unseen Q3 Flashcards

(49 cards)

1
Q

What is Type 2 Diabetes Mellitus (T2DM)?

A

A metabolic disorder characterized by chronic hyperglycemia due to insulin resistance and pancreatic β-cell dysfunction.

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2
Q

What causes hyperglycemia in T2DM?

A

A combination of insulin resistance and impaired insulin secretion from pancreatic β-cells.

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3
Q

What are the two main mechanisms involved in the pathogenesis of T2DM?

A
  • Insulin resistance
  • Pancreatic β-cell dysfunction
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4
Q

What is insulin resistance?

A

A diminished response of peripheral tissues to the action of insulin.

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5
Q

Which tissues are primarily affected by insulin resistance?

A
  • Skeletal muscle
  • Adipose tissue
  • Liver
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6
Q

How does insulin resistance affect skeletal muscle?

A

It impairs glucose uptake and reduces glycogen synthesis.

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7
Q

How does insulin resistance affect adipose tissue?

A

It increases lipolysis and raises free fatty acid levels in the blood.

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8
Q

What is the consequence of elevated free fatty acids?

A

They contribute to insulin resistance and β-cell dysfunction.

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9
Q

How does insulin resistance affect the liver?

A

It reduces insulin’s ability to suppress gluconeogenesis, increasing glucose production.

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10
Q

What is gluconeogenesis?

A

The metabolic process of producing glucose from non-carbohydrate sources.

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11
Q

What is the role of pancreatic β-cells?

A

To produce and secrete insulin in response to blood glucose levels.

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12
Q

What initially happens to β-cells in response to insulin resistance?

A

They increase insulin secretion to compensate.

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13
Q

What is β-cell exhaustion?

A

A decline in β-cell function due to chronic overproduction of insulin.

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14
Q

What is glucotoxicity?

A

Damage to β-cells caused by prolonged high blood glucose levels.

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15
Q

What is lipotoxicity?

A

Damage to β-cells caused by elevated levels of free fatty acids.

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16
Q

How does oxidative stress affect β-cells?

A

It damages β-cell structures and impairs function.

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17
Q

What is endoplasmic reticulum stress?

A

A condition in which protein folding in β-cells is disrupted, contributing to dysfunction.

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18
Q

What happens as functional β-cell mass decreases?

A

Insulin production declines, worsening hyperglycemia.

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19
Q

How do genetic factors influence T2DM?

A

They increase susceptibility, especially with a family history of diabetes.

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20
Q

What environmental factors contribute to T2DM?

A
  • Sedentary lifestyle
  • Excessive caloric intake
  • Obesity
21
Q

What type of obesity is most associated with T2DM?

A

Central adiposity (abdominal fat accumulation).

22
Q

How does obesity promote insulin resistance?

A

By increasing free fatty acids and inflammatory cytokines.

23
Q

What immune cells infiltrate adipose tissue in obesity?

A
  • Macrophages
  • Other immune cells
24
Q

What kind of inflammation is associated with T2DM?

A

Chronic low-grade inflammation.

25
Which cytokines are involved in obesity-related inflammation?
* TNF-α * IL-6
26
How do cytokines like TNF-α affect insulin signaling?
They interfere with insulin receptor signaling pathways.
27
What is the result of inflammation in adipose tissue?
Worsening of insulin resistance.
28
What are incretins?
Hormones that enhance insulin secretion after meals.
29
Name an important incretin hormone.
Glucagon-like peptide-1 (GLP-1).
30
How is the incretin effect altered in T2DM?
It is diminished, reducing insulin secretion in response to meals.
31
What is the consequence of impaired incretin function?
Postprandial hyperglycemia.
32
What is the overall effect of β-cell dysfunction and insulin resistance?
Chronic hyperglycemia and metabolic disturbances.
33
Which mechanisms lead to β-cell damage?
* Glucotoxicity * Lipotoxicity * Oxidative stress * ER stress
34
How do elevated free fatty acids impact T2DM?
They worsen insulin resistance and damage β-cells.
35
How does inflammation link obesity and insulin resistance?
By cytokine release that disrupts insulin signaling.
36
What lifestyle change can help reduce T2DM risk?
Increased physical activity and weight loss.
37
Why is early T2DM often asymptomatic?
Because compensatory insulin secretion initially maintains normoglycemia.
38
What is postprandial hyperglycemia?
High blood sugar levels following meals.
39
What is normoglycemia?
Normal blood glucose levels.
40
What triggers insulin secretion under normal conditions?
Elevated blood glucose levels.
41
What is the role of GLP-1 in glucose regulation?
It stimulates insulin secretion and inhibits glucagon release.
42
How do cytokines impair insulin signaling?
By promoting serine phosphorylation of insulin receptor substrates.
43
Why does insulin resistance increase hepatic glucose output?
Because insulin fails to suppress gluconeogenesis.
44
What happens to insulin levels in late-stage T2DM?
They decline due to β-cell failure.
45
Can T2DM be reversed?
In early stages, lifestyle changes can significantly improve or reverse symptoms.
46
What is central adiposity?
Fat accumulation around the abdomen, linked to metabolic risk.
47
Why are skeletal muscles important in glucose regulation?
They are the main site for insulin-mediated glucose uptake.
48
What does β-cell compensation mean?
Increased insulin secretion in response to insulin resistance.
49
What does the term 'metabolic disturbance' refer to in T2DM?
Disruptions in glucose, fat, and protein metabolism due to insulin dysfunction.