DOCSLIB.ORG

Lipid Metabolism & Obesity

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Lipid Metabolism & Obesity ™ Proteome Profi ler Mouse Obesity Array Kit PRSRT STD R&D Systems Proteome Profi ler Antibody Arrays offer a rapid, sensitive approach to simultaneously detect the relative levels of multiple analytes in U.S. POSTAGE R&D Systems Tools for Cell Biology Research™ a single sample. Each array is designed using carefully selected capture antibodies that are spotted in duplicate onto nitrocellulose membranes. PAID Membranes are incubated with experimental samples containing the proteins of interest and a cocktail of biotinylated detection antibodies. R&D SYSTEMS Streptavidin-HRP and chemiluminescent detection reagents are subsequently added to produce a signal that is proportional to the amount of R&D Systems, Inc. 614 McKinley Place NE analyte bound. The use of these arrays requires no specialized equipment and eliminates the need to perform multiple immunoprecipitation/ Minneapolis, MN 55413 Western blot experiments. TEL: (800) 343-7475 (612) 379-2956 ABUndifferentiated C FAX: (612) 656-4400 Mouse Obesity Array (Catalog # ARY013) www.RnDSystems.com Adiponectin IGFBP-3 Leptin IGF-I 70,000 Contains 4 membranes - each spotted in duplicate with 38 different obesity-related antibodies 60,000 • Adiponectin/Acrp30 • IGFBP-2 • Pentraxin 3 50,000 • AgRP • IGFBP-3 • Pref-1/DLK-1/FA1 Lipid Metabolism & Obesity • ANGPT-L3 • IGFBP-5 • RAGE 40,000 VEGF Pentraxin 3 Resistin Lipocalin-2 • CRP • IGFBP-6 • RANTES/CCL5 • DPPIV • IL-6 • RBP4 Pixel Density Pixel 30,000 • Endocan • IL-10 • Resistin Differentiated 20,000 • Fetuin A • IL-11 • Serpin E1/PAI-1 10,000 • FGF acidic/FGF-1 • Leptin • TIMP-1 Adiponectin IGFBP-3 Leptin IGF-I • FGF-21 • LIF • TNF- 0 • HGF • Lipocalin-2/NGAL • VEGF IGF-I VEGF • ICAM-1/CD54 • MCP-1 Leptin Resistin IGFBP-3 • IGF-I • M-CSF Lipocalin-2 Pentraxin 3 Pentraxin Adiponectin Printed on recyclable paper • IGF-II • Oncostatin M 10% post consumer waste. VEGF Pentraxin 3 Resistin Lipocalin-2 • IGFBP-1 • Pentraxin 2 FluoroNissI and Rhodamine Red are trademarks of Life Technologies. DuoSet, NorthernLights, Parameter, Proteome Profi ler, and StemXVivo are trademarks of R&D Systems. R&D Systems is a trademark of TECHNE Corporation. FL093MAR_Lipid_APR Multiple Proteins in Cell Culture Supernatants from Undifferentiated and Differentiated 3T3-L1 Cells were Assessed using the Mouse Obesity Array. A. The Proteome Profi ler Mouse Obesity Array (Catalog # ARY013) was used to simultaneously assess the relative levels of multiple obesity-related proteins in cell culture supernatants from both undifferentiated 3T3-L1 mouse preadipocytes (top) and differentiated 3T3-L1 adipocytes (bottom). B. Histogram profi les for select proteins were generated by quantifying the mean spot pixel densities from the arrays using image software analysis. Green bars represent protein levels in supernatants from undifferentiated 3T3-L1 cells and gray bars represent the levels detected in supernatants from differentiated cells. C. Proteins detected by the Mouse Obesity Array. Adipogenic Diff erentiation R&D Systems offers base media and supplements specially formulated to direct adipocyte differentiation of human or mouse mesenchymal stem cells (MSCs). Additionally, we offer MSC Functional Identifi cation Kits that contain differentiation supplements and a panel of antibodies for positive Proteins Antibodies ELISAs identifi cation of differentiated adipocytes and other MSC lineages. Product Description Catalog # 5000 1.6 Untreated Insulin Phospho-Insulin R ™ 1.4 Human/Mouse StemXVivo Mesenchymal Complete media for the expansion of MSCs. CCM004 Total Insulin R Stem Cell Expansion Media 4000 ) 450 1.2 Human/Mouse StemXVivo Osteogenic/ Base media used with the appropriate supplement for CCM007 Adipogenic Base Media the differentiation of MSCs into adipocytes. 