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Spatial Regulation of Reactive Oxygen Species via G6PD in Brown Adipocytes Supports Thermogenic Function

Cited 8 time in Web of Science Cited 10 time in Scopus

Sohn, Jee Hyung; Ji, Yul; Cho, Chang-Yun; Nahmgoong, Hahn; Lim, Sangsoo; Jeon, Yong Geun; Han, Sang Mun; Han, Ji Seul; Park, Isaac; Rhee, Hyun-Woo; Kim, Sun; Kim, Jae Bum

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American Diabetes Association
Diabetes, Vol.70 No.12, pp.2756-2770
© 2021 by the American Diabetes Association.Reactive oxygen species (ROS) are associated with various roles of brown adipocytes. Glucose-6-phosphate dehydrogenase (G6PD) controls cellular redox potentials by producing NADPH. Although G6PD upregulates cellular ROS levels in white adipocytes, the roles of G6PD in brown adipocytes remain elusive. Here, we found that G6PD defect in brown adipocytes impaired thermogenic function through excessive cytosolic ROS accumulation. Upon cold exposure, G6PD-deficient mutant (G6PDmut) mice exhibited cold intolerance and downregulated thermogenic gene expression in brown adipose tissue (BAT). In addition, G6PD-deficient brown adipocytes had increased cytosolic ROS levels, leading to extracellular signal-regulated kinase (ERK) activation. In BAT of G6PDmut mice, administration of antioxidant restored the thermogenic activity by potentiating thermogenic gene expression and relieving ERK activation. Consistently, body temperature and thermogenic execution were rescued by ERK inhibition in cold-exposed G6PDmut mice. Taken together, these data suggest that G6PD in brown adipocytes would protect against cytosolic oxidative stress, leading to cold-induced thermogenesis.
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