title: Targeting inflammation in metabolic syndrome.
abstract: The metabolic syndrome (MetS) is comprised of a cluster of closely related risk factors, including visceral adiposity, insulin resistance, hypertension, high triglyceride, and low high-density lipoprotein cholesterol; all of which increase the risk for the development of type 2 diabetes and cardiovascular disease. A chronic state of inflammation appears to be a central mechanism underlying the pathophysiology of insulin resistance and MetS. In this review, we summarize recent research which has provided insight into the mechanisms by which inflammation underlies the pathophysiology of the individual components of MetS including visceral adiposity, hyperglycemia and insulin resistance, dyslipidemia, and hypertension. On the basis of these mechanisms, we summarize therapeutic modalities to target inflammation in the MetS and its individual components. Current therapeutic modalities can modulate the individual components of MetS and have a direct anti-inflammatory effect. Lifestyle modifications including exercise, weight loss, and diets high in fruits, vegetables, fiber, whole grains, and low-fat dairy and low in saturated fat and glucose are recommended as a first line therapy. The Mediterranean and dietary approaches to stop hypertension diets are especially beneficial and have been shown to prevent development of MetS. Moreover, the Mediterranean diet has been associated with reductions in total and cardiovascular mortality. Omega-3 fatty acids and peroxisome proliferator-activated receptor α agonists lower high levels of triglyceride; their role in targeting inflammation is reviewed. Angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and aldosterone blockers comprise pharmacologic therapies for hypertension but also target other aspects of MetS including inflammation. Statin drugs target many of the underlying inflammatory pathways involved in MetS.
authors.affiliation: Division of Cardiology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Mass. Electronic address: fwelty@bidmc.harvard.edu.
authors.forename: Francine K
authors.initials: FK
authors.lastname: Welty
authors.affiliation: Division of Cardiology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Mass.
authors.forename: Abdulhamied
authors.initials: A
authors.lastname: Alfaddagh
authors.affiliation: Division of Cardiology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Mass.
authors.forename: Tarec K
authors.initials: TK
authors.lastname: Elajami
mesh_terms: D050154:Adiposity; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D006801:Humans; D007249:Inflammation / Q000209:etiology / Q000628:therapy*; D007333:Insulin Resistance / Q000502:physiology; D024821:Metabolic Syndrome / Q000150:complications*; D012307:Risk Factors
chemical_list: D000893:Anti-Inflammatory Agents