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Endo > Endocrine functions of pancreas and diabetes mellitus > Flashcards

Endocrine functions of pancreas and diabetes mellitus Flashcards

Wk 8

1
Q

What does the Acini tissue secrete?

A

Digestive juices in the duodenum

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2
Q

What are the two major tissue types of the pancreas?

A

Acini and islets of Langerhans

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3
Q

What does the Islets of Langerhans secrte?

A

pancreatic hormones

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4
Q

What hormones are secreted by the pancreas?

A

insulin, glucagon, somatostatin, pancreatic polypeptide, amylin and ghrelin

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5
Q

What are the five cell types of the pancreas and how much of the pancreas do they make up?

A

Alpha cells – 25%

Beta cells – 70%

Delta cells – less than 5%

PP cells (F cells) - trace amounts

Epsilon cells

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6
Q

What do alpha cells secrete?

A

Glucagon

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7
Q

What do beta cells secrete?

A

isnulin and amylin

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8
Q

What do delta cells secrete?

A

somatostatin

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9
Q

What do PP or F cells secrete?

A

Pancreatic Polypeptide (PP)

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10
Q

what does epsilon cells secrete?

A

Ghrelin

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11
Q

Where are bet cells more abundant?

A

in the centre of the islet.

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12
Q

Where are alpha and delta cells most abundant?

A

in the periphery of the pancreas

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13
Q

can cels within an islet influence the secretion of other cells?

A

yes

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14
Q

How does cells within an islet communicate?

A

Via gap junctions

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15
Q

How does hormones produced by alpha, beta and delta cells regulate each-other’s secretion?

A

paracrine and cell-cell interactions

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16
Q

What does insulin secreted from B cells inhibit?

A

glucagon secretion

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17
Q

What does glucagon activate?

A

Insulin and somatostatin secretion

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18
Q

what does somatostatin inhibit?

A

Glucagon secretion

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19
Q

What does Ghrelin inhibit?

A

Insulin secretion

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20
Q

What is the biosynthesis of insulin?

A

PrePro Insulin  Proinsulin  Insulin and C peptide

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21
Q

What does the amount of C peptide give?

A

measure of Beta function

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22
Q

What are the two polypeptide chains (A and B) of insulin linked by?

A

Disulfide linkages

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23
Q

How is glucose transported into beta cells?

A

via facilitated diffusion using the GLUT 2

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24
Q

What increases insulin secretion?

A

Increased blood glucose

Increased blood AA and FFA

GI hormones

Glucagon, GH and cortisol

Beta adrenergic stimulation

Sulfonyluera drugs

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25
Q

What decreases insulin secretion

A

Decreased blood glucose

Fasting

Somatostatin

Alpha adrenergic activity

Leptin

K + depletion

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26
Q

What is the structure of the insulin receptor?

A

glycoprotein

Heterotetramer with a a and beta subunit complex

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27
Q

What subunit of the glycoprotein binds to insulin?

A

a subunit

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28
Q

What is the mechanism of action for insulin?

A

Insulin binds to a subunit on outside of cell –> autophosphorylates portions of b sub units within the cell. –> activation of tyrosine kinase –> phosphorylates insulin-receptor substrates –> signal activates cascade of kinases (Ras-MAPK) to stimulate gene transcription, protein synthesis and mitotic activity.

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29
Q

What does the autophosphorylation of B subunits of in glyoprotein activate?

A

a local tyrosine kinase that phosphorylates enzymes

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30
Q

Where is the Glut 4 transporter mostly expressed?

A

Adipocytes and muscle cells

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31
Q

What is the Glut 4 transporter?

A

a glucose transporter that has a high affinity for glucose and transports it down the concentration gradient.

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32
Q

What are the actions of insulin on protein metabolism?

A

Increased amino acid uptake

Promotion of protein synthesis

Inhibition of protein degradation

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33
Q

What are the impacts of insulin on protein metabolism just in the liver?

A

inhibits the breakdown of amino acids to form glucose

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34
Q

How does insulin impact carbohydrate metabolism in adipocyte tissue and muscle cells?

A

Increases carrier mediated uptake of glucose into skeletal muscle and adipose tissue

increases glycolysis

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35
Q

How does insulin effect carbohydrate metabolsim?

