Diabetes Flashcards

1
Q

Define diabetes mellitus

A

a heterogeneous complex metabolic disorder characterized by elevated blood glucose concentration secondary to either resistance to the action of insulin, insufficient insulin secretion, or both

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2
Q

What are the sources of glucose?

A

1) From dietary sources​
2) From the breakdown of glycogen stores (glycogenolysis)​
3) From formation of glucose (gluconeogenesis)

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3
Q

Which glucose transporters allow movement at low (basal) glucose levels?

A

GLUT 1, 3 and 4

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4
Q

Which glucose transporter is responsible for insulin dependent response in fat and muscles?

A

GLUT 4

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5
Q

Which glucose transporter is present on beta-islet cells?

A

GLUT 2

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6
Q

Which glucose transporter is responsible for dietary uptake in intestines?

A

SGLT1

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7
Q

Which glucose transporter is found in the kidneys?

A

SGLT2

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8
Q

Are the GLUT transporters energy dependent?

A

No

Promote facilitated diffusion, not energy dependent

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9
Q

Are the SGLT transporter energy dependent?

A

Yes

Use sodium to move glucose against concentration gradient.

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10
Q

What are the substrates for gluconeogenesis?

A

Production of glucose from molecules (not carbohydrates)​
Substrates are:​
- Lactate (from non-oxidative metabolism – Cori cycle)​
- Glycerol (from fats)​
- Glutamine and alanine (from protein)

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11
Q

Where does gluconeogenesis occur?

A

Occurs in both liver and kidneys

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12
Q

How is insulin secreted?

A

Extracellular glucose is transported into the β -cell via GLUT-2.​

Glucose is metabolised which increases adenosine triphosphate to diphosphate (ATP:ADP) ratio within the cell.​

This leads to closure of ATP-dependent K+ channels​

Closure of K+ channels leads to cell membrane depolarisation​

Membrane depolarisation leads to opening of voltage dependent Ca2+ channels and Ca2+ influx​

Ca2+ influx leads to exocytosis of stored insulin vesicles

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13
Q

What are the two phases of insulin secretion?

A

Insulin secretion occurs in two phases (biphasic):​

  • First phase has rapid onset and lasts ~ 10 minutes​
  • Second phase is prolonged plateau lasting as long as hyperglycaemia persists.
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14
Q

What are the actions of insulin?

A

Predominantly anabolic in action​

Action via activation of insulin receptor on target cell membrane​
Outcome depends on which secondary pathway is activated​

Glucose transport​
GLUT 4 predominantly stored in intracellular vesicles​
Insulin promotes fusion of vesicles and transporter insertion into cell walls​
Thus facilitates glucose transport into cells

Glycogen synthesis​
Insulin promotes activation of glycogen synthase​
​
Other actions:​
Inhibit gluconeogenesis​
Glycogen synthesis​
Protein synthesis​
Lipogenesis​
Suppress ketogenesis
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15
Q

What are the actions of glucagon?

A
Promote gluconeogenesis​
Glycogenolysis​
Proteolysis​
Lipolysis​
Ketogenesis
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16
Q

What happens in the post-absorptive state?

A

Post-absorptive (fasted) state

14-16 hours fast​
Glucose levels relatively stable

Insulin : Glucagon ratio favours glucagon​
Primarily catabolic state​
Loss of insulin action to suppress lipolysis and proteolysis​
Production of precursors for gluconeogenesis and production of other fuels (e.g. ketones)

17
Q

What happens in the post-prandial state?

A

Post-prandial (fed) state

Insulin response to rising glucose levels​
Acute exposure to free fatty acids also increases basal and glucose stimulated insulin production ​

Insulin : Glucagon ratio favours insulin​
Primarily anabolic state

18
Q

What do the L-cells of the small intestine produce?

A

L-cells of small intestine produce gastrointestinal insulinotropic polypeptides​
- Glucagon-Like Peptides (GLP)​
- Gastric inhibitory peptide (GIP)​

Augment insulin secretion in response to oral glucose load.

19
Q

What are the symptoms of Type 1 diabetes?

A
Hyperglycaemia
Polyuria
Polydipsia
Weight loss
Ketoacidosis
20
Q

What are the complications of diabetes?

A
Hypoglycaemia (of treatment)​
​
Microvascular​
Nephropathy​
Retinopathy​
Neuropathy​
​
Macrovascular​
Ischaemic heart disease​
Cerebrovascular disease​
Peripheral vascular disease