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Juli Bai, Ph.D was an associate professor of Environmental Medicine Institution at Shanxi University and a postdoctoral fellow of Department of Pharmacology at the University of Texas Health at San Antonio. Her research during her doctorate studies was in the molecular and biological mechanism of carcinogenesis and apoptosis induced by environmental factors. Subsequently, she has headed an independent research laboratory focusing on environmental medicine study and found environmental factors play very important roles in regulating metabolic disorders. Then she started her research in the area of glucose-fatty acid metabolic disorders and its molecular mechanisms. She has authored or co-authored over 30 manuscripts and 2 book chapters in the field of metabolism, environmental science and received awards for advanced research.
Obesity has reached epidemic proportions globally and is associated with various metabolic diseases such as type II diabetes, cardiovascular disease, and many types of cancer. My long term research interest is to determine the mechanisms of key molecules and its regulation on critical metabolic signaling pathway which is associated with the development of metabolic disease such as obesity and diabetes. Chronic sterile inflammation in white adipose tissue, a major depot for chemical energy storage and for hormone and cytokine production in response to nutritional and environmental changes, plays a key role in triggering insulin resistance and associated metabolic diseases. In contrast to white adipose tissue, the major function of brown adipose tissue and beige adipose tissue is to dissipate chemical energy as heat via high levels of mitochondrial uncoupling protein 1 to counteract hypothermia and obesity. It is our hope that better understanding of the mechanism underlying the regulation of thermogenesis and inflammation will provide important information for the treatment of obesity-associated metabolic disorders.
|Juli Bai, Jianzhong He and Yingying Gao|
|Editorial: J Biores Commun 2017, 1:e104|
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