Regulation of Food Intake Flashcards
short term regulation of eating does what?
prevents overeating at each meal
short term regulation of eating is done how?
distention of stomach- stretch signals transmitted by vagus nerve suppress feeding center
GI hormones- secreted from intestine
long term regulation of eating does what?
maintains normal quantities of energy stores in body
long-term regulation of eating is mediated by what?
blood glucose levels (insulin/glucagon)
what is the control center for appetite and energy expenditure
hypothalamus
lateral nuclei of hypothalamus (serves as what?)
serves as feeding center
destruction of the lateral nuclei of hypothalamus causes
lack of desire for food
stimulation of what causes hyperphagia
lateral nuclei of hypothalamus
ventromedial nucleus of hypothalamus (serves as what?)
satiety center
stimulation of the ventromedial nucleus of hypothalamus does what
causes complete satiety
destruction of the ventromedial nucleus of hypothalamus causes what?
voracious and continuous eating
lesions of the paraventricular nucleus often cause what?
excessive eating
lesions of the dorsomedial nucleus usually do what?
depress eating behavior
where do hormones released from GI tract and adipose tissue converge to regulate food intake as well as energy exposure
arcuate nucleus
arcuate nucleus (integrates what kinds of signals)
acts as site of integration of number of neurological and blood-borne signals (lacks complete blood brain barrier)
proopiomelanocortin (POMC) neurons
what do they produce
alpha-melanocyte stimulating hormone (alpha-MSH)
cocaine-amphetamine-regulated transcript (CART)
what two types of neurons form the arcuate nuclei control appetite and energy expenditure
proopiomelanocortin (POMC) neurons
neurons that produce orexigienic substances
the orexigenic substances produces by the arcuate nuclei are?
neuropeptide Y (NPY) agouti-related peptide (AgRP)
activation of POMC neurons does what
decreases food intake and increased energy expenditure
activation of NPY-AgRP neurons does what
increases food intake and reduces energy expenditure
alpha-melanocyte stimulating hormone (alpha-MSH)
what does it act on and where
melanocortin receptors (MCR-3 and MCR-4) in paraventricular nuclei
activation of MCR-3 and MCR-4 si done by what and does what
alpha-melanocyte stimulating hormone (alpha-MSH)
decreases food intake and increased energy expenditure
CART negative mutants are what?
obese
increase in energy expenditure caused by MCR activation is mediated in part by what?
neural pathways that project from paraventricular nuclei to nucleus tracts solitaires (NTS) and stimulate sympathetic nervous activity
most common cause of monogenic human obesity?
mutations of MCR-4
defective signaling of melanocortin system is associated with
extreme obesity
AgRP (is antagonist to what, how does it increase feeding)
natrual antagonist of MCR-3 and MCR-4
probably increases feeding by inhibiting affects of alpha-MSH
AgRP release is inhibited by what?
insulin
excessive formation of AgRP is associated with?
excessive feeding
obesity
when body energy stores are low what is released to stimulate appetite
NPY which binds to Y receptors
the brainstem has what types of receptors that deal with appetite and where and what kind of center
NTS has high density of Y1 and Y5 receptors
satiety center present
nicotinic AChRs are located on what neurons that deal with appetite
POMC neurons
nicotine has what effect on POMC neurons
enhances firing thus activating MCR-4 and reducing food intake and increasing energy expenditure
leptin is what type of protein
adipocyte-derived
when amount of adipose tissue increase what happens to adipocyte production of leptin
goes up
leptin (effect)
anorexigenic
effect is to decrease food consumption and increase energy expenditure
leptin output is increased by what and inhibited by what
increased by insulin
inhibited by fasting and weight loss
leptin increase activity of what?
sympathetic nervous system- increases metabolic rate and energy expenditure
leptin acts where and does what
arcuate nucleus of hypothalamus
represses production o fNPY and AgRP
stimulates procession of POMC products alpha-MSH and CART
leptin decreases secretion of what
insulin
leptin-deficiency causes what
obesity
leptin signals about what type of information
degree of adiposity and nutrition
CCK receptors are found where in the brain and on what nerve
brainstem
vagus nerve
CCK has what effect on food intake
anorexigenic
satiation from CCK could result in part form what?
inhibition of gastric emptying thereby increasing gastric mechanoreceptor firing
effects of CCK dissipate after how long?
24 hours
administration of CCK decreases food intake in humans by
shortening time of meals
ghrelin is produced primarily where
stomach and proximal samll intestine
ghrelin must be what to be activated
acylated
ghrelin stimulates what neurons
NPY/AgRP
ghrelin levels increase with what?
weight loss-low calorie diets, cancer anorexia, anorexia nervosa
stress
sleep deprivation
ghrelin levels decrease with what?
weight gain
exercise
ghrelin plasma levels rise when?
1-2 hours processing normal meals
ghrelin plasma levels drop when?
about 1 hour after meal
glucagon-like peptide-1 (GLP-1) is produced from what, by what cells, and where
produced from proglucagon
by L cells
in ileum and colon
GLP-1 has what affect on food intake
anorexigenic
GLP-1 is released when and when do levels increase
released throughout the day
increase in response to meal
what stimulates secretion of GLP-1
ingested nutrients (especially fats and carbohydrates)
oxyntomodulin (OXM)
what is it, what type of effect does it have, and where is it secreted
proglucagon-derived peptide
anorexigenic
secreted from distal intestine
OXM is secreted in proportion to what
ingested calories
repeated injection of OXM does what
decrease body weight and increase activity related expenditure
PYY (where is it secreted, what type of effect does it have)
distal intestine
anorexigenic
PYY is secreted when and in proportion to what (what type of calories have the greatest effect on secretion)
after a meal in proportion to caloric load (lipids > carbohydrates > proteins)
what GI hormones are anorexigenic
leptin CCK Glucagon-like peptide 1 (GLP-1) Oxyntomodulin (OXM) PYY
what GI hormones are orexigenic
ghrelin
what effect does fasting have on pancreatic polypeptide, PYY, GLP-1, OXM, Ghrelin
decrease pancreatic polypeptide
decrease PYY, GLP-1, and OXM
increase Ghrelin
what effect does being fed have on pancreatic polypeptide, PYY, GLP-1, OXM, Ghrelin
increased pancreatic polypeptide
increase PYY, GLP-1, OXM
increased pancreatic polypeptide has what effect on feeding and through what
anorexigenic
affect vagus nerve, dorsal vagal complex, and arcuate nucleus
endocannabinoids are derived from what?
arachidonic acid
Cannabinoid receptors and endocannabinoids (ECs) have what effect on feeding
increase food intake
particularly sweats and fats
Cannabinoid receptors and endocannabinoids (ECs) levels in obese people
elevated
what effect does leptin have on endocannabinoids
decreased levels of ECs in animals
with aging what happens to anorexigenic and orexigenic substances
anorexigenic substance levels stay the same
orexigenic substance levels go down
anorexia nervosa (what levels are elevated and decreased, when can they go back to normal)
NPY levels elevated
Leptin levels decreased
levels can go back to normal when weight returns to normal
obesity results from?
greater energy intake than energy expenditure
obese person who has reduced to normal weight by strict dietary measures usually develops what kind of hunger compared to that of a lean person
develops intense hunger that is demonstrably far greater than that of a lean person
