Biochemistry I Exam 4 Review
Biochemistry I Exam 4 Review BIO 361
Stony Brook U
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This 6 page Study Guide was uploaded by Jiamin Chen on Thursday January 28, 2016. The Study Guide belongs to BIO 361 at Stony Brook University taught by in Fall 2015. Since its upload, it has received 143 views. For similar materials see Biochemistry I in Biochemistry at Stony Brook University.
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Date Created: 01/28/16
Pentose Phosphate Pathway (PPP) Oxidative Stage irreversible Produce:2 NADPH 1 pentose5P 1 CO2 Regulation step: glucose6phosphate dehydrogenase (G6PDH) deficiency = resistance to malaria Isomerization all reversible; controlled by mass action 2nd step: isomerase/epimerase Transketolase: TPP Transaldolase : use schiff base to stabilize carbanion intermediate NonOxidative Stage glycolytic intermediates recovered convert 3 pentoseP (15C) to 2 fructose6P/ GAP (15C) Glycogen Metabolism Liver glucose maintained at 5mM in blood Muscle Glycogen phosphorylase: add pi to break dimer Phosphoglucomutase: G1P to G6P; use phosphorylated Ser Last Step: conversion of G6P to free glc by glucose 6phosphatase not expressed in skeletal muscle b/c any glycose from glycogen is oxidized directly in the glycolytic pathway reduces chance of glucose in muscle going to blood Glycogen Synthesis Glycogen Synthase PRIMER of at least 4 alpha 1,4linked Glc residues oxonium ion intermediate inhibitor: 1,5gluconolactone; mimic halfchair of oxonium ion ATP,ADP,Pi activate by G6P, AMP Glycogen Storage Disease (GSD) von Gierke’s disease glucose6phosphatase in liver McArdle’s disease glycogen phosphorylase in muscle Gluconeogenesis Occurs in starvation, fasting, intense exercise Liver & Kidney other do but no glucose 6phosphatase/ transporter Pyruvate carboxylase activates by acetylCoA (indication of high energy state) Ureido faciliates e transfer from carboxylate to pyr PEP carboxykinase lactate dehydrogenase (LDH) Warburg effect Ethanol inhibits gluconeogenesis inhibits: malate DH lactate DH = hypoglycermic/low blood glucose =joint pain alcoholics low glucose= buildup of keto bodies in blood= keto acidisis Mighty mouse: overexpression of PEPCK (phosphoenolpyruvate carboxykinase (GTP) = MUCH higher metabolism rate Regulation of Carbohydrate Metabolism: Glucose & Glycogen Glycogen: phosphorylates PK (to a) and GP (to a)= glycogen breakdown epinephrine (emergency) & glycogen different receptor but same response= increase cAMP= glycogen breakdown Liver fed vs. fasting insulin betacell target liver, adipose & muscle inhibits glucose production increase GLUT 4 vs. glucagon alphacell targets liver & adipose, NOT muscle (no glycogen receptor, store glycogen for OWN use) glucagon activates PKA, cAMPdependent PK GS: inhibits by epinephrine, glucagon vs. GP: activates by “”; inhibits by ATP, G6P, & Glucose vs. Muscle covalent modification/phosphorylation Kinase cascade: amplification glycogen phosphorylase b= inactive / T form more sensitive to allosteric regulators glycogen phosphorylase a= active/ R form→ breaks down glycogen has pi phosphoprotein phosphatase1 (PP1c)/dephosphorylation active when bound to glycogen & vice versa active when kicks off 1 pi from glycogen subunit activated by insulin and epinephrine/adrenaline signaling transduction: adenylate cyclase convert ATP to cAMP= activate Protein kinase A (PK a)/ cAMP dependent protein kinase (4 subunit = binds to 4 cAMP) vs. allosteric regulation Glucose/glycolysis/gluconeogenesis PFK activators relieve ATP inhibition Fructose2,6bisphosphate= increase glycolysis not glycolytic intermediate activator of PFK inhibitor of FBPase fructose2,6bisphosphatase(PFK2) bifunctional: 2 oppose