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FHB Exam 4: Endocrinology and Reproduction > Endocrine XI: Metabolic Homeostasis > Flashcards

Endocrine XI: Metabolic Homeostasis Flashcards

1
Q

Define “wasting.”

A

It is a prolonged fasted state, or a state of metabolic starvation.

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2
Q

What are some of the cellular and physiological effects of wasting?

A
  • production of pro-inflammatory cytokines
  • activation of HPA axis
  • dysregulation of GH and IGF-I
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3
Q

What is the metabolic switch?

A

when ketone bodies start to be used as an energy source for the brain (reduced reliance on glucose as a fuel source; protective mechanism)

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4
Q

Metabolic syndrome (or syndrome X) is characterized by the presence of 3 out of 4 of which symptoms?

A
  • visceral obesity
  • insulin resistance
  • dyslipidemia
  • HTN
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5
Q

What is the primary hormone produced by adipocytes?

A

leptin

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6
Q

What are some important transcription factors produced by white adipose tissue?

A

SREBP-1C, PPARγ

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7
Q

What does SREBP-1C do?

A

promotes TG synthesis and increases glucokinase “trapping” of glucose inside cells

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8
Q

What does PPARγ do?

A

It is a nuclear steroid receptor that regulates TG storage and adipocyte differentiation.

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9
Q

What are PPARγ agonists used for, and what are some of their side effects?

A

used to treat insulin resistance and Type 2 diabetes (ex: thiazolidinediones) by making new fat cells with new receptors; because PPARγ induces differentiation of fat cells, a side effect of PPARγ agonists is increased fat storage and weight gain

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10
Q

There is a direct relationship between plasma leptin and what?

A

total fat

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11
Q

What are some stimulators vs. inhibitors of appetite?

A
  • stimulators: neuropeptide Y (NPY), Agouti-related peptide (AGRP)
  • inhibitors: αMSH, cocaine-amphetamine regulated transcript (CART)
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12
Q

What is the net effect of leptin?

A

It decreases food intake by inhibiting appetite stimulators (like NPY and AGRP) and stimulating appetite inhibitors (like αMSH and CART)

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13
Q

What happens to leptin-deficient mice?

A

they are morbidly obese because their appetite is uncontrolled due to lack of leptin

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14
Q

Do higher levels of leptin inhibit appetite more?

A

No, obese humans have high leptin levels and an uninhibited appetite.

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15
Q

What is insulin resistance?

A

an inability to clear glucose from the blood due to insulin not efficiently transporting glucose into cells

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16
Q

What causes insulin resistance?

A

hyperinsulinemia downregulates insulin receptors; over time, pancreas reduces insulin output, which can lead to diabetes mellitus

17
Q

How can Type 1 diabetes be converted to Type 2?

A

beta cell depletion (pancreatic beta cells become dysfunction over time and die)

18
Q

Obese patients have much higher release of _______ despite same level of plasma glucose compared to a patient with normal weight.

A

insulin

19
Q

What is the gold standard for diagnosis of Type II diabetes?

A

elevated HbA1C (greater than or equal to 46 mMol/L, or 6.5%)

20
Q

What are the classic symptoms of T2DM?

A
  • polyphagia (excessive hunger)
  • polyuria (excessive urination)
  • polydipsia (excessive thirst)
21
Q

What are some of the treatments for T2DM?

A
  • Sulfonylureas (ex: Glipizide)- close ATP-dependent K+ channels in beta cells and cause insulin release
  • Biguanides (ex: Metformin)- inhibit hepatic gluconeogenesis and increase insulin receptor activity to increase sensitivity to insulin
  • Alpha-glucosidase inhibitors (ex: Glyset)- delay intestinal absorption of carbs
22
Q

What is more typical for T2DM- relative or absolute insulin deficiency?

A

relative, which is why ketogenesis is absent or minimal

23
Q

True or false- mental acuity is a function of plasma osmolality

A

true!

24
Q

What happens under normal physiological conditions when insulin is present with regard to GH and IGF-I?

A
  • AAs from protein stimulate GH, which stimulates IGF-I in liver
  • IGF-I stimulates glucose uptake in muscle, causing proliferation of visceral organ tissues
  • GH also opposes insulin lipogenesis (maintenance of lean body mass)
25
Q

In a state of starvation, what happens in the body in terms of GH and IGF-I?

A

GH increases due to increased AA proteolysis. No IGF-I is released because no insulin is present, so there is no negative feedback on GH.

26
Q

Why is there no ketogenesis with T2DM?

A

This is because with T2DM, there is SOME insulin present, and insulin inhibits ketogenesis.

27
Q

What is the main distinguishing factor b/t T1DM and T2DM?

A

insulin resistance (Type I=not insulin resistant; Type II=insulin resistant)

28
Q

What is the most highly associated genetic polymorphism associated with risk for T2DM?

A

transcription factor 7-like-2 (TCF72), involved with the Wnt signaling pathway

29
Q

When are pancreatic islet cells formed?

A

during embryonic development; beta cell replication then continues during childhood and adolescence but is stable in adults

30
Q

What are the genes important to islet cell development?

A
  • PDX-1 (islet neogenesis and beta cell prolif.)
  • TCF72 (downstream targets regulate beta cell prolif.)
  • NEUROG3 (encodes protein neurogenin 3, which is key for endocrine cell development)
31
Q

What are some of the environmental risk factors for T2DM?

A
  • impaired beta cell prolif. during childhood (malnutrition, maternal factors during pregnancy)
  • increased propensity for insulin resistance (high calorie diet, lack of physical activity)
  • acquired organ dysfunction for glucose homeostasis (reversible)
32
Q

Explain the changes in beta cell function as T2DM progresses.

A
  • at first, insulin secretion can keep up w/ higher levels of glucose (beta cells compensate and proliferate)
  • insulin levels begin dropping as beta cells die due to glucose and lipid toxicity, as well as amyloid deposition and inflammation
  • beta cells completely die off, and T2DM switches to T1DM that is insulin-dependent
33
Q

What is a key component of the early stage of disease in T2DM?

A

first phase insulin release impairment

FHB Exam 4: Endocrinology and Reproduction (14 decks)

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