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FHB Endocrinology > L77: Metabolic Homeostasis > Flashcards

L77: Metabolic Homeostasis Flashcards

1
Q

What happens in starvation?

A

Brain needs constant supply of glucose (180g /day) -> break down fat stores, liver glycogen, and proteins)

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2
Q

What happens in a prolonged fast?

A

Dominant catabolic state
Metabolic Switch: brain uses ketone bodies rather than glucose for energy -> decrease reliance on glucose as fuel source
Protein breakdown continues but much lower rate

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3
Q

What is obesity?

A

BMI>30

Waist-Hip ratio greater than 0.95M or 0.85W

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4
Q

What is metabolic syndrome?

A

visceral obesity
insulin resistance
dyslipidemia
HTN

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5
Q

What is the primary hormone produced by white adipose tissue?

A

Leptin

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6
Q

What is SREBP-1C?

A

Sterol REgulatory Binding Protein 1C
Promotes TG synthesis
Activated by lipids and insulin

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7
Q

What is PPARy?

A

Peroxisome Proliferator activated Receptor Gamma
Nuclear steroid hormone receptor
Regulates TG storage and adipocyte differentiation

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8
Q

What is a PPARy agonist used clinically?

A

TZD: PPARy agonist used to treat insulin resistance in DM TII
Induces differentiation of adipocytes -> more fat cells
Increased fat storage

Side effect: Weight gain (not desirable for diabetics)

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9
Q

What is the relationship between leptin and fat levels?

A

Higher body fat-> increased levels of leptin

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10
Q

What does leptin do?

A

inhibit appetite and food intake

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11
Q

Why do obese people have high levels of leptin?

A

Potentially insensitive to leptin effects -> very high levesl

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12
Q

What hypothalamic hormones stimulate appetite? What does leptin do to these?

A 
Neuropeptide Y (Arcuate  nucleus)
AGRP (Paraventricular Nucleus)

Leptin inhibits these to decrease food intake

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13
Q

What hypothalamic hormones inhibit appetite? What does leptin do to these?

A

aMSH (Paraventricular Nucleus)
CART (Arcuate Nucleus)

Leptin stimulates these to decrease food intake

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14
Q

What happens in insulin resistance?

A

insulin does not effectively transport glucose into cell -> glucose levels high -> hyperinsulinemia -> down reg insulin receptors (takes time, gradual)

Eventually pancreas reduces insulin output -> DM

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15
Q

What causes a conversion from Type II to Type I DM?

A

Beta cell depletion/exhaustion

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16
Q

What is T2DM?

A

Diabetes Mellitus Type II: impaired beta cell funciton as well as insulin resistance

17
Q

What does HbA1C measure?

A

Measures average blood glucose concentrations over a long period of time as glucose increases the number of glycosylated RBCs

> 6.5% = diabetes

18
Q

Whats diabetic/normal levels of fasting blood glucose?

A 
126+ = T2DM
100-125= prediabetes
19
Q

What are sx of T2DM?

A

Polyphagia
Polyuria- excess glucsoe in blood -> inc plasma osmolarity -> excessive water and sodium loss
Polydipsia

20
Q

What are Tx options for T2DM?

A

Sulfonylureas(glipizide)
Biguanides (Metformin)
a-glucosidase inhibitors

21
Q

What does sulfonylureas do to treat T2DM?

A

Close ATP dependent K+ channels in beta cells -> insulin release

22
Q

What does metformin do to treat T2DM?

A

Inhibit hepatic gluconeogenesis

Increase insulin receptor activiyt -> more sensitive to insulin -> inc glucose uptake

23
Q

What does a-glucosidase inhibitors do to treat T2DM?

A

Delays intestinal absorption of carbs

24
Q

What can cause bet cell dysfunciton oin T2DM?

A 
Islet amyloid buildup
ER stress
Lipotoxicity
Glucose toxicity
Incretin hormone dysregulation
Islet inflammation
25
Q

What characterizes T1DM?

A

Insulin-Dependent Diabetes
Development of ketoacidosis without insulin therapy
Juvenile onset

26
Q

What causes T1DM?

A

Destruction of pancreatic beta cells -> insulin dependent

27
Q

What is used to treat T1DM?

A

Insulin injections, diet, monitor blood glucose

28
Q

What causes diabetic ketoacidosis?

A

T1DM: Decreased insulin + inc counter hormones -> increased FFA released -> inc ketone acid formation -> metabolism of ketone bodies -> inc blood acidity (dec pH)

29
Q

What causes diabetic coma?

A

Severe dehydration and metabolic acidosis

30
Q

What are the counterregulatory hormones to insulin?

A

Glucaon, GH, cortisol, catecholeamines

31
Q

What causes diuresis and dehydration in diabetics?

A

Increased plasma glucose levels -> inc blood osmolality

32
Q

How are plasma osmolality and mental status related?

A

Inc plasma osmolality -> severe dehydration-> increased altered mental status

Seen in T1 and T2DM due to hyperosmotic hyperglycemic states

33
Q

When does islet neogenesis occur?

A

During embryonic development

34
Q

When does beta cell replication occur?

A

During childhood/adolescence but stable in adults

35
Q

What is PDX1?

A

important for islet neogenesis and beta cell proliferation

36
Q

What is TCF72?

A

Downstream targets regulate beta cell proliferation

37
Q

What does Exenatide do?

A 
Incretin Mimetic (GLP-1 agonist)
REstores 1st phase insulin secretion in T2DM patients and improved 2nd phase insulin secretion

FHB Endocrinology (10 decks)

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