Ren Zhang, Ph.D.
Assistant Professor


3240 Scott Hall
540 East Canfield
Detroit, MI 48201
Voice: 313-577-0027
FAX: 313-577-5218
rzhang@med.wayne.edu

 

Assistant Professor (also with Endocrinology); Ph.D., UT MD Anderson Cancer Center, 2005; Obesity and diabetes; the leptin signaling pathway and mechanisms of leptin resistance; molecular evolution and comparative genomics.

Research Interests

The global obesity epidemic poses a major public health issue, because obesity increases the risk of numerous health consequences, such as insulin resistance, type 2 diabetes and coronary heart diseases. Leptin is a hormone secreted exclusively by fat. Leptin deficiency leads to massive obesity that can be cured by leptin replacement therapy. Non-leptin-deficient obese patients, however, develop high serum leptin levels and do not respond to leptin treatment, indicating a state of leptin resistance. One direction of the lab focuses on the leptin signaling pathway and mechanisms of central leptin resistance. Another direction is to use bioinformatics approaches to study the molecular evolution of human obesity related genes. Students will be exposed to techniques of molecular biology, cell culture and mouse genetics.


Selected Publications

Lin, Y. and Zhang, R. (2011) Putative essential and core-essential genes in Mycoplasma genomes. Sci. Rep. 1, 53.

Gao, F and Zhang, R (2011) Enzymes Are Enriched in Bacterial Essential Genes. PLoS ONE 6: e21683.

Zhang, R., Maratos-Flier, E., and Flier, J.S. (2009). Reduced adiposity and high fat diet-induced adipose inflammation in mice deficient for phosphodiesterase 4B. Endocrinology, 150, 3076-3082.

Zhang, R., Dhillon, H., Yin, H., Yoshimura, A., Lowell, B.B., Maratos-Flier, E., and Flier, J.S. (2008). Selective inactivation of Socs3 in SF1 neurons improves glucose homeostasis without affecting body weight. Endocrinology, 149, 5654-5661.

Zhang, R., Murakami, S., Coustry, F., Wang, Y., and de Crombrugghe, B. (2006). Constitutive activation of MKK6 in chondrocytes of transgenic mice inhibits proliferation and delays endochondral bone formation. PNAS, 103, 365-370.


 
 
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