Ablation of PGC-1beta results in defective mitochondrial activity, thermogenesis, hepatic function, and cardiac performance

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Ablation of PGC-1beta results in defective mitochondrial activity, thermogenesis, hepatic function, and cardiac performance

Lelliott, Christopher J. (author): Department of Clinical Biochemistry, University of Cambridge, Cambridge, United Kingdom; AstraZeneca R&D, Mölndal, Sweden

Medina-Gomez, Gema (author): Department of Clinical Biochemistry, University of Cambridge, Cambridge, United Kingdom

Petrovic, Natasa (author): The Wenner-Gren Institute, Stockholm University, Stockholm, Sweden

Kis, Adrienn (author): Department of Clinical Biochemistry, University of Cambridge, Cambridge, United Kingdom

Feldmann, Helena M. (author): The Wenner-Gren Institute, Stockholm University, Stockholm, Sweden

Bjursell, Mikael (author): AstraZeneca R&D, Mölndal, Sweden

Parker, Nadeene (author): Department of Clinical Biochemistry, University of Cambridge, Cambridge, United Kingdom

Curtis, Keira (author): Department of Clinical Biochemistry, University of Cambridge, Cambridge, United Kingdom

Campbell, Mark (author): Department of Clinical Biochemistry, University of Cambridge, Cambridge, United Kingdom

Hu, Ping (author): Division of Cardiology, University of Utah, Salt Lake City, Utah, United States of America

Zhang, Dongfang (author): Division of Cardiology, University of Utah, Salt Lake City, Utah, United States of America

Litwin, Sheldon E. (author): Division of Cardiology, University of Utah, Salt Lake City, Utah, United States of America

Zaha, Vlad G. (author): Division of Endocrinology, Metabolism, and Diabetes and Program in Human Molecular Biology and Genetics, University of Utah, Salt Lake City, Utah, United States of America

Fountain, Kimberly T. (author): Division of Endocrinology, Metabolism, and Diabetes and Program in Human Molecular Biology and Genetics, University of Utah, Salt Lake City, Utah, United States of America

Boudina, Sihem (author): Division of Endocrinology, Metabolism, and Diabetes and Program in Human Molecular Biology and Genetics, University of Utah, Salt Lake City, Utah, United States of America

Jimenez-Linan, Mercedes (author): Department of Clinical Biochemistry, University of Cambridge, Cambridge, United Kingdom

Blount, Margaret (author): Department of Clinical Biochemistry, University of Cambridge, Cambridge, United Kingdom

Lopez, Miguel (author): Department of Clinical Biochemistry, University of Cambridge, Cambridge, United Kingdom

Meirhaeghe, Aline (author): INSERM, Institut Pasteur de Lille, Lille Cedex, France

Bohlooly-Y, Mohammad (author): AstraZeneca R&D, Mölndal, Sweden

Storlien, Leonard (author): AstraZeneca R&D, Mölndal, Sweden

Strömstedt, Maria (author): AstraZeneca R&D, Mölndal, Sweden

Snaith, Michael (author): AstraZeneca R&D, Mölndal, Sweden

Oresic, Matej, 1967- (author): VTT Technical Research Centre of Finland, Espoo, Finland

Abel, E. Dale (author): Division of Endocrinology, Metabolism, and Diabetes and Program in Human Molecular Biology and Genetics, University of Utah, Salt Lake City, Utah, United States of America

Cannon, Barbara (author): The Wenner-Gren Institute, Stockholm University, Stockholm, Sweden

Vidal-Puig, Antonio (author): Department of Clinical Biochemistry, University of Cambridge, Cambridge, United Kingdom

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2006-11-07
2006
English.
In: PLoS biology. - : Public Library of Science (PLoS). - 1544-9173 .- 1545-7885. ; 4:11

Related links:: https://doi.org/10.1...; show more...; https://journals.plo...; https://urn.kb.se/re...; https://doi.org/10.1...; show less...

Journal article (peer-reviewed)

Abstract Subject headings

The transcriptional coactivator peroxisome proliferator-activated receptor-gamma coactivator-1beta (PGC-1beta) has been implicated in important metabolic processes. A mouse lacking PGC-1beta (PGC1betaKO) was generated and phenotyped using physiological, molecular, and bioinformatic approaches. PGC1betaKO mice are generally viable and metabolically healthy. Using systems biology, we identified a general defect in the expression of genes involved in mitochondrial function and, specifically, the electron transport chain. This defect correlated with reduced mitochondrial volume fraction in soleus muscle and heart, but not brown adipose tissue (BAT). Under ambient temperature conditions, PGC-1beta ablation was partially compensated by up-regulation of PGC-1alpha in BAT and white adipose tissue (WAT) that lead to increased thermogenesis, reduced body weight, and reduced fat mass. Despite their decreased fat mass, PGC1betaKO mice had hypertrophic adipocytes in WAT. The thermogenic role of PGC-1beta was identified in thermoneutral and cold-adapted conditions by inadequate responses to norepinephrine injection. Furthermore, PGC1betaKO hearts showed a blunted chronotropic response to dobutamine stimulation, and isolated soleus muscle fibres from PGC1betaKO mice have impaired mitochondrial function. Lack of PGC-1beta also impaired hepatic lipid metabolism in response to acute high fat dietary loads, resulting in hepatic steatosis and reduced lipoprotein-associated triglyceride and cholesterol content. Altogether, our data suggest that PGC-1beta plays a general role in controlling basal mitochondrial function and also participates in tissue-specific adaptive responses during metabolic stress.

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MEDICAL AND HEALTH SCIENCES: MEDICAL AND HEAL ...; and Basic Medicine; and Other Basic Medi ...

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By the university: Örebro University

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Ablation of PGC-1beta results in defective mitochondrial activity, thermogenesis, hepatic function, and cardiac performance

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