L77: Metabolic Homeostasis Flashcards

1
Q

WHO definition of obesity

A

BMI greater than 30

Waist-hip ratio greater than 0.95 (men) and 0.85 (women)

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2
Q

Metabolic syndrome (Syndrome X)

A

visceral obesity, insulin resistance, dyslipidemia, hypertension

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3
Q

visceral obesity, insulin resistance, dyslipidemia, hypertension

A

Metabolic syndrome (Syndrome X)

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4
Q

PPARγ

A

Peroxisome proliferator-activated receptor gamma: Nuclear steroid hormone receptor. Regulates TG storage and adipocyte differentiation - makes more fat cells

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5
Q

Thiazolidinediones (TZD)

A

PPARγ agonists used to treat insulin resistance and

Type II diabetes “Rosiglitazone = Avandia”)

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6
Q

Obese people have high levels of

A

leptin

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7
Q

Leptin is produced by

A

adipocytes

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8
Q

There is a direct relationship between leptin and

A

total fat

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9
Q

Relationship between total fat and plasma

leptin concentrations.

A

Higher body fat
correlates with increased plasma levels of leptin. Leptin inhibits appetite and food intake during the normal fed state. Obese people have
very high levels of leptin, but are potentially insensitive to leptin effects.

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10
Q

Neuropeptide Y

A

hypothalamic stimulator of appetite

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11
Q

Agouti-Related Peptide (AGRP)

A

hypothalamic stimulator of appetite

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12
Q

αMSH

A

hypothalamic suppressor of appetite

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13
Q

Cocaine-amphetamine regulated transcript (CART)

A

hypothalamic suppressor of appetite

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14
Q

Leptin inhibits which hypothalamic regulators of appetite?

A

Neuropeptide Y and AGRP

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15
Q

Leptin stimulates which hypothalamic regulators of appetite?

A

αMSH

CART

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16
Q

Insulin does not efficiently transport glucose into cells. Glucose levels are high

A

Insulin resistance

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17
Q

What promotes conversion from T1DM to T2DM?

A

Beta cell depletion or “exhaustion” will cause conversion from Type II to Type I diabetes

18
Q

Measures average blood glucose
concentrations over a longer period
of time.

A

Elevated HbA1C: ≥48mMol/l (6.5%)

19
Q

Normal vs. pre-diabetic fasting glucose

A

Fasting blood glucose: 100-125 mg/dl (pre-diabetes), 126+ T2DM

20
Q

Leptin deficient mice are

A

morbidly obese

21
Q

HbA1C is effective because the lifespan of RBC is

A

120 days

22
Q

pre-diabetic fasting glucose?

A

100-124mg/dl

23
Q

Fasting glucose for T2DM?

A

126+ mg/dl

24
Q

What are the “3P” symptoms of T2DM?

A

Polyphagia
Polyuria
Polydipsia

25
Q

Polyphagia

A

excessive hunger due to inability of cells to utilize glucose “cellular starvation”

26
Q

Polyuria

A

excess glucose in blood leads to increased plasma osmolarity, excessive water and Na+ loss

27
Q

Polydipsia

A

excessive thirst due to severe dehydration

28
Q

What does Procose or Glyset do? Hint: alpha-glucosidase inhibitors.

A

Delays intestinal absorption of carbs

29
Q

What does metformin do?

A

Inhibits hepatic gluconeogenesis, and enhances insulin receptor activity

30
Q

What does “Glipizide” do? Hint: sulfonylurea drug

A

Closes K+ channel on B-cell, promoting depolarization and Ca+ influx, thus insulin secretion

31
Q

What kind of diabetes exhibits KETOACIDOSIS without insulin therapy?

A

Type 1 DM

32
Q

Side effect of TZD

A

weight gain

33
Q

Direct relationship between plasma leptin and

A

total fat

34
Q

Indirect relationship between ghrelin and

A

obesity

35
Q

Name 4 counter regulatory hormones to insulin

A

GH
Cortisol
Catecholamines
Glucagon

36
Q

Declined mental status in DM results from

A

dehydration accompanying hyper osmotic hyperglycemic state (both T2DM and T1DM)

37
Q

TCF72

A

most highly associated genetic polymorphism in T2DM. This is a Wnt signaling pathway player, co-activatory of beta-catetenin. Downstream targets regulate B-cell proliferation.

38
Q

Which DM is reversible?

A

T2DM

39
Q

PDX-1

A

important for both islet neogenesis and beta-cell proliferation

40
Q

Bonus: what is Exenatide?

A

incretin mimetic