3000 1.0 Human/Mouse StemXVivo Adipogenic Media supplement for the differentiation of human or CCM011 100 0.8 Supplement mouse MSCs into adipocytes. For use with the 80 2000 Osteogenic/Adipogenic Base Media. 60 0.6 Proliferation (RFU) Proliferation 40 Human Mesenchymal Stem Cell Functional Contains adipogenic, chondrogenic, osteogenic, and SC006 Phospho-Insulin R (O.D. Phospho-Insulin R (O.D. 0.4 1000 20 Identifi cation Kit ITS supplements for the differentiation of each lineage. Percent Neutralization Percent 0 0.2 A panel of antibodies for identifi cation of the mature 0.01 0.1 1 10 100 Antibody Concentration (μg/mL) phenotypes are included: anti-Aggrecan, 0 0 anti-Osteocalcin, & anti-FABP4. 0.01 0.1 1 10 100 1000 Leptin (ng/mL) Untreated Insulin Mouse Mesenchymal Stem Cell Functional Contains adipogenic, chondrogenic, osteogenic, and SC010 Identifi cation Kit ITS supplements for the differentiation of each lineage. A panel of antibodies for identifi cation of the mature Leptin Stimulates the Proliferation of Leptin Receptor- AgRP Expression in Mouse Thalamus. Agouti-Related Detection of Insulin Receptor Phosphorylation in Insulin- FABP4 in Diff erentiating Human Adipocytes. Human mesen- phenotypes are included: anti-Collagen II, transfected BaF3 Cells. BaF3 mouse pro B cells transfected Protein (AgRP) was detected in a frozen section of mouse induced HepG2 Cells using the DuoSet® IC ELISA. Lysates chymal stem cells were diff erentiated using Human/Mouse anti-Osteopontin, & anti-FABP4. with human Leptin Receptor were incubated with increasing thalamus using anti-mouse AgRP monoclonal antibody from HepG2 human hepatocellular liver carcinoma cells, un- StemXVivo Osteogenic/Adipogenic Base Media (Catalog # concentrations of recombinant human Leptin (Catalog # (Catalog # MAB634). Tissues were stained using Northern- treated or treated with recombinant human Insulin, were as- CCM007) supplemented with human/mouse StemXVivo Adipo- 398-LP). Cellular proliferation was assessed by a fl uorometric Lights™ 557-conjugated anti-rat secondary antibody (Cata- sessed for Insulin Receptor phosphorylation using the hu- genic Supplement (Catalog # CCM011). Adipocytes were assay using the redox-sensitive dye, Resazurin (Catalog # log # NL013; red) and counterstained with FluoroNissI™ man Phospho-Insulin R DuoSet IC ELISA Development System stained using anti-mouse FABP4 polyclonal antibody provided AR002). Leptin activity in this assay was neutralized by incu- Green. (Catalog # DYC2718; bar graph). The same lysates were also in the Human Mesenchymal Stem Cell Functional Identifi cation bating the recombinant protein with increasing concentra- analyzed by IP-Western blot (inset) using anti-human Insulin Kit (Catalog # SC006) followed by Rhodamine Red™-conjugated tions of anti-human Leptin polyclonal antibody (Catalog # R monoclonal antibody and anti-mouse agarose for immuno- anti-goat secondary antibody. Cells were counterstained with AF398) prior to its addition to Leptin R-transfected BaF3 precipitation. Biotinylated pan anti-Phospho-Tyrosine DAPI (blue). cells (inset). monoclonal (Catalog # BAM1676) and anti-Insulin R poly- clonal antibodies were used for immunoblotting. PRODUCT SELECTION EXPANDING WEEKLY. Please visit our website at www.RnDSystems.com/go/Metabolism for an up-to-date product listing. For research use only. Not for use in diagnostic procedures. For research use only. Not for use in diagnostic procedures. Lipid Metabolism & Obesity Products for Lipid Metabolism & Obesity Research Insulin, secreted by the pancreatic cells, is the main regulator of blood glucose levels. It stimulates glucose uptake in muscle and fat, inhibits glucose production in the liver, promotes glycogen and lipid synthesis, and inhibits lipolysis. Recombinant & Recombinant & Recombinant & Several factors secreted by the adipose tissue either promote or inhibit