Given the disease burden and health costs associated with the increased prevalence of obesity, identifying mechanisms in the pathogenesis of obesity and associated health disorders is crucial for the development of rational therapeutic options. The major interest in the Samad laboratory is to study the extra cellular mediators and intracellular molecular mechanisms involved in the pathogenesis of obesity and related health consequences including increased risk for insulin resistance/type 2 diabetes and cardiovascular disease. Genetic and biochemical studies in the lab focus on gene expression and signal transduction using cultured adipocytes as well as genetic and diet-induced models of obesity to identify specific genes and pathways involved in obesity related pathologies.

Evidence from the lab suggest that secretion of proinflammatory/prothrombotic molecules from an expanded adipose tissue together with increased lipid accumulation in extra adipose tissues such as the liver may contribute to the pathogenesis of these obesity related disorders. How these interrelated phenomena may be mechanistically linked is an important question. Studies in Dr. Samad's lab support a role for sphingolipids, including ceramide, sphingosine and S1P in the onset of these pathogenic disorders and suggest that specific sphingolipids may provide mechanistic links between inflammation/excess nutrients and increased metabolic and cardiovascular risk. They have shown that sphingolipid metabolism is altered in obesity and pharmacological strategies that modulate sphingolipids have beneficial effects on the complications associated with the obesity, including weight gain, insulin resistance and cardiovascular risk. Thus, a major focus in Dr. Samad's lab is aimed at targeting enzymes involved in the biosynthesis of specific sphingolipids, a viable and novel therapeutic option for obesity related disorders.

Obesity and Increased Risk for Breast Cancer >>