It is now well-known that obesity can be a major contributor to cancer. New research by the Rosalind and Morris Goodman Cancer Research Centre published听in Nature shines a light on how obesity is regulated by brown adipose tissue.
Janane F. Rahbani from the Kazak Lab has uncovered how the energy utilization in adipocytes (otherwise known as 鈥渇at cells鈥�) may lead to therapies aimed at normalizing these tissue functions in the context of metabolic disease.
Read the full study here:
Contributions from McGill Core Facilities
- Metabolomics Core - Daina Avizonis
- Transgenic Core (MICAM) - Mitra Cowan and Jade Desjardins
- ABIF (Advanced BioImaging Facility)
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Abstract
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.
