Weiping HAN   
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  Weiping HAN  
  Lab Location:
Institute of Molecular and Cell Biology

Singapore Bioimaging Consortium
#01-02, 11 Biopolis Way


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  Key Publications  

Chen N, Sugihara H, Kim J, Fu Z, Barak B, Sur M, Feng G*, Han W*:
Direct modulation of GFAP-expressing glia in the Arcuate nucleus bi-directionally regulates feeding.
E-Life 5:e18716, October 18, 2016. (*Co-corresponding authors)

Wu B, Wei S, Petersen N, Ali Y, Wang X, Rorsman P, Hong W, Südhof TC*, Han W*:
Synaptotagmin-7 is a GLP-1 effector in its potentiation of glucose-stimulated insulin secretion.
Proceedings of the National Academy of Sciences of the United States of America 112(32):9996-10001, 2015. (*co-corresponding authors)

Lim CY, Bi X, Wu D, Kim JB, Gunning PW, Hong W, Han W:
Tropomodulin 3 is a novel Akt2 effector regulating GLUT4 exocytosis.
Nature Communications 6:5951 doi: 10.1038/ncomms6951, 2015.

Li H, Wei S, Cheng K, Gounko NV, Ericksen RE, Xu A, Hong W*, Han W*:
BIG3 inhibits insulin granule biogenesis and insulin secretion.

The EMBO Reports 15(6):714-722, 2014. (*co-corresponding authors)

Yang W, Thein S, Wang X, Bi X, Ericksen RE, Xu F, Han W: BSCL2/Seipin regulates adipogenesis through actin cytoskeleton remodeling.
Human Molecular Genetics 23(2):502-513, 2014.

Gustavsson N, Wei S-H, Hoang DN, Lao Y, Zhang Q, Radda GK, Rorsman P, Südhof TC, Han W:
Synaptotagmin-7 is a principal Ca2+-sensor for Ca2+-induced glucagon exocytosis in pancreas.
The Journal of Physiology 587(6):1169-1178, 2009.

Gustavsson N, Lao Y, Maximov A, Chuang J-C, Kostromina E, Repa J, Li C, Radda GK, Südhof TC*, Han W*:
Impaired insulin secretion and glucose intolerance in synaptotagmin-7 null mutant mice.
Proceedings of the National Academy of Sciences of the United States of America105:3992-3997, 2008. (*co-corresponding authors)

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  Weiping HAN

Deputy Director, SBIC
Head, Laboratory of Metabolic Medicine, SBIC

Research Director, MHDU, IMCB
Professor, Department of Biochemistry, YLL School of Medicine, National University of Singapore
Professor, Program in Cardiovascular and Metabolic Disorders, Duke-NUS Graduate Medical School

Weiping Han obtained his Ph.D. in Physiology from Cornell University in 1996. He did his postdoctoral work at the University of Pittsburgh and HHMI/UT Southwestern Medical Center in Dallas. In 2003, he was promoted to Research Assistant Professor in the Center for Basic Neuroscience at UT Southwestern Medical Center, where he studied molecular mechanisms of hormone secretion and signaling. In 2005, he moved to Singapore to set up a research program in the Laboratory of Metabolic Medicine (LMM) at Singapore Bioimaging Consortium (SBIC), and was promoted to Research Director / Professor in 2013. Currently he is Deputy Director of SBIC with concurrent appointment as Head of LMM. He is also Research Director at Institute of Molecular and Cell Biology; Professor in the Department of Biochemistry at National University of Singapore and Program in Cardiovascular and Metabolic Disorders, Duke-NUS.

  Metabolism in Human Diseases Unit

Research interests
My research aims to understand the molecular basis of diabetes and its complications, to discover and validate targets for drug development, and to develop animal models for evaluation of therapeutic interventions. My lab uses molecular genetics, cell biology, and physiology techniques to analyze genetically modified animals and cell lines. The current major research projects are:

  • Molecular control of regulated exocytosis in diabetes development and treatment
  • Molecular and cellular mechanisms of adipogenesis and its link to diabetes and other metabolic diseases
  • Post-translational modifications and protein functions in hormone secretion and diabetes development
  • Molecular link underlying increased risk of cognitive impairments in people with diabetes and other metabolic diseases

Figure Legend: Cellular and molecular regulation of insulin secretion
The cellular events leading to insulin secretion start with a rise in glucose level in the blood, which quickly leads to glucose uptake into pancreatic β-cells. Glucose in the cells then undergoes glycolysis and TCA cycle to produce ATP, resulting in an increased ATP/ADP ratio, and consequent closure of KATP-channels. Membrane depolarization due to KATP-channel closure opens L-type calcium channels, allowing calcium influx into the cells, which then triggers insulin granule exocytosis and the release of insulin into blood. The calcium triggering of exocytosis is regulated by calcium-sensors.