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FSHN 470- Unit 2
| Question | Answer |
|---|---|
| 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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