CCK
stimulates the Acinar cells to secrete digestive enzymes.
relaxation of sphincter of Oddi, contraction of the Gall bladder to release bile
Fats >12 Carbons in length (long chain) activate this enzyme. released from I cells of the duodenum. also thought to activate a vago-vagal reflex.
4 levels of protection against pancreatitis
- enzymes in zymogen form
- enzymes stored in zymogen granules
- Geographical separation between pancreas and active enzymes (brush border enterokinase activates trypsin)
- trypsin inhibitor present in zymogen granule
Secretin
acid induces this enzyme secreted by S cells of the duodenum; stimulates bicarb release from duct cells. tightly controlled and pH of 3 is maximal secretion.
Low flow rate electrolyte composition of pancreatic secretion
High Na+, Cl-; Low K and HCO3
High flow rate electrolyte compositin of pancreatic secretion
High HCO3-, Na+; low K and Cl
Most important phase of pancreatic secretion
Intestinal phase-majority of the stimulation, in it is initiated by entry of chyme into intestinal lumen. S cells are activated by the acid (chemoreceptors). I cells detect fat and release CCK
absorption of Bile and B12 occur in one part of the small intestine
ILEUM
Jejunum
CCK, secretin, disaccharides, glucose transporters
What cell secretes gastric lipase; what is the stimulation
chief cells; acetylcholine and gastrin stimulate secretion
primary bile acids
made by liver;
-cholic acid, chenodeoxycholic
usually conjugate to glycine or taurine
secondary bile acids
formed from intestinal bacteria
deoxycholic acid, lithocholic acid
colipase
secreted by pancreas , activated by trypsin
binds to lipid droplets and anchors lipase to bile salt coated fat droplet (without this anchor pancreatic lipase is inhibited from binding of the bile coat)
Bile salt activated lipase
catalyzes the hyrdolysis of carboxyl ester bonds in acylglycerols as well as other dietary fats like cholesterol esters , fat soluble vitamin esters and phospholipids (this lipase comprises 4% of total pancreatic juice protein)
celiac sprue
impaired release of CCK in mucosal disease
Chronic pancreatitis in relation to lipase
insufficient lipase secretion from the pancreas
Zollinger-Ellison Syndrome
inactivation of lipase by low pH
pancreatic phospholipase A2
digest phospholipids (more originates from biliary secretion rather than diet)
Fat soluble vitamins
A, D, E and K
They need BILE!
pancreatic lipase removes esters from A and E
Vit D is transferred from chylomicrons to unoccupied serum Vit D binding proteins
causes of fat malabsorption
1) intraluminal- decreased pancreatic lipase (CF, pancreatitis)or decreased enzyme activation (gastrinoma, pancreatitis)
2) mucosal- decreased bile acid concentration (ilieal resection, baceral overgrowth), decreased exposure to enterocytes (bypass), or defect in enterocyte (sprue)
3) lymphatic- abetalipoproteinemia, intestinal lymphangiectasia
amylose
almost entirely alpha 1,4 linked linear chains of glucose
amylopectin
both alpha 1.4 linked straight chains and alpha 1, 6 linked branch points (every 20 residues or so)
note: isomaltase cleaves the 1,6 linkages!
SGLT1
Na+ and glucose or galactose on luminal side
GLUT-5
fructose on luminal side
GLUT-2
glucose or galacose on submucosa side
fructose on submucosa side
note: also Na, K atpase on submucosal side
maltose
glucose +glucose
digested by sucrase or glucoamylase
sucrose
glucose + fructose
digested by sucrase
lactose
glucose + galactose
