Maria F. Pino, PhD

Postdoctoral Fellow 

Dr. Maria Pino is a post-doctoral research fellow scientist at Translational Research Institute for Metabolism and diabetes, working under the mentorship of Dr. Lauren M. Sparks.  Her research interests are metabolic diseases including Type 2 Diabetes and obesity.  Her current research focuses in exercise and muscle metabolism, specifically understanding the mechanisms underlying the phenomenon called “exercise resistance” observed in some type 2 diabetic individual.

Prior to joining TRI, Dr. Pino was a research associate at MD Anderson Cancer Research Institute at Orlando Health institute, Orlando Fl, where she pursued breast cancer research. She investigated mechanisms involved in breast cancer metastasis. Before coming to Florida, She was a research fellow at Ingram-Cancer Center at Vanderbilt University, Nashville TN, where she conducted research in cell signaling in breast cancer, specifically the p53 family – the most frequently targeted mutation in human tumors . At Vanderbilt, she also conducted research in metabolism and Type 2 diabetes.  She designed mouse models of human mutation found in an enzyme essential for glucose metabolism known as Glucokinase.     

Maria earned her Molecular Biology and B.S. in Microbiology at Michigan State University, East Lansing, Michigan, where her interest in metabolic diseases and Type 2 diabetes began.  She investigated pancreatic beta cell dysfunction which is observed in Type 2 diabetes with emphasis in cell signaling involved insulin gene expression.

    Selected Publications:

    Jennifer M. Rosenbluth, Deborah J. Mays, Maria F. Pino, Luo Jia Tang and Jennifer A. Pietenpol. A gene signature-based approach identifies mTOR as a regulator of p73. Molecular and Cellular Biology. 2008: 5951-64

    Maria F. Pino, Kyoung-Ah Kim, Kathy D. Shelton, Jill Lindler, Stella Odili, Changhong Li, Heather W. Collins, Masa Shiota, Franz M. Matschinsky and Mark A. Magnuson. Glucokinase thermolability and hepatic regulatory protein binding are essential factors for predicting the blood glucose phenotype of missense mutations. Journal of Biological Chemistry. 2007. 282 (18): 13906-16 

    Maria F. Pino, Diana Ye, Katrina Linning, Christopher Green, Barton Wicksteed, Vicent Poitout and L. Karl Olson. Elevated glucose attenuates human insulin gene promoter activity in INS-1 pancreatic beta cells via reduced nuclear factor binding to the A5/core and Z element. Molecular Endocrinology. 2005. 19: 1343-60