insulin sensitivity including Leptin, Adiponectin, TNF-, IL-6, and Resistin (in mice). The ability of these cytokines to infl uence insulin signaling suggests that changes in Molecule Natural Proteins Antibodies ELISAs & Other Kits Molecule Natural Proteins Antibodies ELISAs & Other Kits Molecule Natural Proteins Antibodies ELISAs & Other Kits their levels may contribute to the development of insulin-related metabolic disorders such as Type II diabetes. One of the leading risk factors for Type II diabetes is obesity, a condition characterized by an increase in adipocyte size, mild Adiponectin/Acrp30 H M H M R H M IKK H M R PKA C (pan) H M R infl ammation, and altered adipocytokine secretion. Obesity is associated with reduced Leptin sensitivity and a decrease in the production of Adiponectin, two adipocytokines that normally enhance insulin sensitivity. These changes are AgRP H M H M H IKK H PKA C H H M R Akt Pan Specifi c H M R IKK H M R PKA C H coupled with an increase in the production of Resistin and pro-infl ammatory cytokines such as TNF- and IL-6, which promote insulin resistance. Characterizing the mechanisms by which adipocytokines enhance or interfere with insulin Phospho-Akt (S473) Pan Specifi c H M R H M R IKK H M R PKA R1 H M R signaling pathways is critical to our understanding of how these factors contribute to the pathogenesis of metabolic disorders. Akt1 H H M R H M R IGF-I H M R H M H M PKC H M R R&D Systems offers a wide range of research reagents useful for the study of metabolic signaling pathways. Phospho-Akt1 (S473) H M IGF-I R HH H PKC 1 H R AMPK1 H M R Phospho-IGF-I R HH PKC 2 H M Phospho-AMPK1 (T174) H IGFBP-1 H M H M H PKC H M R Phospho-AMPK1/2 (T174/T172) H IGFBP-2, -3 H M H M H M PKC H LEPTIN FREE FATTY ACIDS IL6 AMPK2 H M R IGFBP-4 HH PKC H M R Appetite H M R H M H M H M t t )FQBUJD(MVDPTF1SPEVDUJPO t1SPNPUF"EJQPDZUF-JQPMZTJT AMPK1 IGFBP-5, -6 PKC / H M R H
Load more

Recommended publications
  • A Novel Lipid Screening Platform That Provides a Complete Solution for Lipidomics Research
    A Novel Lipid Screening Platform that Provides a Complete Solution for Lipidomics Research The Lipidyzer™ Platform, powered by Metabolon® Baljit K Ubhi1, Alex Conner1, Eva Duchoslav3, Annie Evans1, Richard Robinson1, Paul RS Baker4 and Steve Watkins1 1SCIEX, CA, USA, 2Metabolon, USA, 3SCIEX, Ontario, Canada and 4SCIEX, MA, USA INTRODUCTION MATERIALS AND METHODS A major challenge in lipid analysis is the many isobaric Applying the kit for simplified sample extraction and preparation, interferences present in highly complex samples that confound a serum matrix was used following the protocols provided. A identification and accurate quantitation. This problem, coupled QTRAP® System with SelexION® DMS Technology (SCIEX) with complicated sample preparation techniques and data was used for targeted profiling of over a thousand lipid species analysis, highlights the need for a complete solution that from 13 different lipid classes (Figure 2) allowing for addresses these difficulties and provides a simplified method for comprehensive coverage. Two methods were used covering analysis. A novel lipidomics platform was developed that thirteen lipid classes using a flow injection analysis (FIA); one includes simplified sample preparation, automated methods, and injection with SelexION® Technology ON and another with the streamlined data processing techniques that enable facile, SelexION® Technology turned OFF. The lipid molecular species quantitative lipid analysis. Herein, serum samples were analyzed were measured using MRM and positive/negative switching. quantitatively using a unique internal standard labeling protocol, Positive ion mode detected the following lipid classes – a novel selectivity tool (differential mobility spectrometry; DMS) SM/DAG/CE/CER/TAG. Negative ion mode detected the and novel lipid data analysis software.
