AccueilAccueil>L'équipe de Nicolas Venteclef publie le travail de Karima DRARENI dan Cell Reports

L'équipe de Nicolas Venteclef publie le travail de Karima DRARENI dan Cell Reports

L'équipe de Nicolas Venteclef publie le travail de Karima DRARENI intitulé "GPS2 Deficiency Triggers Maladaptive White Adipose Tissue Expansion in Obesity via HIF1A activation" dans « Cell Reports ».

 

  

Après avoir démontré l’importance du coregulateur transcriptionnel GPS2 dans le contrôle de l’inflammation du tissu adipeux (Toubal et al. JCI 2013 et Fan et al. NatMed 2016), le travail de Thèse de Karima Drareni permet de révéler l’implication de GPS2 dans la régulation de l’expansion du tissu adipeux au cours de l’obésité.

 

 

GPS2 Deficiency Triggers Maladaptive White Adipose Tissue Expansion in Obesity via HIF1A activation (Cell Rep. 2018 Sep 11;24(11):2957-2971.e6. doi: 10.1016/j.celrep.2018.08.032.)

Drareni et al.

Summary
Hypertrophic white adipose tissue (WAT) represents a maladaptive mechanism linked to the risk for developing type 2 diabetes in humans. However, the molecular events that predispose WAT to hypertrophy are poorly defined. Here, we demonstrate that adipocyte hypertrophy is triggered by loss of the corepressor GPS2 during obesity. Adipocyte-specific GPS2 deficiency in mice (GPS2 AKO) causes adipocyte hypertrophy, inflammation, and mitochondrial dysfunction during surplus energy. This phenotype is driven by HIF1A activation that orchestrates inadequate WAT remodeling and disrupts mitochondrial activity, which can be reversed by pharmacological or genetic HIF1A inhibition. Correlation analysis of gene expression in human adipose tissue reveals a negative relationship between GPS2 and HIF1A, adipocyte hypertrophy, and insulin resistance. We propose therefore that the obesity-associated loss of GPS2 in adipocytes predisposes for a maladaptive WAT expansion and a pro-diabetic status in mice and humans.

https://www.cell.com/cell-reports/fulltext/S2211-1247(18)31303-2
https://www.ncbi.nlm.nih.gov/pubmed/30208320

 

 

Les Outils