GI 2.1 Final

when does your body enter a post-absorptive state? what 2ndary hormone is released? function?

• haven’t eaten in 5+ hrs

• motilin → released via M cells (sample cells in SI) to start MMC

  • cleans gut, move chyme to LI, dec. bacterial migration from colon to SI

what hormones does low blood glucose trigger? function?

• glucagon, epinephrine, cortisol, GH → raise blood glucose

• ghrelin → stim. appetite, regulate energy homeostasis, fat storage

what are the inhibitory and stimulatory factors of ghrelin? what conditions can these cause?

• hunger hormone

• inhibit: alcohol → low ghrelin = not eating enough

• promote: cannabis + lack of sleep → high ghrelin = hyperphagia

what does ghrelin bind to? what neurons does it activate? function? what occurs if there is a lesion to the LHA?

• arcuate nucleus → activates:

  • AGRP → act. LHA (hunger center) + inhibit ventromedial nucleus

  • NPY → act. LHA (= melanin + orexin → inc. hunger) + PVN (=TRH, CRH, oxytocin, nesfatin → dec. hunger)

• LHA lesion → anorexia (no hunger) = not eating

when does your body enter the absorptive state? what is the order of the hormones released after eating?

• during 4 hrs. after eating

• hormones: gastrin, secretin, CCK, somatostatin

  • when hungry again → motilin + ghrelin

which hormones are released to aid in digestion?

• gastrin

• secretin

• CCK

• insulin

• VIP

what stimulates gastrin release? what is it released by? what does it cause? what inhibits it?

• stomach stretch, partial digested proteins in stomach, vagal nerve stimulation → G cells (pyloric gland)

• stimulate gastric juice (acid, pepsinogen, intrinsic factor (B12))

• inhibit via: stomach acid, somatostatin, GIP, VIP

what causes ZES? what does secretin cause in ZES?

• gastrinoma (tumor w/ excess gastric acid secretion)

• secretin inc. stomach acid

  • normally dec. stomach acid

what releases secretin? when? function? what does it inhibit?

• S cells (duodenum)

• response to stomach acid entering intestine

• secrete HCO3 (neutralize stomach acid in chyme) stimulate delta cells (somatostatin)

• inhibits release: insulin, glucagon, gastrin, CCK, VIP

what releases CCK? when? what does it bind? function?

• I cells (duodenum)

• response to protein (AA) + lipid (FA) in SI, vagal nerve stimulation, GIT infection

• binds CCK1 R on gut vagal nerves → stim. gallbladder contraction, pancreatic digestive enzyme + VIP sec., sphincter of Oddi relax (= more bile)

what releases insulin? when? what is the function of adiponectin?

• B cells in pancreas

• in response to high blood sugar OR osteocalcin (from osteoblasts)

• adiponectin (released by fat cells) → inc. sensitivity to insulin + reduce fat

what releases vasoactive intestinal polypeptide (VIP)? when? function?

• pancreatic + intestine cells

• vagal nerve stim. + GIT infection

• function: muscle relaxation → dec. contraction (stomach, gallbladder, LES, gastric sec.)

what triggers anorexigenic hormones? what are they? function?

• high blood glucose

• PYY, insulin, GIP, GLP1, CCK, amylin, oxyntomodulin, bombesin, somatostatin

• inhibit hunger center via direct ghrelin release inhibition

what releases peptide YY (peptide tyrosine tyrosine or PYY)? when?

• L cells (conc. in ileum + colon/rectum)

• response to food in SI/LI

what releases incretins gastric inhibitory peptide (GIP) and glucagon like peptide (GLP)? function?

• K cells → GIP (also glucose insulin polypeptide)

  • stim: FA, AA, glucose in SI

  • inhibit gastric juice sec. + stim. pancreatic insulin release

• L cells → GLP

  • stim: glucose + FA in SI/LI

  • inhibits glucagon release

what drugs mimic incretins? what is their function?

• ozempic, saxenda, trulicity

• inc. insulin + weight loss

what releases amylin? when?

• B cells in pancreas

• high blood sugar

what releases oxyntomodulin? function?

• fundic cells

• inhibit ghrelin

what does bombesin activate? what does it cause?

act. vagal nerves → trigger satiety

what releases somatostatin? when? what does it inhibit?

• D (delta) cells

• response to high blood glucose, secretin, VIP

• inhibits: gastrin, secretin, CCK, VIP, glucagon, insulin

what releases leptin? function?

• high blood fat levels → adipocytes release leptin

• regulate long-term weight (act. brown fat → inc. calorie burn off) + inhibit insulin release

what inhibits and stimulates leptin?

• inhibit: alcohol + lack of sleep → low leptin = hyperphagia

• stimulate: cannabis + obesity (more adipocyte) → high leptin → leptin resistance → worsens obesity + insulin resistance

where do leptin and anorexigenic hormones bind? what neurons do they activate?

• arcuate nucleus

• act. CART/POMC neurons

  • CART → inhibit LHA (hunger center) + PVN

  • POMC → produce neurotransmitters a-MSH + Y-MSH

what is the function of NT a-MSH and Y-MSH?

• a-MSH → act. arcuate nucleus (+ feedback loop)

• Y-MSH → act. ventromedial nucleus (satiety center) + PVN

  • act. PVN → TRH, CRH, oxytocin, nesfatin

  • VMN lesion → no satiation = hyperphagia

what are the components of total energy expenditure? what organs contribute to basal metabolic rate (BMR)?

• BMR (70%), physical activity (20%), thermic energy (10%)

• BMR contribution: muscle, liver, brain, heart, kidney, fat

what increases basal/ resting metabolic rate (BMR/RMR)? why do females have a lower metabolism?

• high fat-free mass, fat mass, younger age, male (high T3/T4, testosterone, muscle mass)

• females have higher cortisol → inhibit TSH → low T3/T4 → lower metabolism

  • BUT high estrogen → stimulate T3/T4 → inc. metabolism