    [Show full text]
  • Corticosteroid Treatment, Serum Lipids and Coronary Artery Disease D. B. JEFFERYS M
    Postgrad Med J: first published as 10.1136/pgmj.56.657.491 on 1 July 1980. Downloaded from Postgraduate Medical Journal (July 1980) 56, 491-493 Corticosteroid treatment, serum lipids and coronary artery disease D. B. JEFFERYS M. H. LESSOF B.Sc., M.R.C.P. M.D., F.R.C.P. M. B. MATTOCK Ph.D. Department of Medicine, Guy's Hospital, London Bridge SE] 9RT Summary cholesterol out of the tissue and back into the general Serum lipids and the cholesterol concentrations in the metabolic pool, where it may be catabolized. high density lipoprotein (HDL) fractions were meas- In this study the authors have looked at the long- ured in patients receiving long-term corticosteroid term effects of corticosteroids on HDL cholesterol. treatment for connective tissue disorders and asthma. They have studied 3 groups: patients who are receiv- Patients who were not receiving corticosteroid ing corticosteroids; age-, sex- and disease-matched treatment had blood lipid levels which did not differ patients who are not receiving such treatment; and from those of healthy people. However, female (but healthy age- and sex-matched controls. not male) patients who had received prednisolone for a mean period of 3-1 years had a significant elevation Patients and methods in total cholesterol and a large decrease in HDL Subjects cholesterol. It seems possible that high levels of The serum total cholesterol, triglycerides and copyright. corticosteroids may increase the incidence of pre- HDL cholesterol were measured for 16 pre-meno- menopausal ischaemic heart disease in females. pausal female patients (age range 18-34 years) and 15 males (ages 24-38 years) who were all receiving Introduction long-term corticosteroid treatment.
    [Show full text]
  • Tricarboxylic Acid (TCA) Cycle Intermediates: Regulators of Immune Responses
    life Review Tricarboxylic Acid (TCA) Cycle Intermediates: Regulators of Immune Responses Inseok Choi , Hyewon Son and Jea-Hyun Baek * School of Life Science, Handong Global University, Pohang, Gyeongbuk 37554, Korea; [email protected] (I.C.); [email protected] (H.S.) * Correspondence: [email protected]; Tel.: +82-54-260-1347 Abstract: The tricarboxylic acid cycle (TCA) is a series of chemical reactions used in aerobic organisms to generate energy via the oxidation of acetylcoenzyme A (CoA) derived from carbohydrates, fatty acids and proteins. In the eukaryotic system, the TCA cycle occurs completely in mitochondria, while the intermediates of the TCA cycle are retained inside mitochondria due to their polarity and hydrophilicity. Under cell stress conditions, mitochondria can become disrupted and release their contents, which act as danger signals in the cytosol. Of note, the TCA cycle intermediates may also leak from dysfunctioning mitochondria and regulate cellular processes. Increasing evidence shows that the metabolites of the TCA cycle are substantially involved in the regulation of immune responses. In this review, we aimed to provide a comprehensive systematic overview of the molecular mechanisms of each TCA cycle intermediate that may play key roles in regulating cellular immunity in cell stress and discuss its implication for immune activation and suppression. Keywords: Krebs cycle; tricarboxylic acid cycle; cellular immunity; immunometabolism 1. Introduction The tricarboxylic acid cycle (TCA, also known as the Krebs cycle or the citric acid Citation: Choi, I.; Son, H.; Baek, J.-H. Tricarboxylic Acid (TCA) Cycle cycle) is a series of chemical reactions used in aerobic organisms (pro- and eukaryotes) to Intermediates: Regulators of Immune generate energy via the oxidation of acetyl-coenzyme A (CoA) derived from carbohydrates, Responses.
