AsianScientist (Mar. 22, 2016) – Japanese researchers have shown that the lack of a protein called transient receptor potential vanilloid 2 (TRPV2) impairs thermogenesis, or heat production, in brown adipose tissue (BAT) in mice. The mice lacking this protein were more susceptible to obesity after being fed a high fat diet.
Therefore, the activation of TRPV2 in BAT could be an intriguing approach for human obesity prevention and treatment. The research team’s findings were published online in EMBO reports.
The primary function of BAT, or brown fat, is to generate body heat and regulate body temperature in animals or newborns that do not shiver. TRPV2, a Ca2+-permeable cation channel, on the other hand, plays vital roles in the regulation of various cellular functions.
A team made up of researchers from the National Institute for Physiological Sciences, Kyoto University and the National Cerebral and Cardiovascular Center have successfully developed TRPV2 knockout (TRPV2KO) mice, and demonstrated that TRPV2 is expressed in brown fat cells. In the TRPV2KO mice, mRNA levels of thermogenic genes are reduced in both cultured brown fat cells and BAT.
The researchers also found that TRPV2KO brown adipocytes had a lower induction of thermogenic genes when stimulated with β-adrenergic receptor stimulation which downstream of the sympathetic nerve activation.
In addition, TRPV2KO mice had more white adipose tissue and larger brown fat cells, and could not keep constant body temperature of around 37°C upon cold exposure at 4°C. TRPV2KO mice also had increased body weight and fat upon high fat diet treatment, which can be explained by their low thermogenic ability.
Based on these findings, the researchers concluded that TRPV2 plays a role in BAT thermogenesis, and could be a target for human obesity therapy.
The article can be found at: Sun et al. (2016) Lack of TRPV2 Impairs Thermogenesis in Mouse Brown dAipose Tissue.
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Source: National Institutes of Natural Sciences; Photo: Shutterstock.
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