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BRS > Glucose homeostasis and diabetes > Flashcards

Glucose homeostasis and diabetes Flashcards

1
Q

What hormones raise blood glucose?

A

Glucagon, Cortisol, Growth hormone and catecholamines.

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2
Q

What hormones lower blood glucose?

A

Insulin.

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3
Q

What is the endocrine tissue of the pancreas?

A

Islet of langerhans.

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4
Q

What do alpha cells in the pancreas produce?

A

Glucagon.

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5
Q

What do beta cells in the pancreas produce?

A

Insulin.

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6
Q

What do delta cells in the pancreas produce?

A

Somatostatin.

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7
Q

What cells do somatostatin inhibit?

A

Alpha and beta cells. Inhibition of Glucagon and insulin secretion.

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8
Q

What do gap junctions in the islet of langerhans do?

A

Allow small molecules to pass directly between cells.

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9
Q

What do tight junctions in the islet of langerhans do?

A

Create small intercellular spaces.

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10
Q

What stimulates beta cells to produce insulin?

A

Increase in blood glucose, increase in amino acids, increase in GI hormones, parasympathetic nervous system, glucagon.

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11
Q

What inhibits beta cells?

A

Sympathetic nervous activity, somatostatin.

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12
Q

Insulin blood glucose reducing mechanisms

A

Build up of glycogen stores, breakdown of glucose (increased rate of glycolysis), increased uptake of glucose via GLUT4 transporter, increased protein synthesis, increased lipogenesis and decreased lipolysis.
Decreases gluconeogenesis and ketogenesis.

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13
Q

When there is a rise in blood glucose why are glucagon and somatostatin released?

A

To prevent overshoot and result in hypoglycemia.

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14
Q

What stimulates alpha cells to produce glucagon?

A

Low blood glucose, amino acids, GI hormones, sympathetic nervous activity (via alpha adrenergic) and parasympathetic nervous system.

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15
Q

What inhibits alpha cells?

A

Insulin and somatostatin.

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16
Q

What happens to insulin when blood glucose is low?

A

Insulin production is shut down.

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17
Q

Glucagon blood glucose raising mechanisms?

A

Increases gluconeogenesis by increase lipolysis in adipocytes and amino acid transport to liver. Hepatic glycogenolysis takes place.

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18
Q

Beta cells release of insulin mechanism

A

Glucose binds to GLUT 2 without the need for insulin. Glucose gets converted to glucose -6-phosphate which results in an increase in ATP. Increase in ATP results in closure of potassium channels which increases levels of potassium in the cell. This results in opening of calcium channels allowing movement of calcium into cell. Calcium moving into cell causes release of insulin.

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19
Q

How is proinsulin converted to insulin?

A

Proteolytic cleavage of proinsulin. Produces insulin and C peptide.

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20
Q

What are C peptide levels like in a type 1 diabetic patient?

A

Type 1 diabetic patients are producing little insulin from their beta cells. This means they will have a low C peptide.

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21
Q

Why does oral glucose raise insulin more than IV glucose?

A

Due to gastrointestinal hormones such as GLP-1

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22
Q

What does GLP-1 do?

A

Stimulates insulin release and suppresses glucagon release. Increases satiety feeling.

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23
Q

What cells secrete GLP-1?

A

L cells.

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24
Q

What is GLP-1 used to treat?

A

Diabetes.

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25
Q

What is insulin release like in type 2 diabetes?

A

Less of an insulin release and not as fast of a release.

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26
Q

What part of the insulin receptor does insulin bind to?

A

Insulin binds to the alpha subunit which is part of the extracellular domain.

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27
Q

What happens when insulin binds to the insulin receptor?

A

Conformational change in tyrosine kinase domains of beta subunits (intracellular portion of receptor).

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28
Q

Where is GLUT 4 located?

A

Myocytes and adipocytes.

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29
Q

How does insulin mobilise GLUT4?

A

Highly insulin responsive. Stored in vesicles and insulin stimulation mobilises GSV’s (GLUT4 storage vesicles), allowing the vesicles to fuse with cell membrane and insert GLUT4 in plasma membrane.

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30
Q

What hormones inhibits protein breakdown in muscle?

A

Insulin.

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31
Q

What hormone stimulates protein breakdown in muscle?

A

Cortisol.

32
Q

What hormones promote protein synthesis in muscle?

A

Insulin, GH and IGF-1.

33
Q

What hormones stimulate uptake of amino acids by the liver?

A

Glucagon.

34
Q

What hormones stimulate amino acid use for gluconeogenesis in liver?

A

Glucagon, cortisol.

35
Q

What hormones inhibit amino acid use for gluconeogenesis?

A

Insulin.

36
Q

What hormone stimulates protein breakdown in the liver?

A

Glucagon.

37
Q

What hormone stimulates protein synthesis in the liver?

A

Insulin.

38
Q

What stimulates lipoprotein lipase?

A

Insulin.

39
Q

What does lipoprotein lipase do?

