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Phys4 GI Lect9

Phys4 Digestion and Absorption of Lipids

Types of Endogenous Lipids 1.Cholesterol. 2.Phospholipids. 3.Desquamated intestinal villus epithelial cells.
Types of Exogenous Lipids 1.Triglycerides (90%). 2.Cholesterol. 3.Phospholipids.
Emulsification suspension of fat droplets held apart by lecithin, bile salts, and FA. **Inc the SA of the lipids which makes them easier for enzymes to attack.
What is a big emulsifying agent in the stomach? Protein
5 processes of Lipid assimilation 1.Secretion of Bile & lipases. 2.Emulsification. 3.Enzyme hydrolysis of ester linkages. 4.Solubilization of lipolytic products w/in bile salt micelles. 5.Transportation in/out of enterocyte.
Key Lipases not secreted by the Pancreas 1.Lingual Lipase (pH 3-6, does still fnc in stomach). 2.Food Lipases (pH 3.5-9, works all thru GI). 3.Gastric Lipase & Gastric emptying. **All 3 important in newborns b/c their pancreatic enzymes are NOT developed.
Which non-pancreatic lipase would be useful in Zollinger-Ellison disease? Gastric Lipase b/c it can tolerate the high acidity.
What are the 2 most important compounds/enzymes for the assimilation of fat? 1.Pancreatic Lipase. 2.Bile.
Fat stimulates the release of ______? CCK which helps in fat digestion. **also GIP or Vago-Vagal reflex.
Acid stimulates the release of _______? Secretin. **Also somatostatin.
What key function does CCK (stimulated by fat release) have on fat assimilation? 1.Contraction of GallBladder. 2.Relaxation of sphincter of Oddi.
What hormone causes secretion of HCO3- and fluid from pancreatic ductal and centroacinar cells? Secretin. **Secretin is potentiated by ACh and CCK
How does ACh effect the Gall Bladder? it causes CONTRACTION.
What are the 2 main things stimulating pancreatic acinar cells to release digestive enzymes? 1.CCK. 2.ACh.
3 main lipases secreted by the pancreas 1.Lipase. 2.Phospholipase A2. 3.Cholesterol Esterase.
Pancreatic Lipase 1.Secreted: Active form (Co-lipase w/ it is inactivated and must activated by bile salts and prevent bile salt interference w/ lipase). 2.Action: Cleaves FA at the 1 & 3 position of tiglycerides.
Pancreatic Phospholipase 1.Secreted: Inactive form (activated by bile salts). 2.Action: Cleaves FA at the 2 position of triglycerides.
Pancreatic Cholesterol Esterase Secreted: Inactive (Fnc enhanced WITH bile salts). 2.Action: Cleaves FA from Cholesterols, Non-specific esterase that can also cleave 2-monoglycerides.
3 ways by which Lipids cross the Membrane to enter Enterocytes 1.Simple diffusion. 2.Collision (similar to pinocytosis). 3.Carrier proteins.
What is the main function of the Micelle in lipid absorption? they FERRY (transport) lipids across the unstirred water layer of the Acid Microclimate Disequilibrium Zone. **It then dumps the lipid contents at the enterocyte.
Do short and medium chain FA need Micelle transportation to reach the Enterocytes? NO, they can difuse directly through and enter the enterocyte. **Only long chain FA need Micelle transport.
Pathway of Long-chain FAs reforming lipid compounds and joining ApoproteinB within the Enterocyte. 1.Reconverted into triglyc, phospholip, & esters w/in smooth ER. 2.Forms lipid droplets. 3.ApoproteinB synthesized in rough ER join droplets in SER. 4.Chylomicrons & VLDLs glycosylate apoproteinB in golgi.
Pathways of ApoproteinB associated lipid compounds with chylomicrons or VLDLs being reabsorbed back across the basolateral membrane into he lymph. 1.Vesicles bud off golgi carrying chylomicrons or VLDLs and fuse with basolateral membrane. 2.Exocytosis. 3.Chylomicrons & VLDLs cross large interendothelial channels to enter the lymph.
Are short and medium chained FAs absorbed into the BL or Lymph? They move through the enterocyte and directly enter the BL along with glycerol.
What could cause a problem with emulsification? Rapid gastric emptying.
What could cause a problem with the quality or quantity of pancreatic lipases? 1.Hyperacidity (Zollinger Ellison's). 2.Obstruction. 3.Cystic Fibrosis (Dec HCO3- secreted). 4.Chronic Pancreatitis.
What could case a problem within the enterocyte leading to abnormal lipid assimilation 1.abetalipoproteinemia: defective MTP which combines apoproteinB with lipids to form chylomicron. 2.Inadequate Absorption SA (celiac sprue, protazoan infection). 3.Lympthatic transport (Whipple's disease).
What could cause a problem with bile salt micelles and thus abnormal lipid assimilation? 1.Biliary Obstruction. 2.Bile salt synthesis. 3.Bacteria Overgrowth. 3.
Created by: WeeG



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