Glucose Metabolism Flashcards

1
Q

How is glucose manufactured?

A

Gluconeogenesis and glycogenolysis

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2
Q

Which organ does not need insulin for glucose uptake?

A

Brain

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3
Q

How can injection of somatostatin treat hypoglycaemia?

A
  • Somatostatin receptors coupled to voltage gated Ca channels in pancreatic B cells
  • Somatostatin blocks channel
  • Reduces Ca influx and inhibits insulin secretion
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4
Q

Which receptors facilitate non-insulin mediated glucose transport?

A

GLUT 1 and GLUT 3

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5
Q

Which receptors mediate glucose uptake in fat and muscle?

A

GLUT 4

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6
Q

What is the mechanism of GLP1 analogues in treating diabetes?

A
  • GLP1 is an incretin

- Stimulates insulin production

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7
Q

What might be the consequence of glucokinase mutation?

A
  • Inheritable diabetes

- Glucose not broken down to ATP as easily

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8
Q

Which chain of insulin is most active at the receptor?

A

A chain

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9
Q

Insulin is synthesised exclusively in the ____ cells of the _____

A

Beta cells of pancreas

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10
Q

Describe the synthesis and release of insulin.

A
  1. Glucose transported into beta cell by facilitated diffusion via glucose transporter -> inc. [glucose] in beta cell
  2. Glucose -> glycolysis -> ATP -> closure of K+ sensitive channels -> depolarisation
  3. Influx of Ca -> insulin translocation and exocytosis
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11
Q

Why do patients often gain weight after starting on insulin?

A
  • Stimulates triglyceride storage
  • Inhibit lipolysis and FFA production
  • Inhibit ketone production
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12
Q

What is the influence of insulin on carbohydrates?

  • Lier
  • Muscle
  • Adipose
A
  • Liver: inhibit gluconeogenesis and glycogenolysis
  • Muscle: increase glucose transport and glycolysis
  • Adipose: same as muscle
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13
Q

What is the influence of insulin on protein?

A
  • Anabolic

- Increase transport of AA to liver and muscle

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14
Q

What are incretins?

A

Hormones secreted into blood minutes after eating that inc. production of insulin

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15
Q

What is the mechanism of sulfonylureas?

A
  • Close ATP sensitive K channels in beta cell plasma membrane
  • Initiate cascade resulting in insulin release
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16
Q

What do we measure clinically in patients with severe recurrent hypoglycaemia?

A

C peptide

High insulin and low C peptide

17
Q

In the Kreb cycle ____ is oxidised for energy

A

Acetyl CoA

18
Q

How are free fatty acids metabolised?

A
  • Cannot enter Kreb cycle

- Mostly metabolised in liver and muscle to ketone bodies

19
Q

What are three ketones produced in the body?

A
  • Acetoacetate
  • Acetone
  • Beta hydroxybutyrate
20
Q

Which ketone can be measured clinically?

A
  • Beta hydroxybutyrate
21
Q

What is the pathophysiology of diabetic ketoacidosis?

A
  • Lack of insulin, so no glucose in cells (no energy source)
  • Glucose accumulates in blood stream
  • Activation of hormone sensitive lipase -> lipolysis
  • Also breakdown of glycogen
22
Q

What are the clinical findings of a patient with diabetic ketoacidosis?

A
  • Very high blood sugar
  • Severe acidosis
  • Hypotensive
  • Volume depleted
23
Q

What is the range of normal fasting glucose?

A

3.5-5.5 mmol/L

24
Q

What happens when diabetics become hypoglycemic?

A
  • ANS activated ~3.0mmol/L

- NA release - sweating, tremor, increased HR, dilated pupils etc.

25
Q

Which hormones are most important in the counter regulation of hypoglycaemia?

A
  • Adrenaline and glucagon

Also cortisol.

26
Q

What are four causes of hypoglycaemia?

A
  • Insulin in diabetic patients
  • Sulphnylurea therapy
  • Insulinoma
  • Severe hormone deficiency e.g. Addison’s disease