A

Breaks down triglycerides so glycerol and NEFA can enter adipocytes.

40
Q

What hormones stimulate formation of triglycerides?

A

Insulin.

41
Q

What hormones stimulates uptake of glucose in adipocytes so that the glucose can be used to make fatty acids?

A

Insulin.

42
Q

What hormones stimulate breakdown of triglycerides in adipocytes so that glycerol and fatty acids can be released into the blood?

A

Cortisol and growth hormone.

43
Q

What hormones inhibit breakdown of triglycerides in adipocytes?

A

Insulin.

44
Q

What hormones stimulates formation of ketone bodies in liver?

A

Glucagon.

45
Q

What hormones inhibit formation of ketone bodies in liver?

A

Insulin.

46
Q

Metabolic biomarkers for type 1 diabetes?

A

High glucose, low insulin and high levels of ketone bodies.

Normal - Low glucose, Low insulin and increased levels of ketone bodies.

47
Q

What hormones stimulate conversion of glucose-6-phosphate to glycogen in the liver?

A

Insulin.

48
Q

What hormones stimulate conversion of glycogen to glucose-6-phosphate (glycogenolysis)?

A

Glucagon and adrenaline (during fight and flight).

49
Q

What hormones stimulate uptake of glucose via GLUT4 on muscle cells?

A

Insulin.

50
Q

What hormones inhibit uptake of glucose via GLUT4 on muscle cells?

A

Glucagon and growth hormone.

51
Q

What is the difference between glycogen in muscle and liver?

A

Muscle cells can’t release glucose as they lack glucose 6-phosphatase. All glycogen is muscle cells can only be used in muscle cells.

52
Q

What happens during a fasted state?

A

Low insulin to glucagon ratio. Increased proteolysis and lipolysis. Increased hepatic glucose output. Ketogenesis when fasting is prolonged.

53
Q

What happens during a fed state?

A

Insulin is released in two phases. High insulin to glucagon ratio. Stop hepatic glucose output. Insulin blood glucose reducing mechanisms occur.

54
Q

Tests used to diagnose diabetes mellitus?

A

Fasting glucose test. Random glucose test. Oral glucose tolerance test. HbA1c.

55
Q

How is an oral glucose tolerance test?

A

Blood test done under fasted state. Glucose is given. After 2 hours another blood test.

56
Q

How do you confirm someone has diabetes?

A

2 positive tests or 1 positive test + symptoms.

57
Q

What is type 1 diabetes and if left untreated what can it result in?

A

Autoimmune condition resulting in an insulin deficiency. Untreated type 1 diabetes can lead to diabetic ketoacidosis.

58
Q

Symptoms of type 1 diabetes?

A

Weight loss, hyperglycemia, glycosuria with osmotic symptoms (polyuria, nocturia and polydipsia). Ketones in blood and urine.

59
Q

Diagnostic tests for type 1 diabetes?

A

Antibody tests - GAD and IA2
C - peptide
Presence of ketones

60
Q

What can result if too much insulin is given?

A

Hypoglycemia.

61
Q

What is the body’s counterregulatory response to hypoglycemia?

A

Increase in glucagon, cortisol, growth hormone and catecholamines.

62
Q

What can go wrong with the counterregulatory response to hypoglycemia?

A

May not be strong enough if too much insulin is used. Loss of counterregulatory response if body gets used to low blood glucose and so can lead to recurrent hypoglycemia.

63
Q

Key difference between type 2 diabetes and type 1 diabetes?

A

In type 2 there is enough insulin to suppress ketogenesis and proteolysis. Type 2 involves insulin resistance.

64
Q

What happens during insulin resistance?

A

Insulin doesn’t act on PI3K-AKt pathway (metabolic actions). Results in increased insulin production. MAPK pathway leads to high blood pressure.

65
Q

What biomarkers are present in a patient with insulin resistance?

A

High triglycerides, low HDL, Hypertension and inflammation (high CRP).

66
Q

What does type 2 diabetes result in?

A

Hyperglycemia, insulin resistance. Later on may develop insulin deficiency (destruction of beta cells).

67
Q

Diet for type 2 diabetes?

A

More complex carbs, more fibre less sodium.

68
Q

How is type 1 diabetes managed?

A

Exogenous insulin, self monitoring of glucose.

69
Q

How is type 2 diabetes managed?

A

Diet, oral medication, may need insulin later.

70
Q

What GLUT transporter is present in the liver?

A

GLUT2.

71
Q

What GLUT transporter is present in the pancreas?

A

GLUT2

72
Q

What GLUT transporter is present in muscle?

A

GLUT4

73
Q

How is GLUT2 different to GLUT4?

A

GLUT2 is insulin independent while GLUT4 is insulin dependent.

74
Q

What is hypoglycemia blood glucose concentration?

A

Under 4 mmol/l.

75
Q

What is hyperglycemia blood glucose concentration?

A

Above 7 mmol/l.

76
Q

What is normal blood glucose concentration?

A

4-7 mmol/l.

BRS (52 decks)

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