β-Aminoisobutyric acid induces browning of white fat and hepatic β-oxidation and is inversely correlated with cardiometabolic risk factors
The transcriptional coactivator peroxisome proliferator-activated receptor-gamma coactivator-1α (PGC-1α) regulates metabolic genes in skeletal muscle and contributes to the response of muscle to exercise. Muscle PGC-1α transgenic expression and exercise both increase the expression of thermogenic ge...
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| Vydané v: | Cell metabolism Ročník 19; číslo 1; s. 96 |
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| Hlavní autori: | , , , , , , , , , , , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | English |
| Vydavateľské údaje: |
United States
07.01.2014
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| ISSN: | 1932-7420, 1932-7420 |
| On-line prístup: | Zistit podrobnosti o prístupe |
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| Abstract | The transcriptional coactivator peroxisome proliferator-activated receptor-gamma coactivator-1α (PGC-1α) regulates metabolic genes in skeletal muscle and contributes to the response of muscle to exercise. Muscle PGC-1α transgenic expression and exercise both increase the expression of thermogenic genes within white adipose. How the PGC-1α-mediated response to exercise in muscle conveys signals to other tissues remains incompletely defined. We employed a metabolomic approach to examine metabolites secreted from myocytes with forced expression of PGC-1α, and identified β-aminoisobutyric acid (BAIBA) as a small molecule myokine. BAIBA increases the expression of brown adipocyte-specific genes in white adipocytes and β-oxidation in hepatocytes both in vitro and in vivo through a PPARα-mediated mechanism, induces a brown adipose-like phenotype in human pluripotent stem cells, and improves glucose homeostasis in mice. In humans, plasma BAIBA concentrations are increased with exercise and inversely associated with metabolic risk factors. BAIBA may thus contribute to exercise-induced protection from metabolic diseases. |
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| AbstractList | The transcriptional coactivator peroxisome proliferator-activated receptor-gamma coactivator-1α (PGC-1α) regulates metabolic genes in skeletal muscle and contributes to the response of muscle to exercise. Muscle PGC-1α transgenic expression and exercise both increase the expression of thermogenic genes within white adipose. How the PGC-1α-mediated response to exercise in muscle conveys signals to other tissues remains incompletely defined. We employed a metabolomic approach to examine metabolites secreted from myocytes with forced expression of PGC-1α, and identified β-aminoisobutyric acid (BAIBA) as a small molecule myokine. BAIBA increases the expression of brown adipocyte-specific genes in white adipocytes and β-oxidation in hepatocytes both in vitro and in vivo through a PPARα-mediated mechanism, induces a brown adipose-like phenotype in human pluripotent stem cells, and improves glucose homeostasis in mice. In humans, plasma BAIBA concentrations are increased with exercise and inversely associated with metabolic risk factors. BAIBA may thus contribute to exercise-induced protection from metabolic diseases.The transcriptional coactivator peroxisome proliferator-activated receptor-gamma coactivator-1α (PGC-1α) regulates metabolic genes in skeletal muscle and contributes to the response of muscle to exercise. Muscle PGC-1α transgenic expression and exercise both increase the expression of thermogenic genes within white adipose. How the PGC-1α-mediated response to exercise in muscle conveys signals to other tissues remains incompletely defined. We employed a metabolomic approach to examine metabolites secreted from myocytes with forced expression of PGC-1α, and identified β-aminoisobutyric acid (BAIBA) as a small molecule myokine. BAIBA increases the expression of brown adipocyte-specific genes in white adipocytes and β-oxidation in hepatocytes both in vitro and in vivo through a PPARα-mediated mechanism, induces a brown adipose-like phenotype in human pluripotent stem cells, and improves glucose homeostasis in mice. In humans, plasma BAIBA concentrations are increased with exercise and inversely associated with metabolic risk factors. BAIBA may thus contribute to exercise-induced protection from metabolic diseases. The