Feb5 M2-Appetite and Obesity Flashcards
mouth main secretion
amylase by salivary glands
stomach main secretion + other
- pepsinogen by chief cells (zymogen). becomes pepsin bc of low pH
- lipases too to make monoglycerides and FFAs
pancreas main secretions
lipases, proteolytic enzymes, amylase
gallbladder main secretion
bile
2 detergents in bile and what they do
lecithin and bile salts. convert fat globules into very small droplets called micelles (emulsification) so that lipases can act on the fat
main proteolytic enzymes fro mthe pancreas
trypsin, chymotrypsin, carboxypolypeptidase
large intestine function
absorb water and NaCl and store feces
what’s responsible for the preparation to digestion when you smell something or feel hungry
molecules called secretagogues. signaling peptides
what cells secrete HCl in the stomach
parietal cells
what controls HCl release by parietal cells in the stomach
- gastrin (secretagogue) from G cells of the end of the stomach
- vagus may stimulate gastric mucosa to make GRP (gastrin releasing peptide) to act on G cells and make gastrin
how stomach can expand
stretch and pressure trigger vagus to brainstem to vagus reflex to accomodate
2 secretagogues secreted upon entry of gastric chyme in duodenum and why
- secretin bc of low pH
- cholecystokin (CCK) bc of fat and aa content
CCK and secretin function
- CCK + secretin: make pancreas secrete more
- CCK stimulates GB bile secretion
where proteolytic enzymes of the small intestine (enteropeptidases, etc.) are located
on surface of epithelial cell
first brake discovered and what it is (brake = signal regulating chyme propulsion in SI)
ileal brake. strong inhibition of SI peristaltis bc of fat
why people with distal SI obstruction or high volume diarrhea (ex. caused by cholera) are vulnerable to hyovolemia and death
bc of large amounts of fluid secreted by GI tract and that is normally reabsorbed (and reabso is impaired)
appetite vs hunger
hunger = uncomfortable feeling + interest in eating food appetite = conscious desire to eat specific food
what do we call eating triggered by anticipated pleasure
hedonic feeding behavior
feeding and satiety centers in the hypothalamus
feeding centers = lateral nuclei
satiety centers = ventromedial nuclei, inhibit feeding centers
leptin comes from where and what it does
from adipocytes. inhibits feeding centers
ghrelin comes from where and what it does
peptide hormone from stomach. stimulates hunger (feeding center) and increases appetite
CCK does what on hypothalamus
inhibits hunger (feeding, lateral center)
name of hormones that increase feeding vs those that decrease feeding
increase feeding = orexigenic hormones
decrease feeding = anorexigenic hormones
anorexia nervosa def
reduced food intake bc of fear of gaining weight, will to lose weight
how hunger and satiety intensity may vary between people
hunger: may start eating as soon as feel hungry or only when feel very hungry
satiety: may stop eating as soon as they fill full or only after a while
how obesity diagnosed
measure BMI (kg over height in m2)
how risk varies with BMI
health risks increases proportionally with BMI and increases greatly over BMI of 30
how important is fat distribution
greater health risk if central and abd fat but not as much if hips and rear end fat deposition
waist definition
narrowest abd circumference (or halfway between iliac crest and costal margin)
hip circumference def
widest part of the gluteal region
central fat distribution def
WH ratio over 1 in men
WH ratio over 0.85 in women
obesity strong risk factor for what other disease
type 2 diabetes
metabolic syndrome def
combination of insulin resistance (doesn’t have to type 2 DM), high BP, CV disease promoting lipid profile and high uric acid
why epidemic of obesity
- more sendentarity
- more use of processed foods and sugar-sweetened beverages
who becomes obese
people living in obesity-promoting environment (obesogenic) and with obesity predisposition
obesity and genetic
moderately strong genetic link (noticed strong familial links but no genes identified except a few rare). multifactorial and polygenic
thrifty gene hypothesis
notion of a certain genetic profile suitable for food scarce environment but not that predisposes to obesity in the modern environment
in who does obesity NOT occur
doesn’t occur in people who are genetically or metabolically predisposed to a resistance to excessive fat gain
proof that a regulated and modifiable fat ‘‘set point’’ may exist
pregnant women gain 15-20 kg, 25% of which is fat
steps to go about obesity as a physician
- no negative bias
- measure it + risks
- how did it come
- formulate a plan
- exercise
- diet
how to measure obesity
BMI, WH ratio and check for risk factors (BP, diabetes, lipids, liver fat, sleep apnea)
when are risk factors more important
when obesity is more severe and when there are other risk factors (like family history, high BP,..)
when to consider gastric bypass surgery
severe and life long obesity with family history + unlikely to change + very bad risk factors with it (lipids, fatty liver) or comobordities
2 types of exercise that work
- formal
- non-exercise associated thermogenesis
