EK Calton, VS Miller and MJ SoaresBACKGROUND AND OBJECTIVES: The pathogenesis of the metabolic syndrome (MetS) is not well understood. This review is based on the hypothesis that both traditional and emerging risk factors act through adiponectin.
SUBJECTS AND METHODS:We conducted a search of the literature using prominent electronic databases and search terms that included in combination: adiponectin, diet, dietary patterns, exercise, metabolic rate, MetS and testosterone. Articles were restricted to studies conducted on adult humans, reported in English and within the time period 2000-2012. RESULTS AND CONCLUSIONS: Both traditional and emerging risk factors associated with the MetS show some evidence of exerting their influence through adiponectin. High-quality randomized controlled trials that alter adiponectin levels are required to further corroborate this hypothesis.
INTRODUCTIONThe metabolic syndrome (MetS) represents a clustering of risk factors for cardiovascular disease and type 2 diabetes mellitus (T2DM), which include: hypertension, low high-density lipoproteincholesterol (HDL-C), high triglycerides (TG), high fasting blood glucose (FBG) and abdominal obesity. 1 Obesity and insulin resistance (IR) have long been accepted as having a pivotal role in the etiopathogenesis of the syndrome. 2,3 However, emerging evidence indicates that even after controlling for these variables, there remains a substantial unexplained risk. 2,[4][5][6] Adiponectin, a collagen-like protein was first discovered in 1995 by Dcherer and Lodish, who called it adipocyte complementrelated protein of 30 kDa (Acrp30). 7 At a similar time, three other independent groups discovered adiponectin, calling it adipose most abundant gene transcript 1 (apM1), AdipoQ and gelatinbinding protein of 28 kDa (GBP28). 8 Adiponectin is secreted primarily from adipose tissue into the circulation where highmolecular-weight, medium-molecular-weight and low-molecularweight oligomeric forms exist. 8,9 Total adiponectin as well as the individual oligomeric forms have been associated with health benefits. 9 Consistent links between low adiponectin levels and increased TG, FBG, waist circumference, blood pressure (BP) levels and decreased HDL-C explain its potential role in the etiology of MetS. 2,10 Furthermore, genetic studies have linked adiponectin and MetS in individuals of European descent. 11 Specifically, overall adiposity, abdominal adiposity and IR were influenced by gene loci, which also encode adiponectin. 12 This review discusses both traditional and emerging factors that may influence the prevalence of MetS. Furthermore, the possibility that adiponectin may have an important role in the pathogenesis of the syndrome was evaluated. As there is inconsistency in the literature whether total, high-molecular-weight, mediummolecular-weight or low-molecular-weight adiponectin was measured, 4,13,14 this review discusses adiponectin in general terms. We present a model that emphasizes the flow-through effects of several factors on MetS risk through adi...