The following study was conducted by Scientists from UCSF Diabetes Center, San Francisco, USA; Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research, San Francisco, CA, USA; Department of Cell and Tissue Biology, University of California, San Francisco, USA; Department of Electrical Engineering, Department of Materials Science and Engineering, Stanford University, USA; Chan Zuckerberg Biohub, San Francisco, CA, USA. Study is published in Nature Communications Journal as detailed below.
Nature Communications; Volume 11, Article Number: 1730; (2020)
Wireless Optogenetics Protects Against Obesity via Stimulation of Non-Canonical Fat Thermogenesis
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.
Source:
Nature Communications
URL: https://www.nature.com/articles/s41467-020-15589-y
Citation:
Tajima, K., K. Ikeda, et al. (2020). “Wireless optogenetics protects against obesity via stimulation of non-canonical fat thermogenesis.” Nature Communications 11(1): 1730.