transcriptional coactivator peroxisome proliferator-activated receptor-gamma coactivator-1α (PGC-1α) regulates metabolic genes in skeletal muscle and contributes to the response of muscle to exercise. Muscle PGC-1α transgenic expression and exercise both increase the expression of thermogenic genes within white adipose. How the PGC-1α-mediated response to exercise in muscle conveys signals to other tissues remains incompletely defined. We employed a metabolomic approach to examine metabolites secreted from myocytes with forced expression of PGC-1α, and identified β-aminoisobutyric acid (BAIBA) as a small molecule myokine. BAIBA increases the expression of brown adipocyte-specific genes in white adipocytes and β-oxidation in hepatocytes both in vitro and in vivo through a PPARα-mediated mechanism, induces a brown adipose-like phenotype in human pluripotent stem cells, and improves glucose homeostasis in mice. In humans, plasma BAIBA concentrations are increased with exercise and inversely associated with metabolic risk factors. BAIBA may thus contribute to exercise-induced protection from metabolic diseases. |
| Author | Schinzel, Robert T Boström, Pontus Bouchard, Claude Georgiadi, Anastasia Spiegelman, Bruce M Lee, Youn-Kyoung Cowan, Chad A Wang, Thomas J Palma, Melinda J Ramachandran, Vasan S Chen, Ming-Huei Gerszten, Robert E Souza, Amanda L Roberts, Lee D Calhoun, Sondra Larson, Martin G Estall, Jennifer L Dejam, Andre O'Sullivan, John F Lewis, Gregory D Clish, Clary B Soukas, Alexander A Rankinen, Tuomo |
| Author_xml | – sequence: 1 givenname: Lee D surname: Roberts fullname: Roberts, Lee D organization: Cardiovascular Research Center, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA – sequence: 2 givenname: Pontus surname: Boström fullname: Boström, Pontus organization: Dana-Farber Cancer Institute and Harvard Medical School, 3 Blackfan Circle, CLS Building, Floor 11, Boston, MA 02115, USA; Institutionen för Cell-Och Molekylärbiologi (CMB), Karolinska Institutet, von Eulers väg 3, 171 77 Stockholm, Sweden – sequence: 3 givenname: John F surname: O'Sullivan fullname: O'Sullivan, John F organization: Cardiovascular Research Center, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA – sequence: 4 givenname: Robert T surname: Schinzel fullname: Schinzel, Robert T organization: Cardiovascular Research Center, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA; Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA 02138, USA; Center for Regenerative Medicine, Massachusetts General Hospital, Boston, MA 02114, USA; Institut für Biologie-Mikrobiologie, Fachbereich Biologie, Chemie, Pharmazie, Freie Universität Berlin, Königin-Luise-Strasse 12-16,14195 Berlin, Germany – sequence: 5 givenname: Gregory D surname: Lewis fullname: Lewis, Gregory D organization: Cardiovascular Research Center, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA; Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA – sequence: 6 givenname: Andre surname: Dejam fullname: Dejam, Andre organization: Cardiovascular Research Center, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA – sequence: 7 givenname: Youn-Kyoung surname: Lee fullname: Lee, Youn-Kyoung organization: Cardiovascular Research Center, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA; Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA 02138, USA; Center for Regenerative Medicine, Massachusetts General Hospital, Boston, MA 02114, USA – sequence: 8 givenname: Melinda J surname: Palma fullname: Palma, Melinda J organization: Cardiovascular Research Center, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA – sequence: 9 givenname: Sondra surname: Calhoun fullname: Calhoun, Sondra organization: Dana-Farber Cancer Institute and Harvard Medical School, 3 Blackfan Circle, CLS Building, Floor 11, Boston, MA 02115, USA – sequence: 10 givenname: Anastasia surname: Georgiadi fullname: Georgiadi, Anastasia organization: Institutionen för Cell-Och Molekylärbiologi (CMB), Karolinska Institutet, von Eulers väg 3, 171 77 Stockholm, Sweden – sequence: 11 givenname: Ming-Huei surname: Chen fullname: Chen, Ming-Huei organization: Framingham Heart Study of the National Heart, Lung, and Blood Institute and Boston University School of Medicine, Framingham, MA 01702, USA; Department of Neurology, Boston University School of Medicine, Boston, MA 02118, USA; Department of Biostatistics, Boston University School of Public