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FSHN 470- Unit 2

fructokinase vs glucokinase fructokinase Km is very low and highly expressed in liver (essentially unregulated)
2 ways fructose is unregulated 1) enters after PFK (rate-limiting) 2) fructokinase has a low Km and highly expressed
fructose 1-P stimulates what phosphorylation of glucose-> glucose-6-P (more flux thru glycolysis)
fructose and lipemia very high fructose leads to high [TG] postprandial
fructose and blood sugar decreases (compared to glucose) postprandial
T2D and fructose lower glycemic index, but increases hepatic lipid synthesis via increased expression of lipogenic genes
why high carb low fat diets may be bad lower HDL which means higher LDL
insulin resistance and brain metabolism interferes with synaptic plasticity and cognition
how is insulin released beta cells-> high glucose or high ATP
T1/2 of insulin short (3-5 minutes)
glut 4 gene fed vs starved basal, higher with insulin, lower than basal if starved
insulin in liver activates expression of (3 enzymes) glucokinase, acetyl coA carboxylase, fatty acid synthase
insulin in liver down-regulates (by P) glycogen phosphorylase, fructose 2,6 bisphosphatase (bifunctional enzyme)
insulin in liver activates (by P) glycogen synthase, PFK2, ACC
insulin action in muscle glut 4 translocation
insulin action in adipocyte glut 4 translocation AND increase transcription of glut 4 gene
enzyme that converts PEP to pyruvate pyruvate kinase
T1D in adipocytes decreased glucose uptake, increased lipolysis, increased FFA in blood
T2D new equilibrium more glucose and insulin in blood for same response
what is NOT defective in T2D? # of receptors or insulin binding (something else in the cascade)
glucagon and T2D >90 mg/dL blocks secretion
lingual and gastric lipase and infants milk is high in short and medium chain FAs (pancreatic lipase activity is low so this is important)
pancreatic co-lipase has binding sites for lipase and bile salt-stabilized lipid droplet
cholesterol esterase (stimulated by_?) aka non-specific esterase! (hydrolyses CE, phytosterol/phytostanol esters, TG, MG, etc.) *stimulated by bile salts
pancreatic phospholipase A2 (activated by__?) lecithin->lysolecithin (activated by trypsin)
transfer of micelles into enterocytes distal duodenum & jejunum; passive diffusion & maybe binding protein
where are bile acids resorbed? jejunum
how are most fats absorbed? as monoacylglycerol, turned back into TG, into CM
3 ways TG are made 1) monoacylglycerol (enterocytes) 2) glycerol phosphate (hepatocytes) 3) DHAP (adipocytes)
FFA increases due to (4) starvation, stress, diabetic coma, prolonged exercise
FFA are carried by albumin
beta oxidation of unsaturated FAs 4 enzymes that overcome the unsaturation to make saturated fatty acids
where can adipocytes get glycerol 3 phosphate? DHAP via glycolysis (no glycerol kinase)
fasted adipocyte metabolism epinephrine (HSL increases via adenylyl cyclase)-> independent of glucose and insulin
enzyme that breaks down 2 monoacylglycerol -> FFA + glycerol 2-monoacylglycerol lipase
key steps in FAS ATP citrate lyase, acetyl-coA carboxylase, FAS, esterification of FA+glycerol to TG
long term ACC regulation insulin increases transcription of it
coA is also pantothenic acid (B5)
how many times are steps 2-5 repeated in FAS? *always palmitate-> 7 times
short term regulation of FAS none!
fat comes out of ___ when well-fed in form of___ liver, TG
fat comes out of ___ when under-fed in form of___ adipocytes, FFA
can most cells synthesize cholesterol? yes; but they don't because of LDL delivery
HMG CoA reductase translational control mevalonate blocks translation (details unknown)
HMG CoA reductase degradation control cholesterol and mevalonate increase degradation rate
stanol vs sterol stanol= saturated plant sterols
high plant sterols/stanols in the diet does what? blocks cholesterol absorption
are plant stanols or sterols better at lowering plasma cholesterol? stanols
are stanols or sterols better absorbed? sterols
where are bile acids made? liver only
7a hydroxylase- which form (P/deP) is active? phosphorylated (think glucagon)
2 ways to increase fecal bile acid excretion soluble fiber and cholestyramine
how does eating fiber affect plasma cholesterol? bile acids excreted so cholesterol is used to make them, less cholesterol increases transcription of LDLr, increased uptake of cholesterol= lower plasma cholesterol
what happens if bile composition changes? gall stones
what nutrient causes gallstones and why? PUFA because they increase biliary cholesterol which will offset the balance and make bile solid
plasma vs serum both= cells removed, but plasma has an added anticoagulant
what regulates LDLr expression? free cholesterol (lowers it) *but CE don't
oxysterols made by ROS+ cholesterol (not all ROS are bad)
transports dietary TG from intestines to peripheral tissues chylomicrons
carries dietary cholesterol & some TG to liver CM remnant
carries endogenous TG from liver to peripheral tissues VLDL
between VLDL and LDL IDL
transports endogenous & exogenous cholesterol to cells LDL
cholesterol transport away from cells HDL
enzyme that breaks lipids off of lipoproteins lipoprotein lipase
paraoxonase inhibits oxidative modification of LDL (component of HDL)
what does HDL do in atherosclerosis? (4) transports cholesterol out, inhibits adhesins, changes foam cells back to macrophages, inhibits oxidation of LDL
what did Keys find independently? that change in cholesterol is positively correlated w/ sat fat and negatively correlated with unsat fat
what did Hegsted find independently? used individual fatty acids and cholesterol (+sat fat, - unsat fat, ++ cholesterol *too high)
change regarding MUFA after Hegsted and Keys lowers plasma cholesterol slightly (displaces sat fat)
change regarding stearic acid after Hegsted and Keys neutral effect probably because not well absorbed
MRFIT SI protocol stop smoking, weight reduction, hydrochlorothiazide, lower sodium, sat fat <10% kcal, diet chol <300mg, polyunsat >10% kcal
results of MRFIT study same mortality regarding CHD and overall
significant finding in MRFIT study lower mortality for smokers who quit
LRC-CPPT study protocol <400 mg cholesterol per day, cholestyramine supplement
results of LRC-CPPT study small significant decrease in LDL and mortality from CVD
vitamin E study 50% reduction in heart attacks with 300+IU vitamin E
excessive antioxidants act as pro-oxidants
consumption of ___ likely to prevent/limit macrophage accumulation adequate antioxidants and phytochemicals
ATP citrate lyase converts citrate into acetyl coA for fat synthesis
according to Libby et al., where does blood clot occur? before site, then gets stuck
must have ____ with plaque rupture for a ___ ___ to occur; diet is only a small factor in CHD thrombus; coronary event
Created by: melaniebeale
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