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Y3S1 Lectures > Biochemistry of Diabetes and Insulin > Flashcards

Biochemistry of Diabetes and Insulin Flashcards

1
Q

Is insulin anabolic or catabolic? Explain.

A

Anabolic

Promotes synthesis of lipids, proteins and glycogen.

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2
Q

What hormones “take over” in diabetes?

A

Glucagon (liver only), adrenaline and cortisol

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3
Q

What substances are mobilised from muscle and fat respectively in diabetes?

A

Muscie: lactate and AAs
Adipose: glycerol

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4
Q

What is insulin resistance?

A

Decreased sensitivity of target cells to normal circulating insulin levels due to impaired insulin signalling.

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5
Q

What are the BSL levels of people with insulin resistance like?

A

Hyperglycaemia even in the presence of high plasma insulin levels

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6
Q

What are the factors needed to develop insulin resistance?

A

Obesity genes or obesity, insulin resistance genes + environmental factors

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7
Q

What is the early-stage response of the body to insulin resistance?

A

Increased insulin made by beta-cells and adequate compensatory response.
Beta-cell mass increases and function enhances
Compensatory hyperinsulinaemia and maintenance of normal glucose tolerance

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8
Q

How do we transition from insulin resistance to T2DM?

A

Eventually increased demand for insulin causes beta cells to fail to compensate + insulin resistance causes hyperglycaemia and this causes glucolipotoxicity to beta cells.

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9
Q

Does everyone with insulin resistance eventually get DM?

A

No

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10
Q

What type of receptor is the insulin receptor?

A

Tyrosine kinase receptor

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11
Q

What are the rapid and long-term effects of activating the insulin receptor?

A

Rapid: glucose uptake, enzyme activation

Long-term: enzyme synthesis, cell growth

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12
Q

What is the negative control mechanism for insulin receptors?

A

Downstream kinases are activated and phosphorylate IRS proteins on serine residues, preventing propagation of the insulin signal.

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13
Q

What impairs insulin signalling?

A
  1. Genetic variations

2. Excess nutrients and IR induces (cytokines, ROS etc.) that stop signalling

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14
Q

Which important GLUT receptor is insulin-independent and where is it located?

A

GLUT2 in the liver

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15
Q

How does insulin resistance affect lipid metabolism?

A

Increased plasma FFA
Increased plasma TAGs and VLDL
:. Predisposes to hypertriglyceridaemia and NA fatty liver

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16
Q

How does abdominal visceral fat predispose to CVD?

A

Causes insulin resistance AND affects lipid levels, increasing bad cholesterols

17
Q

What are the main features of the metabolic syndrome?

A

CENTRAL OBESITY

  • Raised TAGs <1.7
  • Reduced HDL-C
  • Raised BP >130
  • Raised fasting BGL >5.6 or T2DM
18
Q

What is adiposopathy and how does it occur?

A

Dysfunctional adipose tissue! Low-grade chronic inflammation of expanded adipocytes.
As tissue expansion occurs so does necrosis as the vascular network can’t keep up with growth

19
Q

What are the risk factors for adiposopathy?

A

Caused by adiposity, genetic predisposition and sedentary lifestyle

20
Q

What are the effects of adiposopathy?

A 
Increased FFA release
Abnormal cytokines (adipokines)
Adipose tissue is endocrine tissue! Adiposopathy causes metabolic disturbances including insulin resistance.
21
Q

How to these lipid issues cause damage in non-adipose tissue?

A

Excess FFAs are taken up and lipid storage occurs in droplets near mitochondria, causing lipotoxic effects
Cause beta-cell failure and fatty liver also.
Don’t need to know proposed mechanisms!

22
Q

How go biguanides work?

A

Inhibit hepatic gluconeogenesis

Activate AMPK to increase insulin sensitivity.

23
Q

How do sulphonylureas/meglitinides work?

A

Bind to pancreatic SUR1 receptor to increase insulin secretion
Close K channel to promote insulin release (:. can cause a hypo!)

24
Q

How do thiazolidinediones/glitazones work?

A

Bind to PPAR-gamma to promote peripheral FFA uptake
Sensitise cells to insulin
Increase glucose utilisation

25
Q

How do alpha-glucosidase inhibitors work?

A

Slow down digestion and absorption of some carbs (starch!)

26
Q

What normally happens re glucagon after a meal?

A

Glucose prompts action of beta-cells which in turn inhibit alpha-cells so glucagon is not produced

27
Q

What happens with decreased sensitivity of alpha cells to insulin/decreased insulin?

A

Glucagon is not adequately suppressed and so is oversecreted

Y3S1 Lectures (5 decks)

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