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65 Cards in this Set
- Front
- Back
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Pancreatic exocrine secretion |
- regulated primarily by hormonal mechanisms
- partially by parasympa during cephalic phase of digestion, and even more during gastric phase in response to gastrin
- major secretion occurs during intestinal phase when chyme is in duodenum which releases secretin and CCK |
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role of secretin in pancreatic secretion |
- primary stimulus fo release is acid in duodenum (also fat, hypertonicty and distension)
- secreted by duodenal/jejunal mucosa
- carried by blood to pancreas, stimulating duct cells to increase secretion of NaHCO3 rich fluids to neutralize duodenum |
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role of CCK in pancreatic secretion |
- regulates pancreatic digestive enzyme secretion
- stimulus for release from duodenum is fat and protein products
- circulatory system transports CCK to pancreas where stimulates pancreatic acinar cells to increase digestive enzyme secretion- (lipase and proteolytic enzymes)
- all these enzymes packaged in zymogen granules so all released together |
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Liver functions unrelated to digestion (7 - list) |
1. metabolic processing of (carb,prot,lips) after digestive tract absorption
2. detoxyfying
3. synthesizing plamsa proteins
4. storing glycogen, fats, iron, copper and many vitamins
5. activating Vit D (w/kidneys)
6. removing bacteria and worn out blood cells thanks to macrophages
7. excreting cholesterol and bilirubin (breakdown product product from RBC) |
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hepatocytes and Kupffer cells |
cells of liver
hepatocytes - all metabolic functions of cell, every cell the same - all very specialized from highly developed organelles
Kupffer cells - resident macrophages of liver |
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liver blood flow |
- each hepatocyte in contacet with both arterial blood from aorta and venous blood directly from digestive tract to be detoxified pre-circulation
- in liver portal vein breaks up into capillary netword 'liver sinusoids' where exchange btwn blood and hepatocytes mucks
- hepatic vein then drains into vena cava |
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liver lobules |
- functional units of liver - hexagonal surrounding central vein - at each of 6 corners are 3 vessels - branches of artery, vein & bile duct
- hepatocytes btwn sinusoids 2 cells thick as need access to blood
- bile canaliculus's converge to make common bile duct which pours contents into gallbladder to duodenum |
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sphincter of Oddi |
live/duodenum meeting place, prevents bile from spiling in except during digestion of meals
- when closed ble goes to gallbladder for storage |
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components of bile |
- bile salts
- bilirubin
-cholesterol
-lecithin
-(all derived from hepatocyte activity)
- all in aqueous alkaline solution similar to pancreatic NaHCO3 secretion |
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bile salts |
- cholesterol derivatives - after fat digestion and absorption they are reabsorped into blood by special active transport mechanism in ileum where go back 2 liver thru hepatic portal system |
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enterohepatic circulation |
system of recycling btwn SI and liver |
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bile salts detergent action |
- converts large fat globules into lipid emulsions of many small fat droplets
- lipase has to come into direct contact with triglyceride so bile salts allow lipase to interact with more than just the outside lipids of a globule
- contain a lipid-soluble and water-soluble portion - bile salts adsorb onto surface of fat droplet and waterphillic part sticks out - decreases surface tension/increases surface area and eases breakdown
-water portion sticking outside causes droplets to repel eachother
- pancreas secretes colipase along with lipase - colipase binds to lipase and bile salts to anchor lipase |
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bile salts - micellular formation |
- bile salts + cholesterol + lecithin form micelles important for fat absorption
- lecithin has water/fat soluble portions, cholesterol is almost pure lipid
- fat parts of all 3 in middle core with water-soluble sticking out
- products of digestion like monoglycerides nned to hitch ride w/micelle - goes in inside and water part sheilds it or else it would float on surface of hydro-phillic luminal contents and not get absorbed |
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gallstones |
- when cholestrol secretion overpowers bile salt/lecithin secretion and excess cholesterol precipitates into microcrystals that aggregate into gallstones
-treatment is to ingest lots of bile salts to try to dissolve
- 75 % of gallstones from cholestrol and 25 % from bilirubin precipitate |
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bilirubin |
