Type 2 Diabetes and Obesity

Type 2 Diabetes and Obesity

Overview

According to the World Health Organization (https://www.who.int/), in 2016, more than 1.9 billion adults 18 years and older, were overweight. Of these, over 650 million were obese. Insulin resistance, Type 2 Diabetes (T2D), and atherosclerosis are common complications of obesity. However, treatment options remain limited, in part due to the challenge in identifying suitable drug targets among the complex series of signaling pathways and cellular mediators that control the metabolic syndrome.

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Studies

Research in the Samad lab is focused on understanding how obesity increases the risk of developing 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 (body fat dysfunction) due to chronic inflammation, contributes to many of these obesity-related disorders. The Samad group has identified several blood clotting and inflammatory proteins and signaling pathways that are dysregulated in the obese adipose tissue which contribute to metabolic and cardiovascular disease.

One such dysregulated pathway is caused by changes in sphingolipids leading to inflammation, T2D, and cardiovascular risk. Another unexpected and novel finding is that tissue factor, the initiator of clotting, signals via a protein called protease-activated receptor 2, to promote insulin resistance and obesity. This data from the Samad lab could pave the way to developing innovative medicines to prevent or reduce 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.

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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.

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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

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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.

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Wang J, Badeanlou L, Bielawski J, Ciaraldi TP, Samad F. Sphingosine kinase 1 regulates adipose proinflammatory responses and insulin resistance. Am J Physiol Endocrinol Metab. 2014;306(7):E756-E768.

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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.

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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!

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