appetite regulation (7?)

effect of exercise on energy homeostasi

(burn more energy, etc) - acute exercise been found to boost post-prandial levels of several satiety peptides, while ghelin stays same or decreases -exercise also improves insulin senseititive and glucose uptake in skeltal muscle, which helps overcome insulin resistance

how is insulin involved in peptide mormon reg?

1) responds to moment by moment basis of blood sugar and directly effects metabolism 2) binds directly to receptors on neurons in the hypothalamus thats supressses appetite, thus ** supporting the action of leptin** 3)it is also an adiposity hormone (rises when fat rises)

w/in the ARC there are two miain neuronal pathways...

1= orexigenic: appetite stimulating 2= anorexigenic: appetiti inhibiting these express receptors for appetite regulating hormones (gherlin, lepin, etc) binding leads to release of neirpeptides which ten targets second order neurons associated w/ weight loss or gain

lecture:what inhibits anoergic pathway?

AgRP

lecture:examples of satiety peptodes

CCK, PYY, GLP-1 (sigal satiiation on a moment-by moment basis)

name the satiety peptides (3) and describe breifly

CCK: stims digestion of fat and protein in duodenum. but acts as a satiety peptide by slowing rate of gastric emptying, which delays return of hunger following meal PPY: delays gastric empying, but also directly acts at the hypothalamus to inhibit appetite. Its low during fasting and rises rapidly during meal GLP1: reduces food intake and increases energy expenditure (also an incretin)

lecture: what do adipocytes secrecte/ release

Leptin** turns cortisone to cortisol turns androstendione to E also releases restinin adiponectin (cut due to time)

NT in the anoerigic pathway (2)

POMC--alpha MSH -aMSH binds to MCR (malanocotrin). -MCRs powerfulyl inhibited by AgRP -hypothalamic MCR regulates appetite and sexual behavior CART -increased activity and energy expenditure -prokigner stim has sim effects of cocaine

interplay between ox and anerox

anerxogenic can be over-ridden by orexigenic system. AgRP inhibits melancortin recerptos. Melancortin recetor defecs or chronic inhibition by AgRP are both causes of obesity that arms from interrupt of aroesigenic signal s

in the fed state...

anorexigenic circuits in the hypo are activated by appetite-inbit hormones such as leptin, the reverse for gherlin the anorexigenic release: CART and POMC POMC is proteolycitcally cleaved to alpha-MSH, which binds to the melanocorotin R, on second order neurons that inhibit feeding. however, this can be over-ridden by orexigenic system. AgRP inhibits melancortin recerptos

lecture: what is AgRP

co-expressed with NPY one of the most potent and long-lasting appetite stimulators (appetit stim after organic)

in the hungry state...

elevate ghreline actives receptors on orexigenic ARC neurons in the lateral hypothalus, signals for increased food the orexigenic neurons then secrete 2 peptides: NPY an AgRP. these bind to 2 order neurons w/ NPY receptors conversely: leptin, insulin, PYY oppose these action by inhibiting orexigenic neurons so they don't release NPY and AgRP

fyi

energy hemostats is regulated by many pathways. theses pathways converg on the hypothalamus nutrient (glucose and lipid) sensing neuronal circuilating peptide hormones

lecture: appetitie regulation by GI tract

hormonal: + ghrelin -satiety peptides neural: + gastric empting -gastric distension

lecture: i may have been wrong about the meaning of the word adiposity signals

i think it justs means that its a long-term signal on fat

what is gherlin?

in contrast to satiety peptides, ghrelin is unque in that it increases appetid it binds to the appetitive stim neurons in the hypothalamus can have a long-lasting effect than other peptides it does not affect size of the meal, but just time bet rises before meal, and falls immeaditable after eat (it also promotes GH secretion by binding to GH seretagogye receoor in hpothal)

what are the adiposity hormones

insulin and leptin

lecture: signals from pancress

insulin has an another side to it: its an adiposity signal: it reports to the hypothalamus about fat stores (the basal level, clearly it fluctuates a lot) Amylin: co-secreted with B cells w/ insulin synergistic with insulin (and leptin) inhibits appetits, delays empytying (main job)

what is amylin role in regulating appetite?

its a pancreatic peptide, co-secreted with insulin from B-cells Amylin supresses glucagon secertion its complements and synergistically with that of insulin

lecture: example of adiposity hormones

leptin and insulin

lecture: leptin

major inhibitory peptide. synergistic w/ insulin. opposes ghrelin adiposity signal: tells hypothalamus about extent of fat stores suppresses appetite and increases energy directly at the ARC less leptin tens off reproduce axis at the hypothalamus level

lecture: what is NPY?

most abunntat nueorpeptin in brain many functions, one of which is appetite contoled released more with stess too (appetite stim after oregienic)

lecture: satiety peptides

oppose ghrelin slow gastric emptying and produce satiation most act via vagal afferents potential anti-obesty some GLP-1 are also incretins-stimulate insulting secretion

what is a satiety peptide?

process of satiation (feeling full) is driven primarily by releasing appetite-inhibitory pepties AND by gastric distension peptides are short-acting and define meal size and freq. secreted from stomach and intestines, where they act as neuropeptides on local nerves most affect the rate of gastric emptying

fyi

satiety peptides are the major short-term endocrine regulators of appetite regulation primary longer-term peripheral effectors are leptin and gherlin. leptin and insulin act together to inhib app w/ help by amylin PYY, unlike most other satiety peptides also inhibits appetite at the hypothalamus level. nearly all of the hormone effected are appetite inhib, and are opposed nay by gherkin, the sole appetite stim pep

lecture: what does bariatric surfer do?

satiety peptides go up (come from intestinal, some from stomach ghrelin goes down (from stomach) (and clealry restricts the about of food that can go in)

what is leptin?

secreted by the adipose tissue it beings to receptors on hypothalamic neurons **primary appetitie inhibiiting peptide** *leptin is an adiposity signal: when fat levels are high, leptin is high. (leptin drops during fasting, etc) take away: pepsin mirror fat stores, and it inhibits appetite

lecture: ghrelin

stim appeptie, food intake and decreases energy expenditure secretitec by stomach levels rise before meals, drop after potential clinical application?

what is a metabolic syndrome ?

term that refers to a cluster of conditions that increase the rise of coronary artery disease e.g obestity, type 2 diabetics mellitus , hypertension, cholestorl, etc

lecture: neuronal circuit in the ARC

there are 2, and they connect to second order neorons oreigenic: eat. Ghrelin +, Leptin - anorexigenic: don't eat , Leptin +

fyi

there are 3 major areas in the hypothalamus involved in regulation of appetite and energy: ARC, lateral hypothalamus and ventromedial hypo we will only look at the ARC

descibe the two types of adipose tissue

white and brown brown: many mito, involved in thermogenesis white: energy storehouse, where breakdown of stored fat releases both FA and glycerol. serves as endocrine center. has many receptors and secretes peptide hormones and cytokines