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Allostatic hypermetabolic response in PGC1α/β heterozygote mouse despite mitochondrial defects

Rodriguez-Cuenca, Sergio (författare)
Wellcome-MRC Institute of Metabolic Science, University of Cambridge, Cambridge, UK
Lelliot, Christopher J. (författare)
Discovery Sciences, BioPharmaceuticals R&D, AstraZeneca, Gothenburg, Sweden
Campbell, Mark (författare)
Wellcome-MRC Institute of Metabolic Science, University of Cambridge, Cambridge, UK
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Peddinti, Gopal (författare)
VTT, Technical Research Center of Finland, Espoo, Finland
Martinez-Uña, Maite (författare)
Department of Physiology, University of the Basque Country UPV/EHU, Bilbao, Spain
Ingvorsen, Camilla (författare)
Wellcome-MRC Institute of Metabolic Science, University of Cambridge, Cambridge, UK
Dias, Ana Rita (författare)
Wellcome-MRC Institute of Metabolic Science, University of Cambridge, Cambridge, UK
Relat, Joana (författare)
Department of Nutrition, Food Science and Gastronomy, School of Pharmacy and Food Science, Food and Nutrition Torribera Campus, University of Barcelona (UB), Santa Coloma de Gramenet, Spain; INSA-UB, Nutrition and Food Safety Research Institute, University of Barcelona, Barcelona, Spain
Mora, Silvia (författare)
Department of Cellular and Molecular Physiology, Institute of Translational Medicine, The University of Liverpool, Liverpool, UK
Hyötyläinen, Tuulia, 1971- (författare)
Örebro universitet,Institutionen för naturvetenskap och teknik
Zorzano, Antonio (författare)
Institute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology, Barcelona, Spain; Dept. Biochemistry and Molecular Biomedicine, University of Barcelona, Barcelona, Spain; Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Instituto de Salud Carlos III, Madrid, Spain
Oresic, Matej, 1967- (författare)
Örebro universitet,Institutionen för medicinska vetenskaper,Turku Bioscience Centre, University of Turku and Åbo Akademi University, Turku, Finland
Bjursell, Mikael (författare)
Discovery Sciences, BioPharmaceuticals R&D, AstraZeneca, Gothenburg, Sweden
Bohlooly-Y, Mohammad (författare)
Discovery Sciences, BioPharmaceuticals R&D, AstraZeneca, Gothenburg, Sweden
Lindén, Daniel (författare)
Research and Early Development Cardiovascular, Renal and Metabolism, BioPharmaceuticals R&D, AstraZeneca, Gothenburg, Sweden; Division of Endocrinology, Department of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden
Vidal-Puig, Antonio (författare)
Wellcome-MRC Institute of Metabolic Science, University of Cambridge, Cambridge, UK; Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, UK
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 (creator_code:org_t)
John Wiley & Sons, 2021
2021
Engelska.
Ingår i: The FASEB Journal. - : John Wiley & Sons. - 0892-6638 .- 1530-6860. ; 35:9
Relaterad länk:
https://doi.org/10.1...
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https://urn.kb.se/re...
https://doi.org/10.1...
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  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
Stäng  
  • Aging, obesity, and insulin resistance are associated with low levels of PGC1α and PGC1β coactivators and defective mitochondrial function. We studied mice deficient for PGC1α and PGC1β [double heterozygous (DH)] to investigate their combined pathogenic contribution. Contrary to our hypothesis, DH mice were leaner, had increased energy dissipation, a pro-thermogenic profile in BAT and WAT, and improved carbohydrate metabolism compared to wild types. WAT showed upregulation of mitochondriogenesis/oxphos machinery upon allelic compensation of PGC1α4 from the remaining allele. However, DH mice had decreased mitochondrial OXPHOS and biogenesis transcriptomes in mitochondria-rich organs. Despite being metabolically healthy, mitochondrial defects in DH mice impaired muscle fiber remodeling and caused qualitative changes in the hepatic lipidome. Our data evidence first the existence of organ-specific compensatory allostatic mechanisms are robust enough to drive an unexpected phenotype. Second, optimization of adipose tissue bioenergetics is sufficient to maintain a healthy metabolic phenotype despite a broad severe mitochondrial dysfunction in other relevant metabolic organs. Third, the decrease in PGC1s in adipose tissue of obese and diabetic patients is in contrast with the robustness of the compensatory upregulation in the adipose of the DH mice.

Ämnesord

MEDICIN OCH HÄLSOVETENSKAP  -- Medicinska och farmaceutiska grundvetenskaper -- Fysiologi (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Basic Medicine -- Physiology (hsv//eng)

Nyckelord

PGC-1alpha
adipose tissue
hepatic lipidome
lipotoxicity
mitochondrial dysfunction

Publikations- och innehållstyp

ref (ämneskategori)
art (ämneskategori)

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