Wireless optogenetics protects against obesity via stimulation of non-canonical fat thermogenesis

Kazuki Tajima, Kenji Ikeda, Yuji Tanabe, Ella A. Thomson, Takeshi Yoneshiro, Yasuo Oguri, Marc D. Ferro, Ada S. Y. Poon () and Shingo Kajimura ()
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Kazuki Tajima: UCSF Diabetes Center
Kenji Ikeda: UCSF Diabetes Center
Yuji Tanabe: Stanford University
Ella A. Thomson: Stanford University
Takeshi Yoneshiro: UCSF Diabetes Center
Yasuo Oguri: UCSF Diabetes Center
Marc D. Ferro: Stanford University
Ada S. Y. Poon: Stanford University
Shingo Kajimura: UCSF Diabetes Center

Nature Communications, 2020, vol. 11, issue 1, 1-10

Abstract: Abstract Cold stimuli and the subsequent activation of β-adrenergic receptor (β-AR) potently stimulate adipose tissue thermogenesis and increase whole-body energy expenditure. However, systemic activation of the β3-AR pathway inevitably increases blood pressure, a significant risk factor for cardiovascular disease, and, thus, limits its application for the treatment of obesity. To activate fat thermogenesis under tight spatiotemporal control without external stimuli, here, we report an implantable wireless optogenetic device that bypasses the β-AR pathway and triggers Ca2+ cycling selectively in adipocytes. The wireless optogenetics stimulation in the subcutaneous adipose tissue potently activates Ca2+ cycling fat thermogenesis and increases whole-body energy expenditure without cold stimuli. Significantly, the light-induced fat thermogenesis was sufficient to protect mice from diet-induced body-weight gain. The present study provides the first proof-of-concept that fat-specific cold mimetics via activating non-canonical thermogenesis protect against obesity.

Date: 2020
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DOI: 10.1038/s41467-020-15589-y

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