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Oct 11, 2012
 |  BC Innovations  |  Cover Story

Ember: warming up to brown fat

A team led by Boston-area researchers has shown that inhibiting a cation channel dubbed TRPV4 induced white fat cells to behave like brown fat, thereby protecting mice from diet-induced obesity and insulin resistance.1Ember Therapeutics Inc. has options to in-license the findings as a part of a trio of new deals for brown fat-related targets.

Brown adipose tissue (BAT), or brown fat, has a high mitochondrial content that allows it to burn and dissipate chemical energy as heat more efficiently than white adipose and other tissues. Although human adults have only small deposits of brown fat compared with infants and rodents, a potential strategy for treating obesity and related metabolic conditions is inducing white adipose tissue to take on the mitochondrial and thermogenic properties of brown fat-an approach known as browning.

Peroxisome proliferation-activated receptor-g coactivator 1α (PPARGC1A; PGC-1a) is a key player in oxidative metabolism and thermogenesis in multiple tissue types,2 and a previous study by the Boston team found that exposure to cold and other factors upregulated PGC-1a in brown fat and skeletal muscle.3

Thus, the researchers postulated that compounds that induced PGC-1a expression-directly or indirectly-could help treat metabolic diseases.

The team screened small molecule libraries for compounds that upregulated Pgc-1a in mouse white adipocytes and identified two hits that were known antagonists of transient receptor potential vanilloids (TRPVs), a subfamily of the transient receptor potential ion channels.

To determine if any of the six TRPVs known in humans and mice played a predominant role in activating Pgc-1a, the team...

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