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Endocrinology > Lecture 10: Metabolic Homeostasis > Flashcards

Lecture 10: Metabolic Homeostasis Flashcards

1
Q

How much glucose does the brain require per day?

A

180g

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2
Q

How is starvation related to exercise?

A

initial energy source: 80% fat (release of FFAs, breakdown of liver glycogen/protein)

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3
Q

What does the metabolic switch entail in starvation state?

A

ketone bodies used as energy source - reduced reliance on glucose

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4
Q

What are the 4 criteria for metabolic syndrome?

A

1) visceral obesity
2) insulin resistance
3) dyslipidemia
4) hypertension

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5
Q

What is the primary hormone produced by WAT?

A

Leptin

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6
Q

What are the 2 important transcription factors in WAT?

A

1) Sterol regulatory binding protein 1C (SREBP-1C)

2) PPARy

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7
Q

What does SREBP-1C do?

A

1) promotes TG synthesis
2) increases glucokinase trapping glucose inside cells

(activated by lipids and insulin)

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8
Q

What does PPARy do and what is its receptor?

A

regulates/promotes TG storage and adipocyte differentiation (lipids are the ligand)

INCREASES # of adipocytes

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9
Q

How has PPARy been drugable to treat diabetes type 2?

A

agonists treat insulin resistance (promote TG storage but also makes more fat)

side effect is weight gain

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10
Q

What is the class of PPARy agonists?

A

TZDs (thiazolidinediones)

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11
Q

as leptin increases, what happens to fat?

A

increases (direct relationship)

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12
Q

What are 2 hypothalamic hormone stimulators of appetite?

A

1) Neuropeptide Y

2) Agouti-related peptide

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13
Q

What are 2 inhibitors of appetite?

A

1) aMSH (cleaved from POMC)

2) CART

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14
Q

How does leptin affect appetite?

A

inhibits it!

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15
Q

Why do obese people have high levels of leptin?

A

leptin resistant

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16
Q

What leads to DM?

A

reduced production of insulin by pancreas (beta cell depletion/exhaustion)

17
Q

What happens to insulin receptors in hyperinsulinemia?

A

DOWNREGULATED

18
Q

What is the ultimate diagnosis of T2DM?

A

elevated HbA1c (>48mMol/l)

19
Q

What is HbA1c

A

a measure of glycosylated RBCs (too much glucose in the plasma, eventually starts to stick on RBCs)

20
Q

What is the fasting blood glucose in pre-diabetic patients?

A

100-125mg/dl

21
Q

What is the oral glucose tolerance test?

A

8 hour fast, measure glucose before and 2h after consumption of 75g glucose

22
Q

What does C-peptide tell you?

A

indication of how well the pancreas is working

23
Q

What are 3 symptoms of T2DM?

A

1) Polyphagia (cellular starvation)
2) Polyuria (excess glucose in blood leads to increased plasma osmolarity pulling H2O)
3) Polydipsia (severe dehydration)

24
Q

How do Sulfonylurea drugs help T2DM patients?

A

stimulate insulin release (close ATP dependent K+ channels)

25
Q

What are examples of sulfonylureas?

A

glipizide

glyburide

26
Q

What does metformin do?

A

inhibits hepatic gluconeogenesis

increases insulin receptor activity

27
Q

What do alpha glucosidase inhibitors like precose or glyset do?

A

delay intestinal absorption of carbs

28
Q

What are some leading theories behind beta cell dsyfunction?

A

1) islet amyloid buildup
2) ER stress
3) lipotoxicity

29
Q

Ketoacidosis characterizes which type of diabetes?

A

1 (in the absence of insulin therapy)

30
Q

How does ketoacidosis occur in T1DM?

A

increase FFA release (hepatic precursor for ketone acids) —-> metabolism of ketone bodies for energy —-> increased blood acidity —-> diabetic coma/severe dehydration

31
Q

What is the main difference between absolute and relative insulin deficiency?

A

Absolute: lipolysis (increases ketogenesis)

32
Q

How is mental acuity related to blood sugar?

A

increase blood sugar, increase blood osmolarity (dehydrates)

alert (320mOsm) drowsy (330) stupor (340) coma (360)

33
Q

How are GH and insulin related?

A

AA from protein stimulates GH which stimulates IGF-1

IGF-1 simulates glucose uptake in muscle, proliferation of visceral organ tissues, inhibits proteolysis

GH opposes insulin lipogenesis

34
Q

is GH high or low in times of starvation?

A

HIGH

(increased AA from proteolysis stimulates it)

but no IGF-1 (no insulin) so no negative feedback on GH

35
Q

List the physiological hallmarks of starvation

A

1) No insulin, low glucose
2) catecholamines stimulate glucagon
3) GH increases (increase AA due to proteolysis)
4) no negative feedback on GH (no IGF-1)
5) Cortisol (stress) increases

36
Q

What is the most highly associated genetic polymorphism in T2DM?

A

TCF72 (part of Wnt signaling) participates in islet cell development

37
Q

When does islet neogenesis occur?

A

embryonic development (beta cell replication continues during childhood but is stable in adults)

Endocrinology (16 decks)

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