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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

(53 cards)

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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?

23
Q

Epidemiology of TID?

Study These Flashcards
A

Can develop at any age but usually diagnosed < 20 yo

24
Q

TID is characterized by what of beta cells?

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A

Autoimmune destruction = absolute deficit

25
Twin concordance rate of TID?
30-50%
26
Types of genes implicated in TID?
- Major histocompatibility genes - Genes that teach immune system to "self-tolerate" self tissues
27
Histocompatibility genes?
- HLA DR3 - HLA DR4 - HLA DQ8
28
What genes account for 50% of the genetic risk of TID?
Histocompatibility genes
29
People with one copy of both ______ and ______ show increased risk for TID
DR3 and DR4
30
Histocompatibility gene polymorphisms are within what portion of the gene?
Antigen-presenting portion
31
"Tolerance" genes?
- CTLA-4 - PTPN-22
32
What does CTLA-4 do?
- Down-regulates APCs - Interacts with CD-28 (Treg)
33
What does PTPN-22 do?
Important in the development of central Tregs in thymus
34
Environmental theory of TID of viral infection involvement?
Association with mumps, rubella, coxsackie B, or CMV
35
3 mechanisms for involvement of viral infection in TID?
1. Bystander damage 2. Beta-cell antigen mimickers 3. Precipitating virus
36
Viral infections induce islet injury and inflammation, leading to release of β-cell antigens and activation of autoreactive T cells
Bystander damage
37
Viruses produce proteins that mimic β-cell antigens, and immune response to viral protein cross-reacts with self-tissue
Beta-cell mimicker
38
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
Precipitating virus
39
What likely causes gradual loss of beta-cell mass?
Destruction by cytotoxic T-cells
40
TID disease manifestation appears after _____ of beta-cells are destroyed
90%
41
What cells are the main problem in TID? Why?
T-cells - Self reactive ones not destroyed in thymus - Defects in Treg - Antigens likely attacked
42
What happens as you kill beta-cells?
Remaining cells become hyperproductive
43
What does it mean for beta-cells to be hyperproductive?
When glucose goes up, cells make insulin and glucose go down again
44
Ability of remaining β-cells to become hyper-productive and compensate for failing insulin response
Honeymooning
45
What happens once the honeymooning cells fail?
Deterioration is rapid
46
Typical initial presentation of TID?
Diabetic ketoacidosis
47
Patients presenting with TID generally have a subacute history of what?
- Polyphagia (hunger not satisfied) - Polydipsia (excessive thirst) - Polyuria (excessive urination)
48
As patients lose the ability to use serum glucose to generate ATP, what happens?
Adipose tissues release FAs => ketogenesis
49
How does the liver generating ketones affect blood pH?
Makes it more acidic = pH drop
50
For unclear reasons, patients who experience DKA often experience fairly severe what?
Generalized abdominal pain
51
An absolute insulin deficiency leads to a catabolic state, culminating in ketoacidosis and severe volume depletion - causing what?
CNS compromise and eventual diabetic coma/death
52
Elevated blood glucose => an ______________ in the kidney
Osmotic diuresis
53
Excess sugar in the urine causes?
Drawing water from blood into urine => dehydration

BMS150 Post-MT2 (17 decks)

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