M.D.: Ben-Gurion University
Ph.D.: Ben-Gurion University
Post-Doctoral fellowship: Hospital for Sick Children, Canada
Position: Senior Lecturer
Department of Clinical Biochemistry
Faculty of Health Sciences
E-mail: rudich@bgu.ac.il
The role of adipose tissue dysfunction in obesity and its co-morbidities
Over the past 15 years obesity has become the most prevalent preventable risk factor for morbidity and mortality. Although the reasons for obesity are complex and still incompletely understood, it is clear that in obesity adipose tissue in obesity becomes dysfunctional, and is a major pathogenic contributor to the morbidity that accompanies obesity.
1. Mechanisms for human adipose tissue dysfunction in obesity: Analysis of human adipose tissues is aimed at unraveling how obesity leads to adipose tissue dysfunction. Utilizing expression, molecular, imaging, functional, and ex-vivo studies of human samples, we are identifying the "human adipose tissue stress response" and unravel its functional significance. The causal role of specific pathways and molecular mechanisms identified (such as the role of autophagy, inflammation, and a specific MAP kinase signaling cascade) are further challenged using cellular, ex-vivo and in vivo experimental models. Functionally we mainly focus on two pathogenic axes: an adipocyte-macrophage axis that operates within the adipose tissue, and a fat-liver axis that mediates the pathogenic role of visceral adiposity.
2. Investigating potential life-style interventions to alleviate obesity-related morbidities in large populations: As part of a larger team of investigators (headed by Prof. Iris Shai), intervention trials are being conducted to identify life-style approaches to limit the health burden of the obesity epidemic, and to understand the mechanisms by which such protective effects occur.
3. Circulating monocytes as mediators of the environmental impact on adipose tissue in obesity: Circulating monocytes are the likely precursors of adipose tissue macrophages that accumulate in obesity. We hypothesize that monocytes may constitute a marker of adipose tissue inflammation (and thus, for morbidity-prone obesity), and are also active players in the pathogenesis of obesity-associated morbidity. Specifically, we entertain the possibility that monocytes may communicate a contributing effect of air-borne environmental particles (air pollution) to obesity-associated morbidity.
Nov O., Shapiro H., Ovadia H., Tarnovscki T., Dvir I., Shemesh E., Kovsan J., Shelef I., Carmi Y., Voronov E., Apte R.N., Lewis E., Haim Y., Konrad D., Bashan N. and Rudich A. (2013). Interleukin-1β regulates fat-liver crosstalk in obesity by auto-paracrine modulation of adipose tissue inflammation and expandability. PloSOne 8(1):e53626.
Shapiro H., Pecht T., Shaco-Levy R., Harman-Boehm I., Kirshtein B., Kuperman Y., Chen A., Blüher M., Shai I. and Rudich A. (2013). Adipose tissue foam cells are present in human obesity. J. Clin. Endocrinol. Metab. 98:1173-1181.
Hadad N., Elgazar-Carmon V., Burgazliev O., Solomonov Y., Wueest S., Item F., Konrad D., Rudich A. and Levy R. (2013). Induction of cytosolic phospholipase A2ais required for adipose neutrophil infiltration and hepatic insulin resistance early in the course of high fat feeding. Diabetes 62:3053-3063.
Beck-Haim Y., Tarnovscki T., Bashari D., Rudich A. (2013). A Chromatin Immunoprecipitation (ChIP) protocol for use in whole human adipose tissue. Am. J. Physiol. - Endocrinol. Metab. 305: E1172-E1177.
Pecht T., Gutman A., Bashan N. and Rudich A. (2013). Peripheral blood leucocyte sub-classes as potential biomarkers of adipose tissue inflammation and obesity sub-phenotypes in humans. Obes. Rev. (in press).
