ESPE Yearbook of Paediatric Endocrinology

ESPE Yearbook of Paediatric Endocrinology

ISSN 1662-4009 (online)

Published by BioScientifica

Page 1 of about 2 results

ey0016.11-6 | Tracking, Programming, and Epigenetics | ESPEYB16

11.6. Adipose tissue mitochondrial dysfunction in human obesity is linked to a specific DNA methylation signature in adipose-derived stem cells

M Ejarque , V Ceperuelo-Mallafre , C Serena , E Maymo-Masip , X Duran , A Diaz-Ramos , M Millan-Scheiding , Y Nunez-Alvarez , C Nunez-Roa , P Gama , PM Garcia-Roves , MA Peinado , JM Gimble , A Zorzano , J Vendrell , S Fernandez-Veledo

To read the full abstract: Int J Obes (Lond). 2019;43(6):1256–1268This epigenome-wide association study in stromal/stem cells (ASCs), derived from subcutaneous adipose tissue samples of lean and obese subjects, revealed a specific DNA methylation signature in adipocyte precursors associated with obesity, which has a significant impact on the metabolic phenotype and the mitochondrial...
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ey0020.9-4 | New Findings in Adipose Tissue | ESPEYB20

9.4. SUCNR1 signaling in adipocytes controls energy metabolism by modulating circadian clock and leptin expression

T Villanueva-Carmona , L Cedo , A Madeira , V Ceperuelo-Mallafre , M Rodriguez-Pena , C Nunez-Roa , E Maymo-Masip , M Repolles-de-Dalman , J Badia , N Keiran , M Mirasierra , C Pimenta-Lopes , J Sabadell-Basallote , R Bosch , L Caubet , JC Escola-Gil , JM Fernandez-Real , N Vilarrasa , F Verntura , M Vallejo , J Vendrell , S Fernandez-Veledo

Brief summary: Villanueva-Carmona et al. identified succinate as a mediating metabolite in leptin secretion. Its action is mediated by the succinate receptor SUCNR in adipocytes via the circadian clock in an AMPK/JNK-C/EBPa-dependent manner.Although the regulatory circuits of leptin action on hunger and satiety are well understood, the pathways that mediate acute leptin production in the adipose tissue are less investigated. To investigate how a...
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Published by BioScientifica

ESPE Yearbook of Paediatric Endocrinology
ISSN 1662-4009 (Online)
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