    [Show full text]
  • Fatty Acid Synthesis ANSC/NUTR 618 Lipids & Lipid Metabolism Fatty Acid Synthesis I
    Handout 5 Fatty Acid Synthesis ANSC/NUTR 618 Lipids & Lipid Metabolism Fatty Acid Synthesis I. Overall concepts A. Definitions 1. De novo synthesis = synthesis from non-fatty acid precursors a. Carbohydrate precursors (glucose and lactate) 1) De novo fatty acid synthesis uses glucose absorbed from the diet rather than glucose synthesized by the liver. 2) De novo fatty acid synthesis uses lactate derived primarily from glucose metabolism in muscle and red blood cells. b. Amino acid precursors (e.g., alanine, branched-chain amino acids) 1) De novo fatty acid synthesis from amino acids is especially important during times of excess protein intake. 2) Use of amino acids for fatty acid synthesis may result in nitrogen overload (e.g., the Atkins diet). c. Short-chain organic acids (e.g., acetate, butyrate, and propionate) 1) The rumen of ruminants is a major site of short-chain fatty acid synthesis. 2) Only small amounts of acetate circulate in non-ruminants. 2. Lipogenesis = fatty acid or triacylglycerol synthesis a. From preformed fatty acids (from diet or de novo fatty acid synthesis) b. Requires source of carbon (from glucose or lactate) for glycerol backbone 3T3-L1 Preadipocytes at confluence. No lipid 3T3-L1 Adipocytes after 6 days of filling has yet occurred. differentiation. Dark spots are lipid droplets. 1 Handout 5 Fatty Acid Synthesis B. Tissue sites of de novo fatty acid biosynthesis 1. Liver. In birds, fish, humans, and rodents (approx. 50% of fatty acid biosynthesis). 2. Adipose tissue. All livestock species synthesize fatty acids in adipose tissue; rodents synthesize about 50% of their fatty acids in adipose tissue.
    [Show full text]
  • Seasonal Growth and Lipid Storage of the Circumgiobal, Subantarctic Copepod, Neocalanus Tonsus (Brady)
    Deep-Sea Research, Vol. 36, No. 9, pp, 1309-1326, 1989. 0198-0149/89$3.00 + 0.00 Printed in Great Britain. ~) 1989 PergamonPress pie. Seasonal growth and lipid storage of the circumgiobal, subantarctic copepod, Neocalanus tonsus (Brady) MARK D. OHMAN,* JANET M. BRADFORDt and JOHN B. JILLETr~ (Received 20 January 1988; in revised form 14 April 1989; accepted 24 April 1989) Abstraet--Neocalanus tonsus (Brady) was sampled between October 1984 and September 1985 in the upper 1000 m of the water column off southeastern New Zealand. The apparent spring growth increment of copepodid stage V (CV) differed depending upon the constituent con- sidered: dry mass increased 208 Ixg, carbon 162 Ixg, wax esters 143 Itg, but nitrogen only 5 ltg. Sterols and phospholipids remained relatively constant over this interval. Wax esters were consistently the dominant lipid class present in CV's, increasing seasonally from 57 to 90% of total lipids. From spring to winter, total lipid content of CV's increased from 22 to 49% of dry mass. Nitrogen declined from 10.9 to 5.4% of CV dry mass as storage compounds (wax esters) increased in importance relative to structural compounds. Egg lipids were 66% phospholipids. Upon first appearance of males and females in deep water in winter, lipid content and composition did not differ from co-occurring CV's, confirming the importance of lipids rather than particulate food as an energy source for deep winter reproduction of this species. Despite contrasting life histories, N. tonsus and subarctic Pacific Neocalanus plumchrus CV's share high lipid content, a predominance of wax esters over triacylglycerols as storage lipids, and similar wax ester fatty acid and fatty alcohol composition.
