrine + inhibition of insulin for flight or fight response

75
Q

What is the main pancreatic action of somatostatin?

A

Inhibit activity in GIT - slows down absorption of nutrients to prevent exaggerated peaks in plasma conc.

76
Q

How does somatostatin affect insulin and glucagon release?

A

Strongly supresses the release of both in a paracrine fashion

77
Q

What stimulates the secretion of somatostatin?

A

Elevated plasma [AA] and elevated [BG]

78
Q

How does exercise affect [BG]?

A

Increases entry of glucose into skeletal muscle even in absence of insulin

Also increases insulin sensitivity of muscle, leads to insulin-independent increase in GLUT4 receptors in muscle membrane

79
Q

How long does the effect of exercise on insulin receptors persist?

A

Several hours

Regular exercise can produce prolonged increases in insulin sensitivity

80
Q

What occurs in the body during starvation?

A

Adipose tissue broken down into FFA which can be used by most tissues for energy

Liver converts excess to ketone bodies which can be used by the brain

81
Q

What happens to the brain after a period of starvation?

A

It adapts to be able to use ketones

82
Q

Why is it important to try and use FFA and ketones to fuel the body?

A

To spare protein which would be broken down in gluconeogenesis - this is very weakening, and makes you vulnerable to infection

83
Q

What is the pathophysiology of type 1 diabetes mellitus?

A

Autoimmune destruction of pancreatic B cells

84
Q

How does having poorly controlled type 1 diabetes affect the way you take up ketones?

A

Lack of insulin depresses ketone body uptake –> ketoacidosis (life-threatening acidosis)

85
Q

What is the pathophysiology of type 2 diabetes mellitus?

A

Peripheral tissue become insensitive to insulin (insulin resistance)

i.e. there is abnormal response of insulin receptors in muscle/fat or reduction in their number

86
Q

How are beta-cells affected in type 2 DM?

A

Remain normal, there may actually be hyperinsulinaemia

87
Q

Which kinds of patients typically have type 2 diabetes?

A

> 40 years
Obese
High sugar, animal fat diet, with little exercise

88
Q

What is involved in the initial treatment of type 2 diabetes?

A

Trying to restore insulin sensitivity with lifestyle changes (diet, exercise)

89
Q

What is the first line drug in T2DM?

A

Metformin

90
Q

How does metformin work?

A

Inhibits hepatic gluconeogenesis + antagonises action of glucagon

91
Q

How do sulphonylureas work?

A

Close the KATP in B cells + stimulate Ca entry and insulin secretion

92
Q

Why is [BG] raised in type 1 diabetes?

A

There is inadequate insulin release

93
Q

Why is [BG] raised in type 2 diabetes?

A

Where is inadequate tissue response to the insulin made

94
Q

What are the main diabetic complications?

A

Retinopathy
Neuropathy
Nephropathy
CV disease

Endocrine (11 decks)

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