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BMS150 Post-MT2 > Obesity, Insulin Resistance II, and Type I Diabetes > Flashcards

Obesity, Insulin Resistance II, and Type I Diabetes Flashcards

1
Q

Most important environmental risk factor for insulin resistance?

A

Obesity

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2
Q

Why does insulin resistance usually occur?

A

Combination of factors involving numerous genes and environmental risk factors

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3
Q

Obese people and those with glucose intolerance often have impaired what?

A

Satiety mechanisms - poorly-characterized “leptin resistance”

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4
Q

Satiety signals? (5)

A
  • Leptin (from adipocytes)
  • GLP1 (from SI)
  • CCK
  • PYY (from LI)
  • Vagal afferents
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5
Q

Hunger signal?

A

Ghrelin (released by stomach fasting)

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6
Q

What do non-esterified fatty acids (NEFA) do?

A

Increase insulin resistance

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7
Q

Does central or peripheral fat release more NEFAs?

A

Central fat > peripheral fat

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8
Q

What does increased intracellular [NEFAs] cause?

A

Serine phosphorylation of insulin receptor = inactivation

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9
Q

What are adipokines? What do they do?

A
  • Protein hormones from fat cells
  • Modify sensitivity of insulin receptor
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10
Q

What mediates increased NEFA oxidation?

A

Protein kinase A

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11
Q

What drug activates AMP-K?

A

Metformin

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12
Q

Anti-hyperglycemic adipokines? (2)

A
  • Leptin
  • Adiponectin
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13
Q

Hyperglycemic adipokines? (2)

A
  • Resistin
  • Retinol-binding-protein 4
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14
Q

Pro-inflammatory cytokines secreted by fat cells _______ insulin receptor sensitivity

A

Decreased

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15
Q

Who produces more VLDL?

A

Those that are insulin-resistant

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16
Q

Lipoprotein lipase is ______ in a wide variety of tissues in those that are insulin-resistant

A

Down-regulated

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17
Q

Where especially is LPL reduced in those with insulin-resistance?

A

Skeletal muscle and adipose tissue

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18
Q

What is produced by the liver in an insulin-resistant state that inhibits LPL?

A

ApoC-III Protein

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19
Q

Is HDL increased or reduced during insulin resistance?

A

Reduced

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20
Q

Why is visceral obesity bad for you? (2)

A
  • Excessive lipid buildup = stress on adipocyte (ROS)
  • High [FFA] may bind PAMP-R in adipocyte
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21
Q

What can buildup of stress and high [FFA] in the adipocyte lead to the production of?

A

Pro-inflammatory cytokines IL-6 and TNF-alpha

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22
Q

5-10% of diabetes cases?

A

Type I

23
Q

Epidemiology of TID?

A

Can develop at any age but usually diagnosed < 20 yo

24
Q

TID is characterized by what of beta cells?

A

Autoimmune destruction = absolute deficit

25
Q

Twin concordance rate of TID?

A

30-50%

26
Q

Types of genes implicated in TID?

A
  • Major histocompatibility genes
  • Genes that teach immune system to “self-tolerate” self tissues
27
Q

Histocompatibility genes?

A
  • HLA DR3
  • HLA DR4
  • HLA DQ8
28
Q

What genes account for 50% of the genetic risk of TID?

A

Histocompatibility genes

29
Q

People with one copy of both ______ and ______ show increased risk for TID

A

DR3 and DR4

30
Q

Histocompatibility gene polymorphisms are within what portion of the gene?

A

Antigen-presenting portion

31
Q

“Tolerance” genes?

A
  • CTLA-4
  • PTPN-22
32
Q

What does CTLA-4 do?

A
  • Down-regulates APCs
  • Interacts with CD-28 (Treg)
33
Q

What does PTPN-22 do?

A

Important in the development of central Tregs in thymus

34
Q

Environmental theory of TID of viral infection involvement?

A

Association with mumps, rubella, coxsackie B, or CMV

35
Q

3 mechanisms for involvement of viral infection in TID?

A
  1. Bystander damage
  2. Beta-cell antigen mimickers
  3. Precipitating virus
36
Q

Viral infections induce islet injury and inflammation, leading to release of β-cell antigens and activation of autoreactive T cells

A

Bystander damage

37
Q

Viruses produce proteins that mimic β-cell antigens, and immune response to viral protein cross-reacts with self-tissue

A

Beta-cell mimicker

38
Q

Viral infections early in life persist in pancreas, and re-infection
with a related virus that shares antigenic characteristics leads to immune response against infected islet cells

A

Precipitating virus

39
Q

What likely causes gradual loss of beta-cell mass?

A

Destruction by cytotoxic T-cells

40
Q

TID disease manifestation appears after _____ of beta-cells are destroyed

A

90%

41
Q

What cells are the main problem in TID? Why?

A

T-cells
- Self reactive ones not destroyed in thymus
- Defects in Treg
- Antigens likely attacked

42
Q

What happens as you kill beta-cells?

A

Remaining cells become hyperproductive

43
Q

What does it mean for beta-cells to be hyperproductive?

A

When glucose goes up, cells make insulin and glucose go down again

44
Q

Ability of remaining β-cells to become hyper-productive and compensate for failing insulin response

A

Honeymooning

45
Q

What happens once the honeymooning cells fail?

A

Deterioration is rapid

46
Q

Typical initial presentation of TID?

A

Diabetic ketoacidosis

47
Q

Patients presenting with TID generally have a subacute history of what?

A
  • Polyphagia (hunger not satisfied)
  • Polydipsia (excessive thirst)
  • Polyuria (excessive urination)
48
Q

As patients lose the ability to use serum glucose to generate ATP, what happens?

A

Adipose tissues release FAs => ketogenesis

49
Q

How does the liver generating ketones affect blood pH?

A

Makes it more acidic = pH drop

50
Q

For unclear reasons, patients who experience DKA often experience fairly severe what?

A

Generalized abdominal pain

51
Q

An absolute insulin deficiency leads to a catabolic state,
culminating in ketoacidosis and severe volume depletion - causing what?

A

CNS compromise and eventual diabetic coma/death

52
Q

Elevated blood glucose => an ______________ in the kidney

A

Osmotic diuresis

53
Q

Excess sugar in the urine causes?

A

Drawing water from blood into urine => dehydration

BMS150 Post-MT2 (17 decks)

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