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FHB Exam 4 > Endocrine 11: Metabolic Homeostasis > Flashcards

Endocrine 11: Metabolic Homeostasis Flashcards

1
Q

What are the physiological effects of starvation?

A
  • proinflammatory cytokines
  • constant activation of HPA (catecholamines)
  • dysregulation of GH and IGF1 (no IGF1 b/c no insulin)
  • catabolic state (fat, protein, glycogen)
  • ketogenesis
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2
Q

What are the major physiological conditions associated with Syndrome X/Metabolic Syndrome

A
  • visceral obesity (waist circumference >40in. (M), >35in. (F))
  • insulin resistance (FG > 100 mg/dL)
  • dyslipidemia (TG > 150 mg/dL; HDL 135/80)
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3
Q

Define obesity.

A
  • BMI over 30

- waist-hip ratio greater than 0.95 (M) or 0.85 (F)

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4
Q

Define adipocyte.

A

triglyceride storage cell

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5
Q

List the endocrine secretions of adipocytes.

A
  • main hormone = leptin
  • SREBP-1C (Sterol Regulatory Binding Protein) TF
  • PPARg
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6
Q

Define SREBP-1C.

A

Sterol Regulatory Binding Protein (transcription factor)

  • stimulates TG synthesis
  • activated by lipids and insulin (anabolism)
  • increases glucokinase activity (traps glucose inside cell to be used for storage)
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7
Q

Define PPARg.

A
  • transcription factor
  • steroid nuclear hormone receptor
  • binds to lipids
  • regulates TG storage and adipocyte differentiation
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8
Q

Define TZDs.

A

Thiazolidinediones

  • PPARg agonists
  • promotes differentiation of fat cells => more insulin receptors => increases insulin sensitivity
  • problem = increase fat mass
  • used as Tx for T2DM (called Avandia)
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9
Q

What are the effects of leptin?

A
  • production correlates with amount of fat cells (more fat = more leptin)
  • inhibits appetite by inhibited neuropeptide Y and agouti-related peptide (ARP) in the hypothalamus (these are appetite stimulators)
  • stimulates appetite inhibitors by stimulating aMSH (from POMC) and CART (cocaine-amphetamine related factor)
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10
Q

Describe leptin levels in obese individuals.

A

lots of fat mass = lots of leptin
=> leptin resistance
=> don’t respond to more leptin

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11
Q

Define insulin resistance.

A
  • reversible stage
  • insulin cannot efficiently transport glucose into cells
  • high BG => saturation of insulin independent receptors
  • initially, hyperinsulinemia => downregulation of insulin receptors => resistance
  • over time, beta cell death => T2DM => T1DM
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12
Q

Describe insulin levels in obese individuals.

A

For the same plasma glucose levels, obese individuals produce MUCH more insulin.

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13
Q

What are the diagnostic parameters for T2DM?

A
  • HbA1C > 6.5%
  • fasting glucose > 126 mg/dL
  • oral glucose tolerance test > 200 mg/dL
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14
Q

What are the diagnostic parameters for prediabetes?

A
  • fasting glucose > 100 mg/dL

- oral glucose tolerance test > 150 mg/dL

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15
Q

Describe the symptoms of T2DM.

A
  • polyphagia = ineffective glucose uptake into cells makes body think it is starving
  • polyuria = saturation of glucose reabsorption transporters in kidney => osmotic diuresis of water and electrolytes
  • polydipsia = dehydration from polyuria leads to increased thirst
  • impaired beta cell function and insulin resistance
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16
Q

List treatment options for T2DM.

A
  1. sulfonylureas (glyburide, glipizide) - block ATP-sensitive K channel (keep it closed) => easier to depolarize => pushes out as much insulin as possible from cell (assists in first response)
  2. biguanides (metformin) - blocks hepatic gluconeogenesis and increases peripheral insulin sensitivity, increased glucose uptake
  3. alpha-glucosidase inhibitors (precose, glyset) - slows gastric emptying to allow beta cells to catch up and have proper first response
17
Q

List proposed mechanisms of beta cell dysfunction.

A
  • amyloid plaques
  • stress
  • lipotoxicity
  • glucose toxicity
  • reduced beta cell differentiation in childhood
  • incretin hormone dysregulation
  • islet inflammation
18
Q

Characterize T1DM.

A
  • juvenile onset
  • constant state of catabolism
  • ketogenic
  • tx = lifelong insulin, tight glycemic control
  • destruction of beta cells (autoimmune)
19
Q

Define DKA.

A

Diabetic Ketoacidosis

  • low insulin, high counterregulatory hormones (glucagon, catecholamines)
  • FFA release leads to ketone formation (b/c no glucose uptake)
  • causes acidosis
  • dehydration b/c ketones cause diuresis of cells => neurons shrink =====> coma, death
  • usually, this is how T1DM is treated
20
Q

Describe the physiological state during starvation.

A
  • no glucose = no insulin
  • catecholamines => excess glucagon (no negative feedback b/c no glucose)
  • proteolysis => GH
  • no IGF (no insulin)
  • cortisol => lipolysis, glycogenolysis
21
Q

Describe the physiological state during T1DM.

A

same as starvation except you have high glucose and ketones

22
Q

Describe the physiological state during T2DM.

A

same as T1DM

  • some insulin (also balances glucagon)
  • no ketones
23
Q

What are some genetic risk factors for T2DM?

A
  • most genes affect beta cell differentiation
  • some linked to insulin, obesity, and glucose transport
  • TCF72 is the most common polymorphism (associated with incretin production)
24
Q

What are important genes/factors in beta cell development?

A
  • PDX1 is needed for islet neogenesis and beta cell proliferation (if defective = no islet cells)
  • TCF72 is a TF that regulates beta cell differentiation
  • neurogenin 3 is also required for endocrine cell development
25
Q

List some environmental risk factors for T2DM.

A
  • malnutrition or maternal factors during pregnancy can lead to impaired beta cell development in childhood
  • high calorie diet and lack of physical inactivity can predispose you to insulin resistance
  • acquired organ dysfunction characterized by impaired insulin biphasic response (reversible)
26
Q

Define exenatide.

A
  • GLP1 mimetic
  • improves insulin biphasic response in T2DM
  • warning = pancreas toxicity

FHB Exam 4 (16 decks)

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