Prevalence, Risk Factors, and Genetic Traits in Metabolically Healthy and Unhealthy Obese Individuals

Abstract

Objective. To assess prevalence of metabolically healthy individuals among patients with abdominal obesity (AO) and to determine phenotype and potential genetic traits associated with a benign metabolic status. Methods. 503 AO patients without cardiovascular diseases were examined. Waist circumference (WC), BMI, blood pressure, plasma glucose and serum insulin levels, HOMA-IR, lipid profile, and adiponectin (AN) and leptin (LEP) concentrations in serum were measured. Polymorphisms A19G and Q223R of the LEP and LEP receptor gene, and G276T and T45G of the AN gene were investigated. Results. 91.3% of patients were metabolically unhealthy obese (MUO), and 8.7% metabolically healthy obese (MHO). MHO patients were younger, and had lesser BMI and WC, while duration of obesity, frequency, and duration of physical training were greater than MUO patients (p < 0.05). In MHO and MUO patients distribution of the G19G, G19A, and A19A genotypes of the LEP gene and G276G, G276T, and T276T genotypes of AN gene did not differ. The Т45Т genotype was associated with increase of metabolic disorders' risk for patients with АО (OR = 2.331; 95% CI = 1.121 ÷ 5.132). Conclusions. Prevalence of MHO individuals among patients with AO is low. Benign metabolic status was associated with younger age, lower waist circumference, and higher physical activity, shorter duration of obesity, and G45G adiponectin genotype carriage.

Metabolically healthy obesity across the life course: epidemiology, determinants, and implications

“…Clearly, much work remains to be performed in this area to uncover the influence of genetics, nutrigenetics, and epigenetics on MHO pathogenesis. Berezina et al . examined potential relationships between genetic variants of the adipocytokine genes (leptin, leptin receptor, and adiponectin) and metabolically healthy (without CVD) abdominal obesity among adults.…”

“…Clearly, much work remains to be performed in this area to uncover the influence of genetics, nutrigenetics, and epigenetics on MHO pathogenesis. Berezina et al 90 examined potential relationships between genetic variants of the adipocytokine genes (leptin, leptin receptor, and adiponectin) and metabolically healthy (without CVD) abdominal obesity among adults. Although genetic associations and genenutrient interactions have been previously described between variants of these genes and MetS, 91,92 this study identified for the first time a more than twofold greater likelihood of MUO among the T allele carriers of the adionectin T45T polymorphism relative to the G allele carriers.…”

Gender and age related features of metabolically healthy obesity phenotype prevalence

“…В другом отечественном исследовании коллег из г. Санкт-Петербурга показатель распространенности МÇФО был существенно ниже -всего 8,7% [17]. Более низкие показатели были предопределены тем, что в данной работе к критериям МÇФО была отнесена комбинация минимального количества проявлений метаболического синдрома в сочетании с нормальной чувствительностью тканей к инсулину.…”

The prevalence of metabolically healthy obesity according to the sample of the Moscow region

“…Максимальная распространенность МЗО с учетом критериев МС по IDF 2005 г. была отмечена в Тюмени -52,2%, минимальная -в Воронеже -25,7% при общей распространенности 41% и отсутствии существенных гендерных различий [9]. В другом отечественном исследовании коллег из Санкт-Петербурга показатель распространенности МЗО был существенно ниже -всего 8,7% [10]. Более низкие показатели были предопределены тем, что в данной работе к критериям МЗО была отнесена комбинация минимального количества проявлений метаболического синдрома в сочетании с нормальной чувствительностью тканей к инсулину.…”