obesity Flashcards
fuel storage
liver + muscles: glycogen
adipocytes: fat
obesity
fuel storage
liver + muscles: glycogen
adipocytes: fat
obesity
BMI
weight (kg)/
(height (m))^2
underweight BMI
normal BMI
18.5-24.9
overweight BMI
25.0-29.9
obese BMI
equal or > 30
hypothalamic nuclei involved in regulation of hunger
paraventricular nuclei
dorsal medial nuclei
arcuate nucleus
involve LEPTIN:
lateral hypothalamus (“lateral likes lunch - but lesion/leptin lateral you get little”: stimulation → hunger, INHIBITED by LEPTIN from adipocytes→ anorexia
ventromedial nuclei: STIMULATED by LEPTIN → satiety, lesion → hyperphagia
hypothalamic nuclei involved in regulation of hunger
paraventricular nuclei
dorsal medial nuclei
arcuate nucleus
involve LEPTIN:
lateral hypothalamus (“lateral likes lunch - but lesion/leptin lateral you get little”: stimulation → hunger, INHIBITED by LEPTIN from adipocytes→ anorexia
ventromedial nuclei: STIMULATED by LEPTIN → satiety, lesion → hyperphagia
BMI
weight (kg)/
(height (m))^2
underweight BMI
normal BMI
18.5-24.9
overweight BMI
25.0-29.9
obese BMI
equal or > 30
function of adipocytes
store TG’s from blood (greater capacity than liver cells)
synthesize FA/TG from carbs
break down stored fats → release FA for energy
produce LEPTIN: when adipocytes are full, tell hypothalamus that they have enough energy stored as fat (stop eating!)
hypothalamic nuclei involved in regulation of hunger
paraventricular nuclei
dorsal medial nuclei
arcuate nucleus
involve LEPTIN:
lateral hypothalamus (“lateral likes lunch - but lesion/leptin lateral you get little”: stimulation → hunger, INHIBITED by LEPTIN from adipocytes→ anorexia
ventromedial nuclei: STIMULATED by LEPTIN → satiety, lesion → hyperphagia
leptin control of hypothalamic nuclei: ↓ APPETITE
lateral hypothalamus: INHIBITED by LEPTIN
ventromedial nuclei: STIMULATED by LEPTIN
2 signals for fat utilization of adipocytes
↑ sympathetic tone in both states→↑ NE, epi released from adrenal medulla → epi activates hormone-sensitive TG lipase in fat cells → breakdown TG, mobilization of FA to be used by muscles as energy
1) heavy exercise
2) stress: also stimulates ↑ACTH →↑ cortisol → cortisol ALSO activates TG lipase in fat cells
local atrophy of adipocytes or hyperplasia of adipocytes + abnormal fatty deposits
abdominal obesity with no fat on extremities
associated with cushing syndrome: cortisol triggers mobilization + redistribution of fat = buffalo hump = type of lipodystrophy
lipodystrophy
causes of lipodystrophy
leptin deficiency HIV meds (protease inihbitors) cushing syndrome: buffalo hump
medications that can ↑ weight gain
atypical antipsychotics
mirtazapine (antidepressant)
insulin, TZD, sulfonylurea
some progestins
complications of obesity
gout
gall stones: female, fat, fertile, fourty
fatty liver
osteoarthritis (hips, knees)
candidal infection in skin folds
↑cancer: esophageal, colon, liver, gallbladder, pancreatic, breast/ovarian/uterine, prostate, non-hodgkin lymphoma, MM
PCOS
cause: obesity, type 2 DM, hyperlipidemia, insulin resistance
insulin resistance at liver → excess lipid accumulation in liver
NAFL → NASH → cirrhosis (↑ risk HCC)
can worsen hep C progression
CHRONICALLY elevated ALT/AST + alk phos
nonalcoholic steatohepatitis (NASH)
fat accumulation in hepatocytes causes with inflammation (neutrophils, collagen) of liver + elevated LFTs
looks like early changes seen in heavy drinker (alcoholic fatty liver→alcoholic hepatitis →cirrhosis)
diagnosis of nonalcoholic steatohepatitis (NASH)
liver US, CT scan, MRI MRS: (gold standard)
liver bx