    [Show full text]
  • Lipid–Protein and Protein–Protein Interactions in the Pulmonary Surfactant System and Their Role in Lung Homeostasis
    International Journal of Molecular Sciences Review Lipid–Protein and Protein–Protein Interactions in the Pulmonary Surfactant System and Their Role in Lung Homeostasis Olga Cañadas 1,2,Bárbara Olmeda 1,2, Alejandro Alonso 1,2 and Jesús Pérez-Gil 1,2,* 1 Departament of Biochemistry and Molecular Biology, Faculty of Biology, Complutense University, 28040 Madrid, Spain; [email protected] (O.C.); [email protected] (B.O.); [email protected] (A.A.) 2 Research Institut “Hospital Doce de Octubre (imasdoce)”, 28040 Madrid, Spain * Correspondence: [email protected]; Tel.: +34-913944994 Received: 9 May 2020; Accepted: 22 May 2020; Published: 25 May 2020 Abstract: Pulmonary surfactant is a lipid/protein complex synthesized by the alveolar epithelium and secreted into the airspaces, where it coats and protects the large respiratory air–liquid interface. Surfactant, assembled as a complex network of membranous structures, integrates elements in charge of reducing surface tension to a minimum along the breathing cycle, thus maintaining a large surface open to gas exchange and also protecting the lung and the body from the entrance of a myriad of potentially pathogenic entities. Different molecules in the surfactant establish a multivalent crosstalk with the epithelium, the immune system and the lung microbiota, constituting a crucial platform to sustain homeostasis, under health and disease. This review summarizes some of the most important molecules and interactions within lung surfactant and how multiple lipid–protein and protein–protein interactions contribute to the proper maintenance of an operative respiratory surface. Keywords: pulmonary surfactant film; surfactant metabolism; surface tension; respiratory air–liquid interface; inflammation; antimicrobial activity; apoptosis; efferocytosis; tissue repair 1.
    [Show full text]
  • Soluble Surfactant and Nanoparticle Effects on Lipid Monolayer Assembly and Stability
    Soluble Surfactant and Nanoparticle Effects on Lipid Monolayer Assembly and Stability Dissertation Presented in Partial Fulfillment of the Requirements for the Degree Doctor of Philosophy in the Graduate School of The Ohio State University By Matthew D. Nilsen, B.S., M.Sc. Graduate Program in Chemical Engineering The Ohio State University 2010 Dissertation Committee: Dr. James F. Rathman, Advisor Dr. L. James Lee Dr. Isamu Kusaka c Copyright by Matthew D. Nilsen 2010 Abstract The study of self-assembly dynamics that lead to ultra-thin films at an interface remains a very active research topic because of the ability to generate interesting and useful structures that can perform specific tasks such as aiding in magnetic separa- tions, acting as two-dimensional biosensors and the modification of surfaces without changing their morphology. In some cases this is critical to surface functionality. This area is also important because it may ultimately yield simple screening techniques for novel surfactants and nanoparticle species before they are introduced onto the market, as is already happening. In the work presented here we studied the assembly dynamics of the insoluble lipid DPPC, common to most mammalian cell lines, in the presence of soluble surfactant and nanoparticle species. Preliminarily, we investigated the anomalous behavior of soluble surfactants at the air/water interface as an exten- sion to work done previously and then used these results in an attempt to explain the behavior of the combined surfactant/lipid monolayer under dynamic and static conditions. Separately, we performed nanoparticle dynamics studies for a commer- cially available product and for particles created in-house before performing similar statics/dynamics work on the combined nanoparticle/lipid monolayer.
