lipid metabolism

Medicine Module 3 with Edmonson at Medical College of Georgia

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By: R. C.
Created: 2010-12-29
Size: 26 flashcards
Views: 4

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lipids

energy storage: triglycerides
membranes: phospholipids and glycolipids
cholesterol for steroid hormones and bile acid biosynthesis
ADEK
arachidonic acid: C20 FA for prostaglandin synthesis and other bioactive compounds
phosphoinositides for second messengers

dietary lipids

TGs>CH>CHE>phospholipids

mouth

lingual lipase is secreted by lingual glands, degrades some TGs
attacks c3 ester bond to form 12DAG and FFA
active at pH 2-6

stomach

gastric lipase
secreted by chief cells
active at pH 4-6
more effective in neonates than adults
hydrolyzes short, medium TGs in milk fat to give FFAs and glycerol
fat broken down into lipid droplets
semi-liquid partially digested food is chyme
passes through pyloric valve into duodenum

small intestine

emulsification: lipid droplets are broken down by bile salts in duodenum
detergent synthesized from CH by liver
stored in gallbladder
secreted through bile duct into duodenum

pancreatic juice

bicarbonate: neutralizes acid in partially digested food
maximally active at pH 6
pancreatic lipase: hydrolyzes TGs at C1 and C3 ester bonds
generates 2- MAG and 2 FFAs
colipase (secreted as procolipase) required for activity of lipase

olestra

esterification of FAs with sucrose instead of glycerol
tastes like natural fat but is not hydrolyzed by pancreatic lipase and remains unabsorbed in gut

orlistat

xenical
inhibits pancreatic lipase
reduces fat digestion and absorption
causes steatorrhea and fecal incontinence

cholesteryl esterase

hydrolyzes CHE to CH and FFA

CCK

produced by I cells of duodenum and jejunum
stimulates pancreatic secretion
inhibits gastric motility
stimulates gallbladder contraction for bile release

secretin

secreted by s cells of duodenum and jejunum
stimulates pancreatic secretion of hco3 and water into pancreatic fluid

absorption in jejunum

lipid digestion products: 2-MG, CH, and FFAs and ADEK are mixed with bile salts to form mixed micelles
products enter mucosal cells/enterocytes by passive diffusion
bile salts don't enter mucosal cells; they are reabsorbed in lower ileum, transported to liver, recirculated

niemann-pick C1L1

brush border membrane of enterocytes by passive diffusion
transports CH and plant sterols from mixed micelles into enterocytes

ezetimibe/zetia

CH lowering drug
targets NPC1L1 reduces dietary CH absorption

steatorrhea

pancreatic failure, obstructed bile duct, insufficient bile salt production, extensive loss of intestinal mucosal cells
bulky fatty stools that contain undigested lipids
corrected w tx of pancreatic enzymes and bile salts

mucosal cell

resynthesis of TG and CHE
long-chain FAs react with coa to produce acyl coa
acyl groups are transferred to 2-MG to regenerate TGs
short and medium chain FAs are not esterified to give TGs; these leave mucosal cell to blood

CHE

resynthesized from CH and acyl COA
lysoPL reacts with acyl coa to regenerate PL
acyl transferase catalyzes these rxns

CMs

packaging of TGs, CHE, and fat soluble vitamins
CMs are surfaced by PLs and apoprotien B48
structural component of CMs
defect in apo-b expression can cause apo-b-48 deficiency
CMs will not be formed; tgs accumulate in mucosal cell

familial abetalipoproteinemia

malabsorption of fat, retinitis pigmentosa and ataxia

path of CMs

leave mucosal cells to enter lymph lacteals - thoracic duct - blood circulation
apoE and apo-C2 are added to CMs from HDL

distribution

TGs in CMs hydrolyzed by lipoprotein lipase
enzyme in plasma membrane of endothelial cells lining capillaries

LPL

attacks all 3 ester bonds in TG
converts to glycerol and 3 FFAs
FAs enter muscle cells for oxidation
adipose tissue for resynthesis and storage of TGs
apo-c2 in CMs functions to activate LPL
apo-c2 returns to HDL

familial hyperchylomicronemia/type 1 hyperlipoproteinemia

reduced CM clearance
Apo-c2 deficiency
LPL deficiency
abnormal LPL
massive CM increase in blood plasma
plasma is milky long after meal intake

TG hydrolysis

reduces CM size, generates remnants
these are dietary CH and fat soluble vitamins
taken up by apoE r's in liver
degraded by lysosomal enzymes in liver

familial t 3 hyperlipoproteinemia

apoE deficiency or defect in apoE r's
impaired clearance of CM remnants from blood after fat rich diet
can lead to xanthoma, hypercholesterolemia, atherosclerosis

absorption

TGs with short and med FAs are digested and absorbed just like long-chain TGs
in mucosal cell, FAs are not incorporated into CMs
they pass directly to blood

About this deck

By: R. C.
Created: 2010-12-29
Size: 26 flashcards
Views: 4

About StudyBlue

“I have used this website for three exams, and I see a huge difference in my test results.”
Naj