A

Increased carrier mediated uptake of glucose into skeletal muscle and adipose tissue

Increased glycogenesis in muscle and liver

Increases glycolysis in adipose and muscle

Decreased gluconeogenesis

Decreased glycogenolysis

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36
Q

How does insulin impact fat metabolism in adipose tissue?

A

increases storage of triglycerides via inducing lipoprotein lipase

Increases storage of fatty acids

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37
Q

How does insulin impact fat metabolism in the liver?

A

Inhibits breakdown of fatty acids into ketones

Increases synthesis of triglycerides, cholesterol and very-low-density lipoproteins.

38
Q

What are some other (non metabolic) actions of insulin?

A

Required for growth (with GH) (diabetes in children = failure to grow)

Direct effect on hypothalamic satiety

Increases K uptake = temporary relief of hyperkalaemia

Increases sodium retention by kidney

39
Q

What are the consequences of glucagon in insulin deficiency?

A

insulin contributes signficantly to hyperglycaemia and ketosis

40
Q

What is the origin of glucagon?

A

alpha cells of islets of langerhans

41
Q

what is the structure of glucagon?

A

hyperglycaemic hormone, single polypeptide

42
Q

what stimulates release of glucagon?

A

hypoglycaemia

43
Q

What is the primary and lesser target for Glucagon?

A

Primary target= liver

Lesser target = adipose tissue

44
Q

What are the main actions of insulin?

A

Acts to OPPOSE insulin

Increases blood glucose

increased glycogenolysis

increases gluconeogenesis

Increases lipolysis

45
Q

what factors increase glucagon secretion?

A

Decreased BGL

Amino acids

Acetyl Choline

Catecholamines

46
Q

What factors decrease glucagon secretion?

A

Fatty acids

Insulin

Somatostatin

47
Q

What is the impact of glucagon on fat metabolism?

A

Inhibits storage of triglycerides

Activates adipose cell lipase

Increased fatty acids available for other tissues (ketogenic)

48
Q

What is the impact of glucagon on carbohydrate metabolism?

A

Increases gluconeogenesis (increased uptake of amino acids)

Increased glycogenolysis

Breakdown of liver glycogen

49
Q

What does a high concentration of Glucagon do?

A

enhances strength of heart

increases blood flow into some tissues

increased bile secretion

inhibits gastric secretion

50
Q

What is the mechanism of action of Glucagon?

A

Glucagon activates G protein –> AC –> increased concentration of cAMP –> activates PKA –> phosphorylates multiple enzymes –> activates glycogen phosphorylase –> increased glycogenolysis

51
Q

What happens when PKA deactivates glycogen synthase?

A

decreased glycogen synthesis

52
Q

Where does somatostatin come from?

A

delta cells

53
Q

What does somatostatin inhibit?

A

insulin, glucagon and pancreatic polypeptide secretion

54
Q

what are some actions of somatostatin (apart from inhibition)

A

prolongation of gastric emptying time,

decreased exocrine pancreas secretion, gastric motility and gastric secretion

55
Q

Where is pancreatic polypeptide secreted from?

A

F cells or PP cells

56
Q

What does Pancreatic Polypeptide inhibit?

A

insulin and somatostatin secretion.

57
Q

What is Amylin? (structure)

A

islet amyloid polypeptide

37 AA

co-secreted with insulin from pancretic beta cells

58
Q

When co-secreted from beta cells with insulin, what does Amylin do?

A

decreases glucagon release, decreased body weight (inhibition of food intake) and decreases gastric emptying

59
Q

How does Amylin affect blood glucose concentration?

A

decreases glucagon release (decreases blood glucose via inhibition of hepatic glucose production)

60
Q

What are incretins?

A

Digestive tract hormones that increase insulin secretion from beta cells

61
Q

What are the two major incretins?

A

Glucagon-like peptide and Glucose-dependant insulinotropic polypeptide (PIC).

62
Q

What releases gastroinstetsinal peptides (GLP-1 and GIP), insulin and amylin?

A

ingestion of food

63
Q

Where is GLP1 produced?

A

L cells of small intestine

64
Q

What is the main action of GLP-1?

A

stimulation of glucose-dependant insulin release from pancreatic islets

65
Q

What happens to GLP-1 in type 2 diabetes?