- doesnt play role in digestion, waste product excreted in bile - is the primary bile pigment - yellow from breakdown of RBC (specifically breakdown of heme)
- within digestive tract, modificstions change to brown giving colour of fuckingg shitt
- urines yellow colour
- if bile secretion doesnt occue it gives poo greyish white colour |
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jaundice |
- bilirubin formed more rapidly than excreted -appear yellowish - mostly in whites of eyes
1. prehypatic jaundice - excessive breakdown of RBC
2. hepatic jaundice - liver is diseased and cant deal with normal load of billly
3. posthepatic jaundice - bile duct obstriucted (maybe by gallstone) and cant be pood out |
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signals for bile secretion (3) |
1. Chemical - bile salts (choleretic) - stimulate bile secretion when beng used/needed
2. Hormonal - secretin - aqueous alkaline bile secretion by liver ducts w/o corresponding increase in bile salts
3. Neural - vagus nerve - during cephalic phase, promotes increase in liver bile flow before food reaches stomach/intestine |
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gallbladder |
btwn meals bile shunted into gallbladder
- active transport of salt (and water following) concentrates bile 5-10 fold
- concentrated so primary site for gallstones
- if removed, bile is just stored in common bile duct |
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hepatitis |
- inflammatory disease of liver
- viral infection or exposure to toxic agents (alcohol, CCL4, tranquilizers)
- possible imminent death but also possibly reversible depending on severity |
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cirrhosis |
- repeated/prolonged inflammation (usually in association w/alcoholics
- condition where damaged hepatocytes are permanantely replaced by connective tissue
- can regenerate but is limit
- if exposed to toxic substances so often hepatocyts cant replace, fibroblasts take advantage and lays lots of connective tissue |
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segmentation |
primary method of motility during digestion of a meal - mixes and propels chyme
- concentric oscilating ring-like contractions along SI's length
- moves chyme in both directions
- areas of contraction and relaxation alternate
- segmentation slows down as u move down intestine so food can be slowly moved downwards - because of depolarization frequencies
- contents take 3-5 hour to move thru SI |
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initiation and control of segementation |
- pacemaker cells - produce a basic electrical rhythm (BER) similar to stomach peristalsis
- frequency of segmentation following frequency of BER
- frequency of contraction in duodenum and jejunum is 12 per/min - illiuem is 9
-duodenum responds to distension
-illeum to gastrin
- intensity controlled by distension of intestine, gastrin, extrinsic nerve activity
- para symp enhances |
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migrating-motility complex (intestinal housekeeper) |
- after most meal absorbed and segmentation stopped motilin is released during unfed state by endocrine cells of SI mucosa which causes peristaltic waves from stomach to colon and moves food towards colon
-100 - 150 min |
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ileocecal juncture |
- last part of illeum empties into cecum - illeocecal sphincter is easily pushed open - tightly closed when nothing there to remove LI bacteria from entering and rapidly multiplying in the nutrient rich SI
- gastrin enhances sphincter relaxation at the onset of eating so stuff can move down for new meal |
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succus entricus |
- 'juice of SI' secreted by exocrine glands in SI mucosa - secretion increases post meal when chyme is stimulating - aqueous salt and mucous solution, allows lube and water so hydrolysis can take place as hydrolyisis is what enzymes use to break shitup |
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enzymes of brush border |
- enterokinase (activates trypsinogen from pancreas)
- disacharrides (lactase, maltose, sucrase)
-aminopeptidases
-carb and protein digestion completed within brush border |
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lactose intolerance |
- deficiency of lactase - undigested lactose stays in lumen
consequences: - creates osmotic gradient which drives water in - bacteria of LI can split lactose for energy so they attack but produce CO2 & CH4 - distension from fluid and gas create cramping/diarrhoea -infants may suffer from malnutrition |
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why does illeum hardly digest |
-already done pretty much
-need to absorb bile salts and vitain B12 |
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malabsorption |
-impairment of absorption - may be caused by damage to or reduction of surface area of SI
- one of most common cause is gluten enteropathy (celiac's disease) |
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Celiacs disease (gluten enteropathy) |
- abnormally sensitive to gluten - immunilogical - gluten exposure activates T-cells - that damage villi - normal amount of villi reduced and mucosa becomes flattened - brush border short and stubby - absorption of all nutrients impaired
