Department of Medicine Faculty

Academic Interests

The burgeoning obesity and diabetes epidemics place an enormous strain on health care systems worldwide, threatening both individual health and societal wellness. Reversing these health threats necessitates an understanding of the underlying mechanisms responsible for these scourges in order to devise interventions to mitigate the development of metabolic diseases. An emerging area of interest to explain the rapidity and magnitude of these metabolic epidemics is the contribution of chemical pollutants released into the environment on cellular processes that regulate energy metabolism. My laboratory is focused on understanding the potential mechanisms by which these environmental endocrine disrupting chemicals (EDCs) modulate adipocyte physiology in order to understand how synthetic chemicals hijack human metabolism and thereby predispose to the development of various metabolic diseases. Our recent work has shown the capacity of various EDCs to induce adipocytic insulin resistance, potentially through an augmentation of glucocorticoid signaling. We are currently focused on characterizing the molecular mechanisms by which these EDCs modulate insulin signal transduction in order to specifically understand how these chemicals deleteriously influence adipocyte metabolism as well as to more broadly appreciate how adipose tissue senses cues from the environment to regulate energy metabolism. It is my hope that these studies will also serve as the foundation for the genesis of sound public policy that may be implemented to mitigate the impact of environmental pollution on human metabolic health.

Clinical Interests

Metabolic and endocrine diseases associated with chemical exposures, obesity, diabetes, and general endocrinology

Representative Publications

1. Sargis, RM and Brady, MJ. 2010. Making Fat Work. Perspectives in Biology and Medicine, 53: 630-47.
2. Sargis, RM; Johnson, DN; Choudhury, RA; and Brady, MJ. 2009. Environmental Endocrine Disruptors Promote Adipogenesis in the 3T3-L1 Cell Line through Glucocorticoid Receptor Activation. Obesity, 18: 1283-8
3. Sargis, RM; Wollmann, RL; Pytel, P. 2009. A 59 year old man with sellar mass lesion. Brain Pathology, 19: 161-162.
4. Sargis, RM and Subbaiah, PV. 2006. Sphingomyelin protects membrane cholesterol against free radical-mediated oxidation. Free Radical Biology and Medicine, 40: 2092-2102.
5. Sargis, RM and Subbaiah, PV. 2003. Trans Unsaturated Fatty Acids are Less Oxidizable than Cis Unsaturated Fatty Acids and Protect Endogenous Lipids from Oxidation in Lipoproteins and Lipid Bilayers. Biochemistry. 42: 11533-11543.