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Biochemistry I Exam 4 Review

by: Jiamin Chen

Biochemistry I Exam 4 Review BIO 361

Marketplace > Stony Brook University > Biochemistry > BIO 361 > Biochemistry I Exam 4 Review
Jiamin Chen
Stony Brook U

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About this Document

This is a 6 page concise study guide with some clicker questions for exam 4. It covers topics such as pentose phosphate pathway, glycogen metabolism, glycogen synthesis, gluconeogenesis, regulation...
Biochemistry I
Study Guide
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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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