Dr Cheng, King Yip 鄭競業
Dr. Kenneth King-Yip Cheng is currently a Research Assistant Professor in the Department of Medicine, The University of Hong Kong. He graduated in 2003 with Bachelor of Science (Hons) from The Hong Kong University of Science & Technology and received his Ph.D. from The University of Hong Kong in 2009 after which did a post-doctoral fellowship at The University of Hong Kong. His research focuses on molecular mechanisms underlying obesity and its related metabolic disorders including insulin resistance, β-cell and endothelial dysfunction. He identified the adaptor protein APPL1 as a common regulator of both insulin and adiponectin signaling in various insulin-responsive tissues including liver, endothelium and pancreas, and the related findings have been published in Cell Metabolism, PNAS, Diabetes and Biochemical Journal and etc. (Please refer to Figure 1).
Maintenance of normal glucose levels requires tight coordination of insulin action and secretion. Type 2 diabetes mellitus (T2DM) is characterized by peripheral insulin resistance and pancreatic β-cell dysfunction. We have identified adaptor protein APPL1 as an important signaling regulator in both actions and secretion of insulin. Hepatic overexpression of APPL1 improves hyperglycemia, glucose intolerance and insulin sensitivity in diabetic mice, whereas hepatic silencing of APPL1 causes insulin resistance and hyperglycemia in lean mice. APPL1 can potentiate insulin-mediated activation of Akt, which in turn inhibits the expression of key genes involved in gluconeogenesis. In addition, APPL1 maintains the balance between vasodilation and vasoconstriction by fine-tuning the actions of insulin in endothelium.
Apart from modulating the actions of insulin, APPL1 is a positive regulator of insulin secretion in pancreatic ß cells. Genetic disruption of APPL1 impairs insulin secretion and causes glucose intolerance, whereas transgenic expression of APPL1 prevents dietary-induced glucose intolerance by potentiating insulin secretion. The pancreatic islets lacking APPL1 exhibit a significant reduction of number of docked insulin granules accompanied with decreased exocytosis of insulin as a result of profound decreased expression of exocytotic SNARE proteins, and such effects of APPL1 are mediated via Akt-dependent pathway. Taken together, these findings suggest that APPL1 acts as a master coordinator controlling both secretion and actions of insulin, thus APPL1 may represents a potential therapeutic target to combat T2DM.
|Awardees||Award Date||Honours / Awards / Prizes||Category|
|2006-01-01||Best Poster Presentation Award (11th Medical Research Conference): University of Hong Kong, University of Hong Kong, Hong Kong||Research Achievement|
|2014-01-01||Best Abstract in Basic Science and Translational (Oral Presentation): 19th Medical Research Conference||Research Achievement|
|2009-01-01||Best abstract in animal models (14th Medical Research Conference): University of Hong Kong, University of Hong Kong||Research Achievement|
|2014-01-01||Best Abstract in Basic Science and translational (Oral Presentation): 19th Medical Research Conference||Research Achievement|
|2015-02-01||Research Travel Scholarship 2015: American Academy of Neruology||Research Achievement|
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