    [Show full text]
  • The Mars Project: Avoiding Decompression Sickness on a Distant Planet
    NASA/TM--2000-210188 The Mars Project: Avoiding Decompression Sickness on a Distant Planet Johnny Conkin, Ph.D. National Space Biomedical Research Institute Houston, Texas 77030-3498 National Aeronautics and Space Administration Lyndon B. Johnson Space Center Houston, Texas 77058-3696 May 2000 Acknowledgments The following people provided helpful comments and suggestions: Amrapali M. Shah, Hugh D. Van Liew, James M. Waligora, Joseph P. Dervay, R. Srini Srinivasan, Michael R. Powell, Micheal L. Gernhardt, Karin C. Loftin, and Michael N. Rouen. The National Aeronautics and Space Administration supported part of this work through the NASA Cooperative Agreement NCC 9-58 with the National Space Biomedical Research Institute. The views expressed by the author do not represent official views of the National Aeronautics and Space Administration. Available from: NASA Center for AeroSpace Information National Technical Information Service 7121StandardDrive 5285 Port Royal Road Hanover, MD 21076-1320 Springfield, VA 22161 301-621-0390 703-605-6000 This report is also available in electronic form at http://techreports.larc.nasa.gov/cgi-bin/NTRS Contents Page Acronyms and Nomenclature ................................................................................................ vi Abstract ................................................................................................................................. vii Introduction ..........................................................................................................................
    [Show full text]
  • Lipid Metabolism
    Objectives By the end of lecture the student should: Discuss β oxidation of fatty acids. Illustrate α oxidation of fatty acids. Understand ω oxidation of fatty acids. List sources and fates of active acetate. Oxidation of Fatty Acids 1- β-Oxidation (knoop’s oxidation): . Removal of 2 carbon fragment at a time form Acyl CoA (active FA). .The 2 carbon removed as acetyl CoA. .It occurs in many tissues including liver, kidney & heart FAs to be oxidized must be entered the following 2 steps 2- Transport of acyl 1-Activation of FA COA to mitochondria 1-FA activation Acyl COA synthetase RCOOH RCO~SCOA COASH ATP AMP+P~P 2Pi + E Pyrophosphatase 2- Transport of acyl COA to mitochondria: . Role of carnitine in the transport of LCFA through the inner mithochochondrial membrane Functions of carnitine 1- Transport long chain acyl COA across mitochondrial membrane into the mitochondria so it increases the rate of oxidation of LCFA 2- Transport acetyl-CoA from mitochondria to cytoplasm So it stimulates fatty acid synthesis CoA CoA--SHSH H C α H3C3 α β Cβ Palmitoyl Palmitoyl-CoA -CoA β O ~ S – CoA α H3C α H3C β β CO CO ~ S~ –S CoA – CoA β + + CH3 – CO ~ S –CoA Successive removal of C2 units Acetyl-CoA 8CH3 – CO ~ S – CoA 8CH3 – CO ~ S –Acetyl CoA-CoA Acetyl-CoA Steps of β- Oxidation of FAs Energetics of FA oxidation Palmitic (16C): . β-oxidation of palmitic acid will be repeated 7 cycles producing 8 molecules of acetyl COA . In each cycle FADH2 and NADH+H+ is produced & transported to respiratory chain FADH2 ------------------ 2 ATP NADH+H+ ------------- 3 ATP So 7 cycles 5X7=35 ATP .
    [Show full text]
  • Regulation of Ketone Body and Coenzyme a Metabolism in Liver
    REGULATION OF KETONE BODY AND COENZYME A METABOLISM IN LIVER by SHUANG DENG Submitted in partial fulfillment of the requirements For the Degree of Doctor of Philosophy Dissertation Adviser: Henri Brunengraber, M.D., Ph.D. Department of Nutrition CASE WESTERN RESERVE UNIVERSITY August, 2011 SCHOOL OF GRADUATE STUDIES We hereby approve the thesis/dissertation of __________________ Shuang Deng ____________ _ _ candidate for the ________________________________degree Doctor of Philosophy *. (signed) ________________________________________________ Edith Lerner, PhD (chair of the committee) ________________________________________________ Henri Brunengraber, MD, PhD ________________________________________________ Colleen Croniger, PhD ________________________________________________ Paul Ernsberger, PhD ________________________________________________ Janos Kerner, PhD ________________________________________________ Michelle Puchowicz, PhD (date) _______________________June 23, 2011 *We also certify that written approval has been obtained for any proprietary material contained therein. I dedicate this work to my parents, my son and my husband TABLE OF CONTENTS Table of Contents…………………………………………………………………. iv List of Tables………………………………………………………………………. viii List of Figures……………………………………………………………………… ix Acknowledgements………………………………………………………………. xii List of Abbreviations………………………………………………………………. xiv Abstract…………………………………………………………………………….. xvii CHAPTER 1: KETONE BODY METABOLISM 1.1 Overview……………………………………………………………………….. 1 1.1.1 General introduction