- need to eliminate gluten |
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villus structure |
- epethelial cells - with brush border -connective tissue core made by lamina propria - cappilary network - terminal lymphatic vessel - central lacteal |
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crypts of Lieberkuhn |
- shallow invaginations between villi - secrete water & electrolytes which help constitute succus entericus
- also have stem cells that replace epethial cells of villi - new cells move up villi, pushing older ones out into lumen
- entire epethelial lining replaced every 3 days - high cell division makes very sensitive to anticancer drugs and damage by radiation
- also have Paneth cells - defense for stem cells - they have lysozyme (mucks bacteria) and defensins (small proteins w/antimicrobial powers) |
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epethelial cell life cycle |
- crypts of lieberkuhn with stem cells make new cells that move up villus and as moving up, increase capabilities like more enzymes so a top of villus is best cell but is pushed off into lumen eventually as cells move up but cells in lumen get digested and recyled and other stuff |
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Na absorption in SI |
- Na - passive and active - when electrochemical gradient favours from lumen to blood - passive diffusion thru leaky tight junctions
- thru cell - active - either Na channel or cotransport w/glucose/AA and after pumped out of cell at basolateral border into interstitial fluid where diffuses into cappilaries |
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Water absorption in SI |
- follows Na that is actively pumped into lateral spaces resulting in high osmotic pressure which induces water to move thru cell or thru leaky gap tight junctions
- water in lumen then cause high hydrostatic pressure and is moved into villus interior and is picked up by capillary network |
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order of monosaccaride preference to be transported |
1. galactose then glucose then fructose |
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how are glucose, galactose, fructose & AA absorbed |
G & G & AA -secondary active transport - contransport of Na and the monosaccharide which depends on Na concentration gradient
- after in cell, goes down conc gradient thru passive carrier in basolateral border to enter blood within villus
Fructose - pasive carrier mediated transport all the way
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endogenous proteins and where they come from to be digested |
- proteins from within body
- come from : - digestive enzymes - proteins within cells pushed off of villi - small amounts of plasma proteins normally leaking from cappilaries into digestive tract lumen |
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fat absorption |
- micelles bring to epethlial cells and monoglycerides and free fatty acids can freely difuse across lipid membrane into cell
- after dropping off, micelle can pick up more digested lipid stuffs until end of digestion where bile salts are reabsorped at illeum
- once in cells, packaged into triglycerides which conglomerate into droplets and coated with lipoprotein (water soluble coat) and then considered chylomicrons who are extruded via exocytosis into villus interstitial fluid where they enter central lacteals as cappilaries have basement membrane and deny access
- directly is passive process but energy needed to secrete bile salts from liver and synthesive to triglycerides and package chylomicrons take energy |
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vitamin absorption |
- water soluble vitamins passivley absorbed
- fat soluble carried in micelles and absorbed passivley with end products of digestion
- also some bidn with carries
- Vit B12 needs gastric instrinsic factor for receptor mediated endocytosis in illeum |
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why to women absorb more iron than men? |
lose it in period blooooood |
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iron absorption |
- fe 2+ more easily absorbed than Fe 3+
- Vit C increases absorbtion as changes from 3+ to 2
- phosphate and oxalate combine with iron to make unabsorbable iron salts
- after actively transported into epethelial - has 2 fates:
1. needed for blood - is absorbed and transported by plasma protein transferrin and erythropoetin is also believed to enhance Fe absorbtion into blood - then used in synthesis of hemoglobin
2. not immediately needed - remains stored in epethial cells as grnular ferritin (cant be absorbed into blood) if blood iron too high, gets dumped in with absorbed ferritin. Excreted by feces within 3 days as epethelial cells slough off
- lots of iron in feces gives it dark colour
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calcium absorption |
- PTH - Vit D system doe
- two- thirds of calcium intake absorbed - rest to shitt |
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absorbed nutrients and the liver |
- venules from villi join hepatic portal vein - detoxification of harmful stuff and metabolic processing before general circulation
