You are currently viewing the editor's summary.
View Full TextLog in to view the full text
AAAS login provides access to Science for AAAS members, and access to other journals in the Science family to users who have purchased individual subscriptions.
Register for free to read this article
As a service to the community, this article is available for free. Existing users log in.
More options
Download and print this article for your personal scholarly, research, and educational use.
Buy a single issue of Science for just $15 USD.
BAT Signal
The high numbers of mitochondria in brown adipose tissue (BAT) oxidize fat to produce heat (a process referred to as thermogenesis). Thus, increasing the amount or activity of BAT has been proposed as a potential method of countering metabolic diseases such as obesity and type II diabetes; however, the signaling pathways that regulate the differentiation of BAT have not been completely elucidated. Haas et al. have uncovered a key role for protein kinase G I (PKGI) in the differentiation and thermogenic function of BAT. Brown fat cells from mice lacking PKGI had lower mitochondrial content and reduced amounts of adipogenic factors compared to those from wild-type mice. Strikingly, PKGI-deficient mice exhibited lower body temperatures than those of wild-type mice. Thus, treatments that increase the activity of the PKGI pathway in BAT could enhance BAT function and its calorie-burning effects.
