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Jandee Lee, Woong Youn Chung, The Role Played by the Peroxisome Proliferator-Activated Receptor-β/δ (PPARβ/δ) Activator, GW501516, in Control of Fatty Acid Metabolism: A New Potential Therapeutic Target for Treating Metabolic Syndrome, Endocrinology, Volume 152, Issue 5, 1 May 2011, Pages 1742–1744, https://doi.org/10.1210/en.2011-0211
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Obesity is increasing in significance as a global health hazard by virtue of an association with metabolic syndrome, which is characterized by abdominal obesity, hyperglycemia caused by insulin resistance, glucose intolerance, atherogenic dyslipidemia, and hypertension (1). The prevalence of obesity has increased dramatically (by about 75%) since 1980; in the United States, 33% of adults are obese and 22% have metabolic syndrome (2, 3). Although many different factors can cause metabolic syndrome, derangement of lipid homeostasis attributable to a combination of excess lipid intake and lack of physical exercise plays a major role (4). It has been suggested that adipocyte dysfunction causes excessive accumulation of intraabdominal fat that, in turn, promotes ectopic fat deposition (5–7). Recently it was shown that dyslipidemia associated with metabolic syndrome is initiated principally by hepatic overproduction of plasma lipoproteins that carry triglycerides, the very low-density lipoproteins (VLDL). Such overproduction induces a series of changes in lipoproteins, eventually resulting in the atherogenic lipid abnormalities of metabolic syndrome (8). To date, the approaches to treating the syndrome using either single drugs or drug combinations (e.g. statins, fibrates, and/or angiotensin converting enzyme inhibitors) have been less than ideal, in part because of limitations in therapeutic efficacy and drug side effects (9). Thus, it is important to develop a new and effective pharmacological therapy to prevent development of atherogenic dyslipidemia in patients with metabolic syndrome.
