Crosstalk Between Dietary Pattern, Anthropometric Parameters, and Adiponectin Concentration Among Patients with Metabolic Syndrome.

Adiponectin is known to mediate antidiabetic and cardioprotective metabolic effects. Current evidence suggests that diet, both its quantity and quality, affects adiponectin concentration. The purpose of this study was to evaluate the association of adiponectin with cardiometabolic risk factors, anthropometric features, and diet characteristics in obese patients with multiple cardiometabolic risk factors. The group of 113 nondiabetic patients (90 males, mean age: 48 ± 9 years) fulfilling the criteria of metabolic syndrome (IDF, 2005) was divided into 2 subgroups according to median adiponectin concentration calculated for that cohort (6.83 μg/mL)-low-adiponectin (LA) and high-adiponectin (HA) subgroup. Biochemical and anthropometric measurements were recorded and nutrients intake was assessed using 24-hr dietary recall method and diet history questionnaire. No significant differences between LA and HA were noted regarding the anthropometric parameters. However, there were significant differences in biochemical indices, and HA was characterized by a more favorable insulin level, homeostasis model assessment of insulin resistance (HOMA-IR) value, and plasma lipid profile than LA. Both LA and HA subgroups were comparable in terms of energy, protein, carbohydrate, and total fat intake, but there were significant differences between the level of polyunsaturated fatty acids (PUFA) consumption (6.06 ± 1.0 and 6.37 ± 1.1, respectively) and omega-3/omega-6 ratio (as follows: 0.09 ± 0.01 and 0.16 ± 0.04). These results highlight interactions between diet, adiponectin concentration, and biochemical profile. Nondiabetic patients with metabolic syndrome with higher PUFA consumption, including higher omega-3/omega-6 ratio, were characterized by higher circulating adiponectin level and more favorable biochemical profile. Thus, it might be assumed that the protective role of omega-3 fatty acids might be mediated by adiponectin in patients with metabolic syndrome.