Education and Outreach

Einav Shnaidman, Ph.D.

Division of Computational Biology

Education

Ph.D., Metabolism and Human Nutrition, The Hebrew University of Jerusalem, Israel, 2007
M.S., Metabolism and Human Nutrition, The Hebrew University of Jerusalem, Israel, 2002
B.S., Clinical Nutrition, The Hebrew University of Jerusalem, Israel, 1998

Research

The objective of my research is to explore the signal transduction pathways and gene expression patterns controlling mitochondrial biogenesis in human white adipocytes. Mitochondrial biogenesis is a process in which mitochondrial number and function are increased to meet energetic challenges of the cell, as in the case of exercising muscle and during adaptive thermogenesis in brown adipocytes. Generating a high density of functional mitochondria could contribute to energy expenditure and weight loss. On the other hand, insufficient mitochondrial mass and activity has been linked with various elements of metabolic disease and it seems to be involved in increases in fat mass, particularly in the visceral depots, and in the development of diabetes.

Using human subcutaneous and visceral adipocytes of lean, over-weight and obese subjects, I will test whether the ability of the white cell-mitochondria for oxidative metabolism is impaired with increasing BMI. I am testing several hypotheses regarding the molecular mechanisms responsible for defects in mitochondrial biogenesis by examining the catecholamine and nuclear receptor signaling pathways that control brown adipocyte metabolism and mitochondrial biogenesis. These include PKA, p38α MAPK, PGC-1α, UCP1, LXRα, among others. I am also exploring whether defects in oxidation as a function of increasing BMI will be most pronounced in visceral adipocytes as they are more strongly associated with development of the metabolic syndrome.

Selected Publications

Yehuda-Shnaidman E., Kalderon B. and Bar-Tana J. Modulation of mitochondrial transition pore components by thyroid hormone. (2005) Endocrinology;146:2462-2472.