Obesity Flashcards

1
Q

what BMIs consistute

  • underweight
  • overweight
  • obese
A
  • underweight: < 18.5
  • overweight: 25-29
  • obese: > 30
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2
Q

how do number and size of fat cells change

  • throughout age?
  • when energy in exceeds energy out (fat gain)?
  • when energy out exceeds energy in (fat loss)?
A
  • throughout age? # increases
  • energy in > energy out (fat gain): size and # increase
  • energy out > energy in (fat loss): size decreases (but not #)
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3
Q

fat cells capable of increasing in size / # by what degree?

A

size: by 20-fold
number: by 1000-fold

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4
Q

what are hyperplastic and hypertrophic obesity?

A
  • Obesity due to an increase in the number of fat cells is hyperplastic obesity.
  • Obesity due to an increase in the size of fat cells is hypertrophic obesity.
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5
Q

what is lipotoxicity?

A

= adverse affects caused by fat in non-adipose tissue

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6
Q

what are adipokes?

clinical significance?

A
  • metabolic changes produced by adipose tissue
    • indicate disease risk
    • tend to preceed chronic inflammation
    • oa pts adipokine profile will begin to improve with 5% weight loss
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7
Q

what is the role of lipoprotein lipase (LPL)?

how does it change across demographics?

A
  • moves trigerglycerides (TAGs) from the blood into –> adipose / muscle tissue
  • demographics:
    • more LPL activity in obese people
    • men vs women:
      • men: abundant LPL made by abdominal fat
      • women: abundant LPL made by breasts / hips / thigh
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8
Q

what is the set point theory?

A

Body tends to maintain a certain weight by means of its own internal controls

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9
Q

what physiological factors remain fairly stable under a variety of conditions?

A
  • blood glucose
  • blood pH
  • body temperature
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10
Q

prader-willi syndrome

  • clinical presentation
A
  • a genetic disorder that leads to
    • excessive appetite
    • massive obesity
    • short stature
    • mental retardation
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11
Q

leptin

  • expressed on what gene?
  • comes for what tissue?
  • acts where?
  • has what effects?
  • clinical significance?
A
  • Ob gene (obesity gene)
  • expressed in adipose tissue
  • acts on hypothalamus
    • serves to:
      • suppress appetite
      • increase energy expenditure
  • can be used to inc appetite & thus weight loss in lipid deficient/resistant people:
    • give as injection
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12
Q

how do lepin levels change based on body fat?

A

made by adipose tissue, so when

  • body fat increases –> leptin inc –> appetite increases
  • body fat decreases –> leptin dec –> appetite decreases

leptin “maintains homeostasis”

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13
Q

grehlin

  • produced where?
  • acts where?
  • has what effects?
A
  • produced by the stomach cells
  • acts on the hypothalamus
  • effects:
    • promotes weight gain by –> stimulating appetite / induces smell sensitivity / promoting efficient energy storage
      • levels flucutate - rise before eating / fall after eating
        • this fluctuation is contintent about psychological “mindset” surroudning eating
    • promotes sleep
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14
Q

how does lack of sleep affect

  • leptin
  • grehlin
A

lack of sleep

  • increases ghrelin –> appetite/sensitive smell/energy storage
  • decreases leptin –> inhibits satiety
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15
Q
  • white vs brown adipose tissue
    • roles in the body?
    • what factors affect their distribution
A
  • white adipose tissue - stores fat for other cells to use
  • brown adipose tissue - releases stored energy as heat
    • small amounts in:
      • adults
      • obesity pts (especially little)
    • greater amounts in:
      • babies
      • pts who exercise a lot (white –> brown conversion)
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16
Q

what is myokine irisin?

what is its significance?

A
  • a protein released by muscle cells d_uring exercise_
    • ​induces white fat cells to “undergo browning” into brite fat cells
17
Q

what BMIs and wait circumferences are indicative of “risk” to health

A
  • BMI
    • 25-29: overweight
    • > 30: obese
  • waist circumference
    • men: > 40 in
    • women > 35 in
18
Q

what is “NEAT”?

A

the energy expended in the everyday spontaneous activities: “nonexercise activity thermogenesis”

19
Q

metabolic syndrome

  • generally centered around what issue?
  • defined by what wet of criteria?
A
  • insulin resistance central to development of metabolic syndrome

criteria:

  • waist circumference: > 35 in females, > 40 in men
  • triglycerdies: > 150 mg/dL
  • HDL: < 50 mg/dL females, < 40 men mg/dL
  • BP: >183 / 85
  • fasting blood glucose: > 100 mg/dl
20
Q

PCOS

  • definition
  • cause
  • presentation
A
  • endocrine disorder leading to
    • hyperandrogenism
    • anovulation
  • cause:
    • exact cause unknown
    • but centered on insulin resistance - exacerbated by metabolic syndorme
21
Q

what molecules are often elevated in metabolic syndrome?

A

= pro-inflammatory molecules

  • C-reactive protein (CRP)
  • TNF-a: from macrophages/monocyte in adipose tissue
  • resistin: a type of adipocyte (from adipose tissue) - promotes insulin resistance
  • ILs: 1B, 6, 8, 10
22
Q

what molecules are reduced in metabolic syndrome?

A
  • Vitamin D
  • adiponectin: an _anti-inflammator_y adipokine - regulate glcuose/FA breakdown
23
Q

adiponectin

  • encoded by what gene?
  • synthesized by what tissue?
  • has what effects / roles?
A
  • encoded by ADIPOQ
  • made by adipose tissue > muscle/brain
  • is an anti-inflammatory molecule that is decreased in metabolic syndrome
    • regulates blood glucose / FA breakdown
24
Q

what conditions are metabolic syndrome comorbidities?

what are their major clinical manifestations?

A
  • PCOS - anovulation / androgen excessive
    • manifestation of metabolic syndrome
  • non-alcoholic fatty liver disease - steatosis / cirrhosis
    • incidence inc by metabolic syndorme
  • OSA (sleep disturbance)
  • gout (hyperuricemia)
25
Q

when is surgery indicated for obesity?

A

= gastric bypass surgery

  • in clinically severe obesity: BMI > 40