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SGUL - Physiology 1 > Control of Blood Glucose & Endocrine Pancreas > Flashcards

Control of Blood Glucose & Endocrine Pancreas Flashcards

1
Q

How does glucose get into cells in the gut?

A
  • Secondary active transport
  • SGLT 1
  • Sodium transports glucose into the cell
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2
Q

How does glucose get reabsorbed in the PCT?

A

SGLT 1 and SGLT2

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3
Q

Where is GLUT 1 found and in what ranges does it work?

A
  • In the brain + erythrocytes
  • High affinity for glucose
  • Constant uptake at 2-6mM
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4
Q

Where is GLUT 2 found and what is the affinity like?

A
  • Liver, kidney, pancreas, gut
  • Low affinity
  • Transport rate increases with glucose concentration
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5
Q

Where is GLUT 3 found and what is its affinity?

A
  • Brain
  • High affinity
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6
Q

Where is GLUT 4 found and what is its affinity?

A
  • Muscle and adipose tissue
  • Medium affinity
  • Glucose uptake is insulin dependent
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7
Q

What are the islets of Langerhans?

A

Clusters of endocrine cells surrounded by an exocrine pancreas where hormones are synthesised

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8
Q

What do the following secrete?

α-cells (A cells)
β-cells (B cells)
δ-cells

A

α-cells (A cells) - glucagon
β-cells (B cells) - insulin
δ-cells - somatostatin

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9
Q

How do we get mature insulin from the precursor? PART 1

A
  • Formed from preproinsulin by proteolytic processing.
  • Removal of signal sequence at the amino acid terminus of preproinsulin and the formation of 3 disulphide bonds produces proinsulin.
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10
Q

How do we get mature insulin from the precursor? PART 2

A
  • Further proteolytic cuts remove the C peptide from proinsulin to produce mature insulin, composed of A and B chains.
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11
Q

What is the blood supply of the pancreas?

A

Branches of celiac, superior mesenteric and splenic arteries

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12
Q

What is the venous drainage of the pancreas?

A

Into the portal system

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13
Q

Describe the release of insulin into the circulation.

A
  • Half of the secreted insulin is metabolised by the liver in its first pass
  • Remainder is diluted into peripheral circulation.
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14
Q

What is the clinical significance of C peptide?

A
  • Not metabolised by the liver
  • Good index of insulin circulation
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15
Q

List some factors stimulating insulin secretion (ie. affecting B-cells).

A
  • plasma glucose
  • incretin hormones
  • alpha adrenergic
  • parasympathetic
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16
Q

List some factors inhibiting insulin secretion.

A

Somatostatin

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17
Q

List some factors stimulating glucagon secretion.

A
  • beta-adrenergic
  • parasympathetic
18
Q

List some factors inhibiting glucagon secretion.

A

insulin
plasma glucose
somatostatin

19
Q

How do β-cells sense a rise in glucose? PART 1

A
  • Glucose uptake via GLUT2 transporter.
  • Glucose metabolised to G6P, which generates ATP.
  • ATP stimulates an ATP-sensitive K+ channel, so K+ efflux is stopped.
20
Q

How do β-cells sense a rise in glucose? PART 2

A
  • Cell depolarisation, which activates VGCCs.
  • Ca2+ influx signals vesicle mobilisation (the vesicles contain insulin).
21
Q

Describe the glucagon receptor action pathway.

A
  • Binds to its receptor, activating αGs subunit.
  • Stimulates Adenylate Cyclase, which generates cAMP
  • Activates PKA
22
Q

What type of receptor are insulin receptors?

A

Tyrosine kinase

23
Q

What are the general effects of insulin binding to its receptor?

A
  • Activates cascade of protein phosphorylation, which stimulates or inhibits specific metabolic enzymes
  • Modulates activity of metabolic enzymes by regulating gene transcription
24
Q

What are the specific effects of insulin binding to its receptor?

A
  • Translocation of GLUT4 transporters to plasma membrane ∴ influx of glucose
  • Glycogenesis
  • Glycolysis
  • Fatty acid synthesis
25
Q

How do insulin and glucagon act together?

A
  • Counter-regulatory hormones that act principally through PKA activity
  • Glucagon phosphorylates key enzymes in metabolic pathways.
  • Insulin action leads to dephosphorylation of these same enzymes.
26
Q

Describe Type 1 Diabetes Mellitus.

A

Absolute insulin deficiency (due to destruction of pancreatic β-cells)

27
Q

Describe Type 2 Diabetes Mellitus

A

Combination of insulin resistance and insulin deficiency

28
Q

How do we diagnose diabetes mellitus?

A
  • Random plasma glucose would be ≥11.1 mmol/L
  • Fasting plasma glucose would be ≥7.0 mmol/L
  • Oral glucose tolerance test (OGT) would be ≥11.1 mmol/L
29
Q

How does insulin affect plasma glucose?

A
  • Plasma glucose is kept within constant limits by insulin and glucagon
  • Insulin is released in response to high plasma glucose, acting to lower it to within a suitable range.
30
Q

What is the importance of glycaemic control?

A
  • Reduces macrovascular complications (increased risk of CVD and stroke, etc.)
  • Reduces microvascular complications (damage to capillary beds in retina, kidney, etc.)
31
Q

What would be a good indicator of glycaemic control?

A
  • HbA1C (glycosylated Hb) - ideally found in low levels
  • Less than 6.5% is good
  • With every 1% fall in A1C, there is a 20-30% relative risk reduction in microvascular complications.
32
Q

Why would a doctor not administer an injection to maintain glycaemic control?

A
  • Accidental overdoses can occur
  • Patient may become hypoglycaemic
33
Q

Give examples of incretin hormones and where they are released from.

A
  • GLP-1 and GIP.
  • Released by gut endocrine cells in response to nutrients in the gut.
34
Q

What is the general mechanism of action of incretin hormones?

A
  • Circulate in bloodstream until they reach the pancreas
  • Potentiate production of insulin from β-cells ∴ blood glucose decreases
35
Q

How does GLP-1 work?

A
  • Activates adenylate cyclases
  • Increases cAMP ∴ increases PKA
  • Increased release of insulin-rich secretory granules.
36
Q

What are some drug treatments for Type 2 Diabetes Mellitus? PART 1

A
  • Metformin: decreases gluconeogenesis
  • Sulfonylureas: bind and close ATP-sensitive K channels, depolarising β-cells and releasing insulin
37
Q

What are some drug treatments for Type 2 Diabetes Mellitus? PART 2

A
  • Thiazolidinediones: activate PPARγ receptors (controllers of lipid metabolism), which reduces insulin resistance
  • SGLT2 inhibitors: promote glucose excretion via the kidney
38
Q

What are some drug treatments for Type 2 Diabetes Mellitus? PART 3

A
  • Incretin-targeting drugs: potentiate insulin release in response to rising plasma glucose (such as synthetic GLP-1 analogues)
39
Q

Why is insulin resistance not down to one reason?

A

Many intracellular pathways

40
Q

What enzyme starts lipogenesis and how?

A
  • ACC(Acetyl CoA-carboxylase)
  • Insulin reduces PKA which inhibits ACC

SGUL - Physiology 1 (68 decks)

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