L77: Metabolic Homeostasis

Question 1

WHO definition of obesity

Answer 1

BMI greater than 30

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

Question 2

Metabolic syndrome (Syndrome X)

Answer 2

visceral obesity, insulin resistance, dyslipidemia, hypertension

Question 3

visceral obesity, insulin resistance, dyslipidemia, hypertension

Answer 3

Metabolic syndrome (Syndrome X)

Question 4

PPARγ

Answer 4

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

Question 5

Thiazolidinediones (TZD)

Answer 5

PPARγ agonists used to treat insulin resistance and

Type II diabetes “Rosiglitazone = Avandia”)

Question 6

Obese people have high levels of

Answer 6

leptin

Question 7

Leptin is produced by

Answer 7

adipocytes

Question 8

There is a direct relationship between leptin and

Answer 8

total fat

Question 9

Relationship between total fat and plasma

leptin concentrations.

Answer 9

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.

Question 10

Neuropeptide Y

Answer 10

hypothalamic stimulator of appetite

Question 11

Agouti-Related Peptide (AGRP)

Answer 11

hypothalamic stimulator of appetite

Question 12

αMSH

Answer 12

hypothalamic suppressor of appetite

Question 13

Cocaine-amphetamine regulated transcript (CART)

Answer 13

hypothalamic suppressor of appetite

Question 14

Leptin inhibits which hypothalamic regulators of appetite?

Answer 14

Neuropeptide Y and AGRP

Question 15

Leptin stimulates which hypothalamic regulators of appetite?

Answer 15

αMSH

CART

Question 16

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

Answer 16

Insulin resistance

Question 17

What promotes conversion from T1DM to T2DM?

Answer 17

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

Question 18

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

Answer 18

Elevated HbA1C: ≥48mMol/l (6.5%)

Question 19

Normal vs. pre-diabetic fasting glucose

Answer 19

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

Question 20

Leptin deficient mice are

Answer 20

morbidly obese

Question 21

HbA1C is effective because the lifespan of RBC is

Answer 21

120 days

Question 22

pre-diabetic fasting glucose?

Answer 22

100-124mg/dl

Question 23

Fasting glucose for T2DM?

Answer 23

126+ mg/dl

Question 24

What are the “3P” symptoms of T2DM?

Answer 24

Polyphagia
Polyuria
Polydipsia

Question 25

Polyphagia

Answer 25

excessive hunger due to inability of cells to utilize glucose "cellular starvation"

Question 26

Polyuria

Answer 26

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

Question 27

Polydipsia

Answer 27

excessive thirst due to severe dehydration

Question 28

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

Answer 28

Delays intestinal absorption of carbs

Question 29

What does metformin do?

Answer 29

Inhibits hepatic gluconeogenesis, and enhances insulin receptor activity

Question 30

What does "Glipizide" do? Hint: sulfonylurea drug

Answer 30

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

Question 31

What kind of diabetes exhibits KETOACIDOSIS without insulin therapy?

Answer 31

Type 1 DM

Question 32

Side effect of TZD

Answer 32

weight gain

Question 33

Direct relationship between plasma leptin and

Answer 33

total fat

Question 34

Indirect relationship between ghrelin and

Answer 34

obesity

Question 35

Name 4 counter regulatory hormones to insulin

Answer 35

GH Cortisol Catecholamines Glucagon

Question 36

Declined mental status in DM results from

Answer 36

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

Question 37

TCF72

Answer 37

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.

Question 38

Which DM is reversible?

Answer 38

T2DM

Question 39

PDX-1

Answer 39

important for both islet neogenesis and beta-cell proliferation

Question 40

Bonus: what is Exenatide?

Answer 40

incretin mimetic