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- W2259857027 abstract "The global epidemic of obesity is constantly growing and represents an enormous challenge for health care systems worldwide. Obesity fuels the development of metabolic syndrome that includes components such as elevated glucose levels, insulin resistance, elevated blood pressure, and increased levels of triglycerides (1). Obesity and metabolic syndrome increase the risk of metabolic diseases, such as type 2 diabetes (T2D), cardiovascular disease, and atherosclerosis, and contribute to a reduction in life expectancy (2). In the U.S., the obesity rate in adults has reached 36% and obesity affects more than 1 billion people worldwide (3). Currently, 9.3% of the U.S. population has diabetes. In adults, T2D accounts for 90–95% of all diagnosed cases of diabetes, and the estimated total economic burden of diabetes in the U.S. is $245 billion (4). Thus, it is imperative that we increase our understanding of the mechanisms that lead to the development of obesity-induced insulin resistance and T2D, which will help identify therapeutic targets to reduce the impact of these syndromes on morbidity and mortality.The first piece of evidence that obesity, insulin resistance, and inflammation are interconnected was provided more than a century ago when Dr. R.T. Williamson (5) observed that the anti-inflammatory drug sodium salicylate improved glucose control in patients with diabetes. Almost 90 years later, Hotamisligil et al. (6) revisited this observation as they found that the neutralization of tumor necrosis factor (TNF)-α improved insulin resistance, and thus a link between inflammation and diet-induced insulin resistance was established. Subsequent studies elucidated that a complex immune cellular network regulates inflammation and insulin responsiveness in metabolic tissues. Recently, interleukin (IL)-1β antibodies in monotherapy or in …" @default.
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- W2259857027 date "2015-06-17" @default.
- W2259857027 modified "2023-10-10" @default.
- W2259857027 title "New Piece in the Jigsaw Puzzle: Adipose Tissue–Derived Stem Cells From Obese Subjects Drive Th17 Polarization" @default.
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- W2259857027 doi "https://doi.org/10.2337/db15-0437" @default.
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