The Bile Acid Chenodeoxycholic Acid Increases Human Brown Adipose Tissue Activity

The interest in brown adipose tissue (BAT) as a target to combat metabolic disease has recently been renewed with the discovery of functional BAT in humans. In rodents, BAT can be activated by bile acids, which activate type 2 iodothyronine deiodinase (D2) in BAT via the G-coupled protein receptor T...

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Vydané v:	Cell metabolism Ročník 22; číslo 3; s. 418
Hlavní autori:	Broeders, Evie P M, Nascimento, Emmani B M, Havekes, Bas, Brans, Boudewijn, Roumans, Kay H M, Tailleux, Anne, Schaart, Gert, Kouach, Mostafa, Charton, Julie, Deprez, Benoit, Bouvy, Nicole D, Mottaghy, Felix, Staels, Bart, van Marken Lichtenbelt, Wouter D, Schrauwen, Patrick
Médium:	Journal Article
Jazyk:	English
Vydavateľské údaje:	United States 01.09.2015
Predmet:	Adipocytes, Brown - drug effects Adipocytes, Brown - metabolism Adipose Tissue, Brown - drug effects Adipose Tissue, Brown - metabolism Administration, Oral Adult Cells, Cultured Chenodeoxycholic Acid - administration & dosage Chenodeoxycholic Acid - blood Chenodeoxycholic Acid - pharmacology Energy Metabolism - drug effects Female Humans Receptors, G-Protein-Coupled - metabolism Signal Transduction - drug effects Young Adult
ISSN:	1932-7420, 1932-7420
On-line prístup:	Zistit podrobnosti o prístupe
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Abstract	The interest in brown adipose tissue (BAT) as a target to combat metabolic disease has recently been renewed with the discovery of functional BAT in humans. In rodents, BAT can be activated by bile acids, which activate type 2 iodothyronine deiodinase (D2) in BAT via the G-coupled protein receptor TGR5, resulting in increased oxygen consumption and energy expenditure. Here we examined the effects of oral supplementation of the bile acid chenodeoxycholic acid (CDCA) on human BAT activity. Treatment of 12 healthy female subjects with CDCA for 2 days resulted in increased BAT activity. Whole-body energy expenditure was also increased upon CDCA treatment. In vitro treatment of primary human brown adipocytes derived with CDCA or specific TGR5 agonists increased mitochondrial uncoupling and D2 expression, an effect that was absent in human primary white adipocytes. These findings identify bile acids as a target to activate BAT in humans.
AbstractList	The interest in brown adipose tissue (BAT) as a target to combat metabolic disease has recently been renewed with the discovery of functional BAT in humans. In rodents, BAT can be activated by bile acids, which activate type 2 iodothyronine deiodinase (D2) in BAT via the G-coupled protein receptor TGR5, resulting in increased oxygen consumption and energy expenditure. Here we examined the effects of oral supplementation of the bile acid chenodeoxycholic acid (CDCA) on human BAT activity. Treatment of 12 healthy female subjects with CDCA for 2 days resulted in increased BAT activity. Whole-body energy expenditure was also increased upon CDCA treatment. In vitro treatment of primary human brown adipocytes derived with CDCA or specific TGR5 agonists increased mitochondrial uncoupling and D2 expression, an effect that was absent in human primary white adipocytes. These findings identify bile acids as a target to activate BAT in humans.The interest in brown adipose tissue (BAT) as a target to combat metabolic disease has recently been renewed with the discovery of functional BAT in humans. In rodents, BAT can be activated by bile acids, which activate type 2 iodothyronine deiodinase (D2) in BAT via the G-coupled protein receptor TGR5, resulting in increased oxygen consumption and energy expenditure. Here we examined the effects of oral supplementation of the bile acid chenodeoxycholic acid (CDCA) on human BAT activity. Treatment of 12 healthy female subjects with CDCA for 2 days resulted in increased BAT activity. Whole-body energy expenditure was also increased upon CDCA treatment. In vitro treatment of primary human brown adipocytes derived with CDCA or specific TGR5 agonists increased mitochondrial uncoupling and D2 expression, an effect that was absent in human primary white adipocytes. These findings identify bile acids as a target to activate BAT in humans. The interest in brown adipose tissue (BAT) as a target to combat metabolic disease has recently been renewed with the discovery of functional BAT in humans. In rodents, BAT can be activated by bile acids, which activate type 2 iodothyronine deiodinase (D2) in BAT via the G-coupled protein receptor TGR5, resulting in increased oxygen consumption and energy expenditure. Here we examined the effects of oral supplementation of the bile acid chenodeoxycholic acid (CDCA) on human BAT activity. Treatment of 12 healthy female subjects with CDCA for 2 days resulted in increased BAT activity. Whole-body energy expenditure was also increased upon CDCA treatment. In vitro treatment of primary human brown adipocytes derived with CDCA or specific TGR5 agonists increased mitochondrial uncoupling and D2 expression, an effect that was absent in human primary white adipocytes. These findings identify bile acids as a target to activate BAT in humans.