Health, Boston, MA 02118, USA – sequence: 12 givenname: Vasan S surname: Ramachandran fullname: Ramachandran, Vasan S organization: Framingham Heart Study of the National Heart, Lung, and Blood Institute and Boston University School of Medicine, Framingham, MA 01702, USA; Cardiology Section, Boston Medical Center, Boston University School of Medicine, Boston, MA 02118, USA – sequence: 13 givenname: Martin G surname: Larson fullname: Larson, Martin G organization: Framingham Heart Study of the National Heart, Lung, and Blood Institute and Boston University School of Medicine, Framingham, MA 01702, USA; Department of Mathematics and Statistics, Boston University, Boston, MA 02215, USA – sequence: 14 givenname: Claude surname: Bouchard fullname: Bouchard, Claude organization: Pennington Biomedical Research Center, Baton Rouge, LA 70808, USA – sequence: 15 givenname: Tuomo surname: Rankinen fullname: Rankinen, Tuomo organization: Pennington Biomedical Research Center, Baton Rouge, LA 70808, USA – sequence: 16 givenname: Amanda L surname: Souza fullname: Souza, Amanda L organization: Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA – sequence: 17 givenname: Clary B surname: Clish fullname: Clish, Clary B organization: Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA – sequence: 18 givenname: Thomas J surname: Wang fullname: Wang, Thomas J organization: Cardiovascular Research Center, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA; Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA; Cardiology Division, Vanderbilt University, Nashville, TN 37232, USA – sequence: 19 givenname: Jennifer L surname: Estall fullname: Estall, Jennifer L organization: Institut de Recherches Cliniques de Montreal, Montreal, QC H2W 1R7, Canada – sequence: 20 givenname: Alexander A surname: Soukas fullname: Soukas, Alexander A organization: Center for Human Genetic Research, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA – sequence: 21 givenname: Chad A surname: Cowan fullname: Cowan, Chad A organization: Cardiovascular Research Center, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA; Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA 02138, USA; Center for Regenerative Medicine, Massachusetts General Hospital, Boston, MA 02114, USA; Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA – sequence: 22 givenname: Bruce M surname: Spiegelman fullname: Spiegelman, Bruce M organization: Dana-Farber Cancer Institute and Harvard Medical School, 3 Blackfan Circle, CLS Building, Floor 11, Boston, MA 02115, USA – sequence: 23 givenname: Robert E surname: Gerszten fullname: Gerszten, Robert E email: rgerszten@partners.org organization: Cardiovascular Research Center, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA; Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. Electronic address: rgerszten@partners.org |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/24411942$$D View this record in MEDLINE/PubMed |
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| SubjectTerms | Adipocytes, Brown - drug effects Adipocytes, Brown - metabolism Adipocytes, Brown - pathology Adipocytes, White - drug effects Adipocytes, White - metabolism Adipocytes, White - pathology Adipose Tissue, Brown - cytology Adipose Tissue, Brown - drug effects Adipose Tissue, Brown - metabolism Adipose Tissue, White - cytology Adipose Tissue, White - drug effects Adipose Tissue, White - metabolism Aminoisobutyric Acids - blood Aminoisobutyric Acids - pharmacology Animals Cardiovascular Diseases - metabolism Cardiovascular Diseases - pathology Cell Differentiation - drug effects Exercise Gene Expression Regulation - drug effects Glucose Tolerance Test Humans Induced Pluripotent Stem Cells - drug effects Induced Pluripotent Stem Cells - metabolism Liver - drug effects Liver - metabolism Metabolic Diseases - metabolism Metabolic Diseases - pathology Mice Organ Specificity - drug effects Organ Specificity - genetics Oxidation-Reduction - drug effects Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha Phenotype Physical Conditioning, Animal PPAR alpha - metabolism Risk Factors Transcription Factors - metabolism Transcription, Genetic - drug effects Weight Gain - drug effects |
| Title | β-Aminoisobutyric acid induces browning of white fat and hepatic β-oxidation and is inversely correlated with cardiometabolic risk factors |
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