- fat that travels thru lacteals enters circulation first then comes to liver - so liver doesnt get more than it can handle |
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what is only secretory product that escapes from the body |
bilirubin |
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SI absorbs 9 litres of fluid per day how? we only ingest 2500 ml/g of fluid and food per day |
- 7000 ml comes from plasma |
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diarrhoea |
- leads to acid-base imbalance - passage of highly fluid fecal matter and lots of times - beneficial when ridding of something harmful - ingested materials are lost but also secreted materials that would've been absorbed are lost too - excessive loss causes: - dehydration, loss of nutrient material, metabolic acidosis from loss of HCO3
- usually occurs b/c SI is unable to absorb fluid as extensively as normal causes:
1. viral infection/local irritation of gut wall/emotional stress - excessive SI motility - doesnt give enuf absorption time
2. excess osmotically active particles like those in lactase deficiency are present in lumen - cause excessive fluid to enter and be retained
3. toxins like cholera and other microorganisms - promote excessive secretions of fluid by SI mucosa gives profuse diarrhea - leading cause of death of kids in developing nations - oral reydration therapy uses glucose cotranspot carrier and saves lives |
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structure of LI |
- starts at cecum (appendix hanging off), ascending colon, transverse colon, descending colon, sigmoid colon, rectum, anal canal with internal anal sphincter (smooth muscle) and external (skeletal muscle)
- a haustra is a pouch of LI (goes all way until rectum)
- taeniae coli - 3 seperate, longitudinal bands of smooth muscle, run along each colon
appendix - lymphoid tissue- houses lymphocytes |
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LI |
- absorption of salt/water in upper half - strorage in lower half
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why are haustra in pouches not stretched out? |
- taeniae coli are shorter than them and mucosal layers |
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haustral contractions |
- initiated by autonomous rhythmicity of smooth muscle cells
- similar to segmentation but istead of 9/min its one per 30 mins
- non-propulsive, just slowly shuffle, exposes materials to absorptive mucosa
- controlled by locally mediated reflexes involving intrinsic plexuses |
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mass movements and gastrocolic reflex |
3-4 times a day generally after meals - ascending/transverse colons contract simultaneously driving feces along within seconds
- when food enters stomach, MM triggered primarily by gastrocolic reflex - mediated from stomach to colon by gastrin and extrinsic autonomic nerves
- makes room for meal incoming and prepares for defacation reflex |
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defacation reflex |
- after mass movements, distension of rectum stimulates stretch receptors initiating reflex
- sensory stretch impulses sent to sacral portion of spine reflex signal sent via parasympa to distal colon
- causes rectum and sigmoid colon to contract vigourously and internal anal sphincter (smooth muscle) to relax
- external sphincter just needs to open but is skeletal and is voluntary
- when defecation occurs, voluntary straining causes contraction of abdominal muscles and forced expiration against closed glottis - valsal manouvre used to increase intra-abdominal pressure which helps exples shitt |
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constipation |
- when defecation delayed and colonic contents retained too long too much water is absorped and pooo becmes hard and dry
- abdominal discomfort, dull headache, loss of apetite, nausea, mental depression
- symptoms arent cause by bacteria which liver takes care of, its because of distension of LI, particularly rectum
causes:
- ignoring urge to defecate - aging, emotion, low-bulk diet inducing decreased motility - obsruction of fecal movements caused by tumour or colonic spasm - impairment of defacation reflex thru nerve damage |
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appendicitis |
- if hardened fecal matter is lodged in appendix, obstructs normal circulation and mucous secretion in small appendix and emflames it
- swells and fills with pus
- tissue may die due to local circulatory interference
- may rupture and spew infectious contents into abdominal cavity |
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LI secretion |
- no digestive enzymes - its done - NaHCO3 alkaline mucous solution - protect LI mucose from chemical/mechanical injury - provides lube for shitt - neutralizes irritating acids
- secretion increases due to mechanical and chemical stimulation of mucosa mediated by short reflexes and parasympathetic innervation
-colonic bacteia to digest some cellulose fo their own use |
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colon |
- b/c of slow movements bacteria grow and accumulate
- not all bacteria destroyed by HCL and lysozyme - surving are typically harmless and we have more in LI than cells in whole body
-what do they do doe?