domains; kinase (increase F2,6,BP) vs phosphatase(activate by pi) phosphorylates pyruvate kinase= inactivating= slow glycolysis turn PEP to pyruvates Regulation in 1st, 3rd, 10th step 1st step: isozymes Muscle: hexokinase, inhibited by G6P Liver: glucokinase, not inhibited by G6P; takes glucose even if high, higher Km=lower affinity Integration of Metabolism I 3 Levels of regulation: cell, tissue, organism Organism: Hormone insulin= increase fuel uptake & storage (use and store) glucagon & catecholamine= increase fuel mobilization= make glucose in liver Brain only glucose & ketone bodies? Skeletal Muscle cori cycle Protein: muscle aminotransferase can convert pyruvate to alanine: alanine in circulation Heart treatment of angina= inhibition of beta oxidation ranolazine Adipose insulin inhibits hormonesensitive lipase (HSL) Liver cannot use keto bodies VLDL: very lowdensity lipoprotein Kidney Glucose Transporter GLUT 4: muscle & Fat; insulin membrane receptor important effect: INTRACELLULAR vesicle becomes part of membrane gene expression to make more GLUT 4=take up more glucose Diabetes mellitus detect in regulating blood glucose 3rd leaving cause of death cause blindness Type I/insulindependent (IDDM) ”juvenile” in preadolescents loss of betacell; no insulin treat w/insulinreplace Type II: Noninsulin (NIDDM) insulin resistances; produce insulin but no response treatment: diet/ drug activates AMP dependent protein kinase (AMPK) Maintain homeostasis: AMPK: AMP dependent protein kinase heterotrimer: alpha, beta, gamma 2 AMP binding sites: allosteric opens activation loop=> phosphorylates =activates/try to get ATP inhibits by ATP activated by low energy: high ratio of AMP/ATP activates glucose intake in HEART and MUSCLE stimulates FA oxidation in liver? inhibits gluconeogenesis in liver Heart targets bifunctional FPK2/FBPase2= increase F2,6,P= increase glycolysis in HEART Liver inhibits synthesis of FA,cholesterol, glucose Skeletal Muscle promotes FA oxidation, glucose intake (recruit GLUT 4) inhibits glycogen synthesis Adipose: opposite AMPK inhibits breakdown of TG to FA to glucose?? why Hormone (5) Adiponectin: activates AMPK by phosphorylation from adipose tissue decrease adiponectin= insulin resistance associates to LMW homotrimer to hexamers/dodecamers= linked by disulfides to HMW oligermers (more active b/c bind to multiple receptors)= activate AMPK Leptin: inhibits appetite= eat less DB/diabetes: receptor for leptin OB/obese: produce leptin nearly identical phenotype obesity: absence of leptin/receptor from adipose inhibits secretion of neuropeptide Y doesn’t not regulate AMPK?? doesn’t inhibit synthesis of ghrelin Insulin Neuropeptide Y (NPY)=counteracts leptin stimulate appetite=eat more by hypothalamus NPY receptor= GPCR inhibits cAMP production=? Ghrelin: hunger=counters leptin from stomach & pancreas cross BBB to ghrelin receptor also GPCR PYY 336: suppress/reduce appetite acts on NPY receptors? Drug decrease insulin resistance/ treat type II metformin: suppress glucose release in liver thiazolidinedione (TZD): increase glucose use in muscle rosiglitazone/avandia: may increase risk of heart attack/stroke Pathologies w/diabetes shortterm: ketoacidosis longterm: blindness glucose modification: Hemoglobin A1c (HbA1c): monitor diabetics increase w/plasma glucose protein crosslinking= diabetic cataract Clicker/Exam Questions: Inhibition of COX enzymes produces which of the following effects? A. Reduction of free fatty acid level B. Increased production of PGE2 C. Induction of fever D. None of the above Under anaerobic conditions in the muscle, what is the net yield of ATP from glycolysis when glycogen is used as a starting material? 3 ATP
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