Circulating Osteonectin and Adipokine Profiles in Relation to Metabolically Healthy Obesity in Chinese Children: Findings From BCAMS

Abstract

Background The role of adipokine dysregulation in determining the metabolic fate of obesity is not well studied. We aimed to examine whether the matricellular protein osteonectin and the profiles of certain adipokines could differentiate metabolically healthy obese ( MHO ) versus metabolically unhealthy obese phenotypes in childhood. Methods and Results This study included 1137 obese children and 982 normal‐weight healthy ( NWH ) controls recruited from the BCAMS (Beijing Child and Adolescent Metabolic Syndrome) study. MHO was defined by the absence of insulin resistance and/or any metabolic syndrome components. Six adipokines—osteonectin, leptin, adiponectin, resistin, FGF21 (fibroblast growth factor 21), and RBP‐4 (retinol binding protein 4)—were assessed. Approximately 20% of obese children displayed the MHO phenotype. MHO children had a more favorable adipokine profile than metabolically unhealthy obese children, with lower osteonectin, leptin, and RBP ‐4 and higher adiponectin (all P <0.05). Compared with normal‐weight healthy controls, MHO children displayed increased leptin, resistin, and RBP ‐4 levels and reduced adiponectin concentrations (all P <0.05) but similar osteonectin and FGF 21 levels. Among obese subjects, decreased osteonectin (odds ratio [OR]: 0.82; 95% confidence interval [CI] per standard deviation, 0.70–0.97), RBP ‐4 (OR: 0.77; 95% CI per standard deviation, 0.64–0.93), and leptin/adiponectin ratio (OR: 0.58; 95% CI per standard deviation, 0.43–0.77) were independent predictors of MHO . In addition, compared with children without abnormalities, those with any 3 adipokine abnormalities were 80% less likely to exhibit the MHO phenotype ( OR : 0.20; 95% CI , 0.10–0.43) and 3 times more likely to have metabolic syndrome ( OR : 2.77; 95% CI , 1.52–5.03). Conclusions These findings suggest that dysregulation of adipokines might govern the metabolic consequences of obesity in children. Low osteonectin levels, along with a healthy adipokine profile, might be used as an early marker of the MHO phenotype.

Leptin and Adiponectin Signaling Pathways Are Involved in the Antiobesity Effects of Peanut Skin Extract

“…In addition, the leptin signaling pathways of mice in the HFD and HFD plus PSE groups are also evidently changed. The significant increase of leptin gene expression, leptin protein level in adipose tissue and plasma leptin, and reduction of leptin in the hypothalamus of mice in the HFD group (Figures 2(b) and 4(c)) are consistent with other reports [26, 27]. The results displayed in Figures 2(c), 2(e), Table 1 and Figure 4(c) suggest that PSE can improve the leptin resistance of obese mice induced by HFD and leptin/leptin receptor/AgRP/NPY and adiponectin/ADR signaling pathways involved in the antiobesity effects of PSE for obese mice.…”

“…Adiponectin mainly targets adiponectin receptors (AdipoR1 and AdipoR2) to regulate energy metabolism and exert functions, such as antiatherogenic, anti-inflammatory, antidiabetic, and cardioprotective effect [23–25]. Increased leptin gene expression in adipocytes and increased plasma leptin have been reported in obese individuals [26, 27]. The gene expression of adiponectin and plasma adiponectin in obese patients, pigs, and rodents are also significantly reduced [28, 29].…”

Prevalence and Clinical Characteristics of Children and Adolescents with Metabolically Healthy Obesity: Role of Insulin Sensitivity

“…Furthermore, serum leptin levels were also significantly higher in MUO compared to MHO, confirming the role of this adipokine in determining insulin resistance and metabolic impairment independently of the age and BMI-z score of the population studied [38]. In our series, adiponectin levels did not differ significantly between MUO and MHO individuals, at variance with the positive correlation reported by others between serum adiponectin concentrations and the MHO phenotype in children and adolescents with overweight or obesity [39,40]. This difference might be due to different ethnicities or to the assay utilized for the determination of adiponectin (radioimmunoassay-RIA vs. enzyme-linked immunosorbent assay-ELISA).…”

Adipose Tissue Distribution, Inflammation and Its Metabolic Consequences, Including Diabetes and Cardiovascular Disease

“…Notable differences in the adipokine profile between MHO and MUHO subjects have been reported, which could contribute to their respective risks for T2DM and CVD. Leptin has been shown to be higher in MUHO than MHO obese Chinese children in one study (202), but was not found to differ between adult groups in several other studies (203)(204)(205). By contrast, adiponectin has consistently been shown to be higher in subjects with MHO than in those with MUHO, despite both populations having lower adiponectin than metabolically healthy lean controls (203,(205)(206)(207)(208)(209).…”