Obesity Flashcards
what BMIs consistute
- underweight
- overweight
- obese
- underweight: < 18.5
- overweight: 25-29
- obese: > 30
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)?
- throughout age? # increases
- energy in > energy out (fat gain): size and # increase
- energy out > energy in (fat loss): size decreases (but not #)
fat cells capable of increasing in size / # by what degree?
size: by 20-fold
number: by 1000-fold
what are hyperplastic and hypertrophic obesity?
- 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.
what is lipotoxicity?
= adverse affects caused by fat in non-adipose tissue
what are adipokes?
clinical significance?
-
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
what is the role of lipoprotein lipase (LPL)?
how does it change across demographics?
- 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
what is the set point theory?
Body tends to maintain a certain weight by means of its own internal controls
what physiological factors remain fairly stable under a variety of conditions?
- blood glucose
- blood pH
- body temperature
prader-willi syndrome
- clinical presentation
- a genetic disorder that leads to
- excessive appetite
- massive obesity
- short stature
- mental retardation
leptin
- expressed on what gene?
- comes for what tissue?
- acts where?
- has what effects?
- clinical significance?
- Ob gene (obesity gene)
- expressed in adipose tissue
- acts on hypothalamus
- serves to:
- suppress appetite
- increase energy expenditure
- serves to:
- can be used to inc appetite & thus weight loss in lipid deficient/resistant people:
- give as injection
how do lepin levels change based on body fat?
made by adipose tissue, so when
- body fat increases –> leptin inc –> appetite increases
- body fat decreases –> leptin dec –> appetite decreases
leptin “maintains homeostasis”
grehlin
- produced where?
- acts where?
- has what effects?
- 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
- levels flucutate - rise before eating / fall after eating
- promotes sleep
-
promotes weight gain by –> stimulating appetite / induces smell sensitivity / promoting efficient energy storage
how does lack of sleep affect
- leptin
- grehlin
lack of sleep
- increases ghrelin –> appetite/sensitive smell/energy storage
- decreases leptin –> inhibits satiety
- white vs brown adipose tissue
- roles in the body?
- what factors affect their distribution
- 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)
- small amounts in:
what is myokine irisin?
what is its significance?
- a protein released by muscle cells d_uring exercise_
- induces white fat cells to “undergo browning” into brite fat cells
what BMIs and wait circumferences are indicative of “risk” to health
- BMI
- 25-29: overweight
- > 30: obese
- waist circumference
- men: > 40 in
- women > 35 in
what is “NEAT”?
the energy expended in the everyday spontaneous activities: “nonexercise activity thermogenesis”
metabolic syndrome
- generally centered around what issue?
- defined by what wet of criteria?
- 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
PCOS
- definition
- cause
- presentation
- endocrine disorder leading to
- hyperandrogenism
- anovulation
- cause:
- exact cause unknown
- but centered on insulin resistance - exacerbated by metabolic syndorme
what molecules are often elevated in metabolic syndrome?
= 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
what molecules are reduced in metabolic syndrome?
- Vitamin D
- adiponectin: an _anti-inflammator_y adipokine - regulate glcuose/FA breakdown
adiponectin
- encoded by what gene?
- synthesized by what tissue?
- has what effects / roles?
- 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
what conditions are metabolic syndrome comorbidities?
what are their major clinical manifestations?
- 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)