Author	Broeders, Evie P M Mottaghy, Felix Roumans, Kay H M Deprez, Benoit Schaart, Gert Nascimento, Emmani B M Tailleux, Anne Brans, Boudewijn van Marken Lichtenbelt, Wouter D Schrauwen, Patrick Havekes, Bas Bouvy, Nicole D Staels, Bart Charton, Julie Kouach, Mostafa
Author_xml	– sequence: 1 givenname: Evie P M surname: Broeders fullname: Broeders, Evie P M organization: Department of Human Biology and Human Movement Sciences, NUTRIM, School for Nutrition and Translational Research in Metabolism, Maastricht University Medical Center, Maastricht 6200 MD, the Netherlands; Department of General Surgery, NUTRIM, School for Nutrition and Translational Research in Metabolism, Maastricht University Medical Center, Maastricht 6200 MD, the Netherlands – sequence: 2 givenname: Emmani B M surname: Nascimento fullname: Nascimento, Emmani B M organization: Department of Human Biology and Human Movement Sciences, NUTRIM, School for Nutrition and Translational Research in Metabolism, Maastricht University Medical Center, Maastricht 6200 MD, the Netherlands – sequence: 3 givenname: Bas surname: Havekes fullname: Havekes, Bas organization: Department of Endocrinology, NUTRIM, School for Nutrition and Translational Research in Metabolism, Maastricht University Medical Center, Maastricht 6200 MD, the Netherlands – sequence: 4 givenname: Boudewijn surname: Brans fullname: Brans, Boudewijn organization: Department of Nuclear Medicine, NUTRIM, School for Nutrition and Translational Research in Metabolism, Maastricht University Medical Center, Maastricht 6200 MD, the Netherlands – sequence: 5 givenname: Kay H M surname: Roumans fullname: Roumans, Kay H M organization: Department of Human Biology and Human Movement Sciences, NUTRIM, School for Nutrition and Translational Research in Metabolism, Maastricht University Medical Center, Maastricht 6200 MD, the Netherlands – sequence: 6 givenname: Anne surname: Tailleux fullname: Tailleux, Anne organization: University of Lille, Institut Pasteur de Lille, Inserm UMR 1011, EGID, 59000 Lille, France – sequence: 7 givenname: Gert surname: Schaart fullname: Schaart, Gert organization: Department of Human Biology and Human Movement Sciences, NUTRIM, School for Nutrition and Translational Research in Metabolism, Maastricht University Medical Center, Maastricht 6200 MD, the Netherlands – sequence: 8 givenname: Mostafa surname: Kouach fullname: Kouach, Mostafa organization: University of Lille, Centre Universitaire de Mesures et d'Analyses, 59000 Lille, France – sequence: 9 givenname: Julie surname: Charton fullname: Charton, Julie organization: University of Lille, Institut Pasteur de Lille, Inserm UMR1177, Biostructures and Drug Discovery, 59000 Lille, France – sequence: 10 givenname: Benoit surname: Deprez fullname: Deprez, Benoit organization: University of Lille, Institut Pasteur de Lille, Inserm UMR1177, Biostructures and Drug Discovery, 59000 Lille, France – sequence: 11 givenname: Nicole D surname: Bouvy fullname: Bouvy, Nicole D organization: Department of General Surgery, NUTRIM, School for Nutrition and Translational Research in Metabolism, Maastricht University Medical Center, Maastricht 6200 MD, the Netherlands – sequence: 12 givenname: Felix surname: Mottaghy fullname: Mottaghy, Felix organization: Department of Nuclear Medicine, NUTRIM, School for Nutrition and Translational Research in Metabolism, Maastricht University Medical Center, Maastricht 6200 MD, the Netherlands; Nuclear Medicine, University Hospital Aachen, 52072 Aachen, Germany – sequence: 13 givenname: Bart surname: Staels fullname: Staels, Bart organization: University of Lille, Institut Pasteur de Lille, Inserm UMR 1011, EGID, 59000 Lille, France – sequence: 14 givenname: Wouter D surname: van Marken Lichtenbelt fullname: van Marken Lichtenbelt, Wouter D organization: Department of Human Biology and Human Movement Sciences, NUTRIM, School for Nutrition and Translational Research in Metabolism, Maastricht University Medical Center, Maastricht 6200 MD, the Netherlands – sequence: 15 givenname: Patrick surname: Schrauwen fullname: Schrauwen, Patrick email: p.schrauwen@maastrichtuniversity.nl organization: Department of Human Biology and Human Movement Sciences, NUTRIM, School for Nutrition and Translational Research in Metabolism, Maastricht University Medical Center, Maastricht 6200 MD, the Netherlands. Electronic address: p.schrauwen@maastrichtuniversity.nl
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PublicationTitle	Cell metabolism
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Snippet	The interest in brown adipose tissue (BAT) as a target to combat metabolic disease has recently been renewed with the discovery of functional BAT in humans. In...
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SubjectTerms	Adipocytes, Brown - drug effects Adipocytes, Brown - metabolism Adipose Tissue, Brown - drug effects Adipose Tissue, Brown - metabolism Administration, Oral Adult Cells, Cultured Chenodeoxycholic Acid - administration & dosage Chenodeoxycholic Acid - blood Chenodeoxycholic Acid - pharmacology Energy Metabolism - drug effects Female Humans Receptors, G-Protein-Coupled - metabolism Signal Transduction - drug effects Young Adult
Title	The Bile Acid Chenodeoxycholic Acid Increases Human Brown Adipose Tissue Activity
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