Body Energy Stores Flashcards
Metabolism controlled mostly through what mechanism
hormonal
Maintenance of Body energy depends on what two things
- how much energy we ingest
2. how much energy we consume (energy output - our metabolism)
Much of our food intake is controlled by
Neuotransmitters, some hormones, other factors
Body’s primary controller of complex vegatative function
Hypothalamus
Lateral hypothalamic nucleus
causes behaviors that are associated with hunger
Ventromedial nucleus
region associated with satiety
dorsomedial nucleus
more directly involved in the control of metabolism
arcuate nucleus
source of major inputs to the lateral and ventromedial hypothalamic nuclei
Orexigenic chemicals
Neuropeptide Y
Ghrelin
AGRP
anorexigneic chemicals
CCK Seratonin Melanocortin CART Leptin GLP-1
NPY
produced by arcuate nucleus
acts on lateral hypothalamic nucleus
NPY-1 receptor
increases food ingestion
most potent trigger of short term feeding behavior
release increased by ghrelin and decreased with leptin
AGRP
antagonist of MSH expressed by arcuate nucleus, work on lateral hypothalamic nuclei also works on dorsomedial and ventromedial synapses, wher it blocks the anorexigenc actions of melanocortin stimulated by ghrelin inhibited by leptin
Ghrelin
produced by parietal cells
endogenous ligand for GHS receptor
actions of ghrelin are independent of its ability to increase growth hormone secretion
increases as time after meal increases.
ingestion of food decreases grehlin release
acts on arcuate nucleus to increase NPY and AGRP
increases gastric motility
CCK
released with presence of fat in duodenum
by chemoreceptors involved in control of intermeal duration.
activate ventromedial nucleus to induce satiety
Seratonin
ventromedial nucleus
role in satiety
decrease apetite
MSH
released from subset of neurons in arcuate nucleus
project to dorsomedial and ventromedial nuclei,
binds there to MC-4R receptor.
GPCR
decreasing feeding behavior.
CART
arcuate neurons express Cart, released from synapses in the dorsoand ventromedial nuclei
anorexic effect
Leptin
peptide hormone secreted by adipose tissue
needs receptor on cells of BBB to be transported to CSF
binds to receptor on neurons of arcuate nucleus
inhibits synthesis and release of NPY and AGRP,
increases release of melanocortin and CART
GLP-1
induction of satiety
Short Term control of eating, what is it?
How much we eat at a meal
Short term control of eating, how it works
- input from mechanoreceptors in the stomach and the intestine (distention) sent up through vagus nerve. causes inhibition of lateral nucleus, and excitation of ventromedial nucleus
- CCK (presence of fats in duodenum) causes us to stop eating
Intermediate Control of eating, what is it
how long between meals
Intermediate control, how it works
- intestinal and hepatic chemoreceptors
- hypothalamic chemoreceptors
- action of ghrelin
Intestinal and hepatic chemoreceptors
chemoreceptros sensitive to one of the three nutrien groups and relay info to the brain.
via vagus nerve.
cause inhibition of lateral feeding areas
stimulation of medial satiety centers
important for determining time between meals (snack experiment)
Hypotholamic chemoreceptors
set of neurons (glucostats, lipostats, aminostats) which sense content of those macromolecules - now believed that there is a common set of neurons for all 3 nutrients
inhibit lateral centers
stimulate medial centers
believed that glucokinase phosphorylates a K channel blocking efflux leading to AP, and belived to release 5HT
Role of ghrelin in intermediat control
secreted from stomach
increases as time between meals increases, peak just before meal
acts on arcuate nucleus to increase NPY and AGRP in lateral and medial hypothalamic nuclei
NPY - stimulates hunger
AGRP - blocks satiety
NOTE - ghrelin has short term inhibition of feeding behavior,, but also plays role in meal initiation
Long term control of Energy intake, what is it
How much do I weigh?
Long Term control of Energy intake, how do we do it?
- leptin is released in proportion to adipose present in body
- leptin binds receptor at bbb to get into csf
- leptin ginds receptros in arcuate nucleus and
increases MSH and CART release in medial nuclei to produce satiety
decreases NPY and AGRP release to prevent hunger - hypothalamic chemoreceptors and ghrelin may play role
Causes of obesity
genetic (small portion)
leptin (we thought so, but not really, hypothalamus of obese person sees same amt of leptin as normal weight bc of desensitization of receptors)
GLP-1 (obese ppl have low GLP1).
Ghrelin (lower in overweight)
Melanocortin - different levels may lead to obesity
overweight ppl eat a diet higher in fats
(more calories per gram, doesnt spike metabolism the same way, and overweight pppl dont compensate for fat calories as well)
Dz related anorexia
seen with illness, IL-1, IL-5, TNF
Hypothalamic damage
damage to lateral nucleus, leads to loss of feeding behavior
damage to medial nuclei, leads to loss of satiety