Il est maintenant bien connu que l'ob茅sit茅 peut 锚tre un contributeur majeur au cancer. Une nouvelle 茅tude听du Centre de recherche sur le cancer Rosalind听et Morris Goodman publi茅e dans Nature met en lumi猫re la fa莽on dont l'ob茅sit茅 est r茅gul茅e par le tissu adipeux brun.
Janane F. Rahbani du laboratoire Kazak a d茅couvert comment l'utilisation de l'茅nergie dans les adipocytes (autrement appel茅s 芦cellules graisseuses禄) pouvait conduire 脿 des th茅rapies visant 脿 normaliser ces fonctions tissulaires dans le contexte d'une maladie m茅tabolique.
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Contributions des plateformes听de 苹果淫院
- Metabolomics Core - Daina Avizonis
- Transgenic Core (MICAM) - Mitra Cowan et听Jade Desjardins
- ABIF (Advanced BioImaging Facility)
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搁茅蝉耻尘茅
Obesity increases the risk of mortality because of metabolic sequelae such as type 2 diabetes and cardiovascular disease. Thermogenesis by adipocytes can counteract obesity and metabolic diseases,. In thermogenic fat, creatine liberates a molar excess of mitochondrial ADP鈥攑urportedly via a phosphorylation cycle鈥攖o drive thermogenic respiration. However, the proteins that control this futile creatine cycle are unknown. Here we show that creatine kinase B (CKB) is indispensable for thermogenesis resulting from the futile creatine cycle, during which it traffics to mitochondria using an internal mitochondrial targeting sequence. CKB is powerfully induced by thermogenic stimuli in both mouse and human adipocytes. Adipocyte-selective inactivation of听Ckb听in mice diminishes thermogenic capacity, increases predisposition to obesity, and disrupts glucose homeostasis. CKB is therefore a key effector of the futile creatine cycle.