    [Show full text]
  • In-Situ Measurement of Metabolic Status in Three Coral Species from the Florida Reef Tract
    TITLE: In-situ measurement of metabolic status in three coral species from the Florida Reef Tract AUTHORS: Erica K. Towle*1, Renée Carlton2, 3, Chris Langdon1, Derek P. Manzello3 1Rosenstiel School of Marine and Atmospheric Science, University of Miami, 4600 Rickenbacker Cswy, Miami, FL 33149 2Cooperative Institute for Marine and Atmospheric Studies, Rosenstiel School of Marine and Atmospheric Science, University of Miami, 4600 Rickenbacker Cswy, Miami, FL 33149 3Atlantic Oceanographic and Meteorological Laboratories (AOML), NOAA, 4301 Rickenbacker Cswy, Miami, FL 33149 *Corresponding author: Erica K. Towle, [email protected] Key words: Coral calcification, lipids, Florida Keys, Florida Reef Tract Abstract: The goal of this study was to gain an understanding of intra-and inter-specific variation in calcification rate, lipid content, symbiont density, and chlorophyll a of corals in the Florida Reef Tract to improve our insight of in-situ variation and resilience capacity in coral physiology. The Florida Keys are an excellent place to assess this question regarding resilience because coral cover has declined dramatically since the late 1970s, yet has remained relatively high on some inshore patch reefs. Coral lipid content has been shown to be an accurate predictor of resilience under stress, however much of the current lipid data in the literature comes from laboratory- based studies, and previous in-situ lipid work has been highly variable. The calcification rates o three species were monitored over a seven-month period at three sites and lipid content was quantified at two seasonal time points at each of the three sites. Montastraea cavernosa had the highest mean calcification rate (4.7 mg cm-2 day-1) and lowest mean lipid content (1.6 mg cm-2 ) across sites and seasons.
    [Show full text]
  • CHAPTER-IV LIPID METABOLISM BETA-OXIDATION Beta-Oxidation Is
    CHAPTER-IV LIPID METABOLISM BETA-OXIDATION Beta-oxidation is the process by which fatty acids, in the form of acyl-CoA molecules, are broken down in mitochondria and/or peroxisomes to generate acetyl-CoA, the entry molecule for the citric acid cycle. The beta oxidation of fatty acids involve three stages: 1. Activation of fatty acids in the cytosol 2. Transport of activated fatty acids into mitochondria (carnitine shuttle) 3. Beta oxidation proper in the mitochondrial matrix Fatty acids are oxidized by most of the tissues in the body. However, some tissues such as the adrenal medulla do not use fatty acids for their energy requirements and instead use carbohydrates. Energy yield The ATP yield for every oxidation cycle is 14 ATP (according to the P/O ratio), broken down as follows: Source ATP Total [citation needed] 1 FADH2 x 1.5 ATP = 1.5 ATP (some sources say 2 ATP) 1 NADH x 2.5 ATP = 2.5 ATP (some sources say 3 ATP) 1 acetyl CoA x 10 ATP = 10 ATP (some sources say 12 ATP) TOTAL = 14 ATP For an even-numbered saturated fat (C2n), n - 1 oxidations are necessary, and the final process yields an additional acetyl CoA. In addition, two equivalents of ATP are lost during the activation of the fatty acid. Therefore, the total ATP yield can be stated as: (n - 1) * 14 + 10 - 2 = total ATP For instance, the ATP yield of palmitate (C16, n = 8) is: (8 - 1) * 14 + 10 - 2 = 106 ATP Represented in table form: Source ATP Total 7 FADH2 x 1.5 ATP = 10.5 ATP 7 NADH x 2.5 ATP = 17.5 ATP 8 acetyl CoA x 10 ATP = 80 ATP Activation = -2 ATP NET = 106 ATP For sources that use the larger ATP production numbers described above, the total would be 129 ATP ={(8-1)*17+12-2} equivalents per palmitate.
    [Show full text]