Type 2 Diabetes and Obesity

Type 2 Diabetes and Obesity

Overview

According to the World Health Organization, in 2014, more than 1.9 billion adults 18 years and older, were overweight. Of these over 600 million were obese. Insulin resistance, Type 2 Diabetes, and atherosclerosis are common complications of obesity. However, treatment options remain limited, in part due to the challenge of identifying suitable drug targets among the complex series of signaling pathways and cellular mediators that control the metabolic syndrome.

Donate Now Help us give every patient a fighting chance.

Studies

Research in the Samad lab is focused on understanding how obesity increases the risk for developing type 2 diabetes (T2D) and cardiovascular disease, with the ultimate goal of identifying novel targets for drug development. Over the past two decades, Dr. Samad has worked on the overarching theme that adipose dysfunction due to chronic inflammation contributes to many of these obesity-related disorders. Her group has identified a number of pro-thrombotic (Plasminogen activator inhibitor-1, Tissue factor) and inflammatory proteins and signaling pathways that are dysregulated in the obese adipose tissue and that contribute to metabolic and cardiovascular disease.
One such pathway is caused by changes in sphingolipids (e.g., ceramide, sphingosine 1 phosphate). These changes lead to inflammation, T2D, and cardiovascular risk. Another is an unexpected and novel finding that tissue factor, the principal initiator of coagulation, signals via protease-activated receptor 2 to promote insulin resistance and obesity. Current research efforts are focused on identifying methods to limit chronic adipose inflammation and dysfunction in obesity. Data derived from the Samad lab could pave the way to developing innovative medicines that could prevent or limit obesity-related metabolic and cardiovascular complications.

Select Publications

Wang J, Ciaraldi TP, Samad F. Tissue factor expression in obese type 2 diabetic subjects and its regulation by antidiabetic agents. J Obes. 2015;2015:291209.

PDF

Neels GN, Badeanlou L, Hester KD, and Samad F. Keratinocyte-derived Chemokine in Obesity: Expression and Role in Adipose Macrophage Infiltration and Glucose homeostasis. J Biol Chem 2009;284(31):20692–8.

PDF

Samad F, Uysal KT, Weisbrock SM, Pandey M, Hotamisligil GS, Loskutoff DJ. Tumor necrosis factor-a: A key component in the obesity-linked elevation of plasminogen activator inhibitor-1. Proc Natl Acad Sci USA. 1999;96(12): 6902–07

PDF

Badeanlou L, Furlan-Freguia C, Yang G, Ruf W, Samad F. Tissue factor-protease activated receptor 2 signaling promotes diet-induced obesity and adipose inflammation. Nat Med. 2011;17(11): 1490–7.

PDF

Wang J, Badeanlou L, Bielawski J, Ciaraldi TP, Samad F. 2014. Sphingosine kinase 1 regulates adipose proinflammatory responses and insulin resistance. Am J Physiol Endocrinol Metab. 1;306(7):E756-68. Epub 2014 Jan 28.

PDF

Samad F, Yamamoto K, Loskutoff DJ. Distribution and regulation of plasminogen activator inhibitor-1 in murine adipose tissue in vivo: Induction by tumor necrosis factor-a and lipopolysaccharide. J Clin Invest. 1996; 97(1): 37–46.

PDF

We need your help


Our research programs are funded primarily by grants from the National Institutes of Health (NIH). Private donations help to accelerate the progress of research through the purchase of laboratory supplies and equipment or the recruitment of additional laboratory personnel. Thank you!

Donate Now