A

impaired insulin response to GLP-1 = reduction in postprandial GLP-1 secretion

66
Q

What is the action of GIP in the fasting state (hypoglycemia)?

A

enhances glucagon activity

67
Q

what is GIP stimulated by?

A

glucose, fat and protein ingestion

67
Q

What is the action of GIP in hyperglycemia?

A

potentiates (increases) glucose-induced insulin secretion

68
Q

what is the normal blood glucose range for fasting and random?

A

fasting = 3.0 - 6.9 mmol/L
random = 3.0-8.0mmol/L

69
Q

When is Growth hormone in blood glucose regulation and what does it do?

A

Hypoglycaemic trigger

decreased glucose and increased fat use

70
Q

When is cortisol triggered in BGL regulation and what does it do?

A

hypoglycaemic trigger

decreased glucose uses and increased fat use

increased gluconeogenesis, hepatic glycogenesis sand ketogenesis

71
Q

what are the most common causes of diabetes?

A

defect insulin secretion, defect insulin action or both

72
Q

Describe the physiology of how thirst and polyuria occurs in type 1 diabetes Mellitus.

A

Increased blood glucose –> Increased filtered load of
glucose –> The non-reabsorbed glucose acts as an osmotic
solute in urine, producing an osmotic diuresis, polyuria,
and thirst

73
Q

What is insulin deficiency?

A

from the destruction of pancreatic-B cells

caused by ‘organ specific’ autoimmune disease

74
Q

What does insulin deficiency (and glucagon excess) result in?

A

Decreased glucose uptake

increased protein catabolism

increased lipolysis

75
Q

What is the consequence of decreased glucose uptake?

A

Hyperglycaemia, glycosuria, osmotic diuresis, electrolyte depletion

76
Q

What does thyroid hormone do for BGL?

A

makes them raise because it increases glucose absorption

77
Q

What is the consequence of increased protein catabolism in insulin deficiency?

A

increased plasma amino acids

nitrogen loss in urine

and all decreased glucose uptake consequences

(Hyperglycaemia, glycosuria, osmotic diuresis, electrolyte depletion)

78
Q

What is the consequence of increased lipolysis (insulin deficiency)?

A

Increased plasma FFA, ketogenesis, ketouria and ketonemia

79
Q

What is hyperglycaemia due to?

A

Decreased insulin action
–Increased insulin production
(Hyperinsulinemia)
* Leads to beta cell failure

80
Q

what percent of diabetes are type 2?

A

90%

81
Q

What is insulin resistance?

A

– impaired biological response to insulin

Insulin is secreted normally by the beta
cells
– But insulin can not activate its receptors in
the target cells

82
Q

what is the primary defect for patients with type 2 diabetes?

A

insulin resistance

83
Q

what are the main differences between type 1 and type 2 diabetes?

A

Type 1 = insulin dependant whilst type 2 is non insulin dependent

type 1 = severe symptoms of thirst and ketoacidosis whilst type 2 = insidious onset of symptoms

type 1. = spontaneous ketosis but type 2 = no ketoacidosis

Type 1= c-peptide absent, 2 = c-peptide present

84
Q

When should we medically consider Type 1 Diabetes Mellitus?

A

If there is:

Ketonuria
polyuria
weight loss
young age
family history of autoimmune disease
rapid onset of symptoms

85
Q

What is the difference between insulin deficiency and insulin resistance ?

A

deficiency = don’t actually make it because beta cells are destroyed

resistance = make it but does not activate receptors in target cells

86
Q

What is diabetes insidious vs mellitus

A

Insipidus= very diluted urine = ADH deficiency

Mellitus= sweet urine due to excess glucose secreted = insulin inactivity

87
Q

What do GH, Corisol and Thyroid hormone all do?

A

Hyperglucemic hormones = incerased blood glucose levels

88
Q

Describe the sequence of actions if there is Increased BG?

A

Alpha cell inhibited = decreased glucagon

Beta cell activated = increased insulin

= deceased to normal levels

89
Q

Describe the sequence of actions if there is decreased BG?

A

alpha cell activated = increased glucagon

beta cell inhibited = decrased insulin

= raise to normal levels

Endo (14 decks)

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