1. enhance intestinal immunity by competing with pathogenic microbes for nutrients and space
2. promote motility
3. help maintain mucosal integrity
4. make nutritional contributions - ex. synthesisve vit K and raise colonic acidity, promoting absorption of Ca, Mg, zinc
- some glucose from bacterial processing of cellulose is absorbed by colonic mucosa |
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Salt and water in LI |
- Na actively absorbed, Cl follows passively and water osmotically
- absorbs barely any but some- other electrolytes, and Vit K synthesized by colonic bacteria
- forms firm fecal mass as water leaves |
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what is in shitt
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undigested cellulose, bilirubin, bacteria, small amounts of salt |
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intestinal gases/ faaaaarts |
- derived from 2 sources
1. swallowed air 2. gas produced by bacterial fermentation in colon
- mixture of N and CO2, small amounts of H, CH4 and H2S
- borborygmi - gurggling souns as gas percolates thru lumen
- burping removes some but some stays and passes thru to intestine
- SI - gas is either absorbed or quickly passes to LI
- depends on food - beans have carbs we cant digest and only bacteria in LI can which create products that contribute to fart
- abdominal contractions raise pressure against contracted anal sphincter enough so that voluntary relaxing lets escape but hole not big enough for poo so thats why, high velocity thru small hole means vibrating and noise |
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gastrin (all functions) |
- protein in stomach stimulates release
1. increase HCl secretion and pepsinogen
2. enhances gastric motility, stimulates ileal motility, relaxes ileocecal sphincter, induces mass movements-keep stuff moving thru tract
3. trophic to stomach mucosa and small-intestinal mucosa
- inhibited by accumulation of acid in stomach and duodenal lumen |
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Secretin (all functions) |
- presence of acid in duodenum stimulates release
1. inhibits gastric emptying to prevent further acid from entering duodenum until present acid is neutralized
2. inhibits gastric secretion to control acid production
3. stmulates pancreas duct cells to produce NaHCO3 secretion - into duodenum to neutralize
4. stimulates secretion by liver of NaHCO3 rich bile to also go to duodenum to neutralize, pancreatic digestive enzymes are inhibited by acid
5. along with CCK, is trophic to exocrine pancreas |
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CCK (all functions) |
- as chyme enters duodenum, fat and protein products cause CCK release
1. inhibits gastric motility/secretion - allowing duodenal stuff to be digested/absorbed
2. stimulates acinar cells to increase secretion of pancreatic enzymes
3. contranction to gallbladder and relaxation of sphincter of Oddi to release bile
4. with secretin, is trophic to exocrine pancreas
5. long term changes in pancreatic enzyme secretion based on long-term diet change
6. satiety - sensation of having had enough to eat |
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GIP (glucose-dependant insulinotrophic peptide) |
- released by duodenal K cells
1. promote metabolic proccesing of absorbed nutrients 2. stimulates inssulin release from pancreas
3. lesser extent - inhibits water/electrolytle absorption in SI
- glucose in duodenum increases GIP secretion |
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GLP-1 (glucagon-like peptide-1) |
- intestinal L cells - dependant on prescence of nutrients in SI lumen
- tries to connect consumption of nutrients with glucose metabolism
effects 1. promotes insulin sensitivity 2. increases pancreatic insulin secretion 3. decreases pancreatic glucagon secretion 4. increases insulin sensitivty in alpha & beta cells 5. increases beta cells mass and insulin gene expression 6. inhibits gastric secretion and gastric emptying in stomach 7. contributes to satiety |
