Instructor | ||
Ph.D.: 2013 South China Normal University | ||
Postdoctoral research: UMass Chan Medical School | ||
Office: | UMass Chan Medical School 364 Plantation Street, LRB-570-X Worcester, MA 01605 |
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Phone: | 508-856-5635 | |
Email: | Lei.Huang@umassmed.edu |
Research
My research interests are focused on understanding epigenetic and transcriptional regulation of brown fat (BAT) development and inguinal white adipose tissue (iWAT) browning. Adipose tissue that mediates lipid storage and mobilization is a remarkably complex organ and plays a crucial role in glucose balance and energy homeostasis. In particular, brown adipose tissue (BAT) and brown-like adipocytes (also called beige adipocytes) are characterized by mobilization of fuels and dissipation of the stored chemical energy as heat in humans and rodents, mainly mediated through a process named adaptive thermogenesis. In contrast, white adipose tissue (WAT) is responsible for energy storage in times of excessive nutrients. The dysfunction of adaptive thermogenesis contributes to metabolic disorders and associated diseases, including obesity, hypertension, cardiovascular diseases, and type II diabetes. My first project explored Jumonji domain-containing protein D3 (JMJD3) functions on BAT development and white fat plasticity using cell and mouse models (Developmental Cell, 2015 Dec 7; 35:568-583). Further, I investigated a crucial transcription factor H2.0 homo box protein (HLX) enriched in BAT, and I deeply explored the roles of HLX in iWAT browning and the related molecular mechanism (Nature Communications, 2017 Jul 12; 8:68). Recently, I identified a KRAB domain-containing protein zfp961 repressing adipose thermogenesis and energy expenditure through interaction with PPARα (Advanced Science, 2021 in press)