Journal
OBESITY REVIEWS
Volume 10, Issue 3, Pages 265-268Publisher
WILEY-BLACKWELL PUBLISHING, INC
DOI: 10.1111/j.1467-789X.2008.00559.x
Keywords
Brown adipose tissue; obesity; PRDM16
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Funding
- NIDDK NIH HHS [P30 DK072476] Funding Source: Medline
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [P30DK072476] Funding Source: NIH RePORTER
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In the 1970s and 1980s, it was observed that rodents could offset excess calories ingested when they were fed a human-like 'cafeteria diet'. Although it was erroneously concluded that this so-called diet-induced thermogenesis was because of brown adipose tissue (BAT), it led to efforts to test whether variations in brown fat in humans may explain the susceptibility to obesity. However, from evidence on the inability of ephedrine or beta-3 adrenergic agonists to induce BAT thermogenesis, it was concluded that the thermogenic role of BAT was unimportant in adult humans largely because humans had low numbers of brown adipocytes. Solid evidence on the actual numbers of brown adipocytes in humans was not available. We are now re-evaluating the role of BAT for the treatment of obesity given the following recent observations (i) studies in nuclear medicine by using PET/CT scanning reveal the presence of BAT in adult humans; and (ii) recent data suggest that a new transcription factor called PDRM16 may control the induction of BAT. These recent discoveries should revamp our effort to target the molecular development of brown adipogenesis in the treatment of obesity.
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