Key result
LMW-adiponectin levels strongly differentiate insulin-resistant from non-insulin-resistant individuals with an AUC of ~0.82.
Why the study?
The contribution of adiponectin oligomers, resolvin-E1, and chemerin levels to insulin resistance and adiposopathy status in obesity was unclear.
Cross-Sectional (n=230)
An imbalance in serum levels of LMW-adiponectin, resolvin-E1, and chemerin is associated with adiposopathy and insulin resistance in individuals with obesity, potentially serving as early risk markers.
Answers are grounded in this paper and cite their sources.
LMW-adiponectin may support biomarker use for insulin resistance in obesity; cross-sectional data leave clinical adoption and causality open.
Objective: The aim was to establish if the balance adiponectin-oligomers, resolvin-E1 and chemerin levels could contribute to the insulin resistance (IR) setting of subjects with obesity, based on their serum levels and its relationship with inflammatory markers, metabolic profile and adiposopathy status.Methods: This study included 230 individuals, classified according to World Health Organization criteria by body mass index (BMI) kg/m 2 in two groups: withoutobesity (from 18.5 to 29.9) and with-obesity (from 30.0 to 39.9).Body fat mass distribution, metabolic and inflammatory markers were measured by anthropometric, enzymatic and immuno-turbidimetry methods, respectively.Serum insulin, resolvin-E1, chemerin, and adiponectin-oligomers were evaluating by ELISA method.Analysis performed were correlations IR-indexes with adiposity, receiver operating characteristic (ROC) curves and the adiponectin-oligomers, resolvin-E1 and chemerin tertiles.Results: Subjects' with-obesity showed adiposopathy status, characterized by metabolic dysregulation and a subclinical inflammatory profile.They presented higher levels (x ±SD, ng/mL) of resolvin-E1 (1227 ±668 versus 909 ±769, P= 0.017), chemerin (91 ±31 versus 79 ±23, P= 0.013) and LMW-Adiponectin (2257 ±797 versus 1030 ±1055, P= 0.011), whereas HMW-Adiponectin was lower (2470 ±1095 versus 3236 ±1848, P= 0.010), compared to the without-obesity individuals.Individuals' with-obesity also displayed positive correlation of IR markers (rho from 0.163 to 0.479) along body fat measurements, metabolic and inflammation profiles.Moreover, a negative correlation of HMW-Adiponectin (rho from -0.564 to -0.214) with body fat measurements, metabolic and inflammation profiles.IR-indexes, LMW-Adiponectin and resolvin-E1/chemerin relationship showed differences between groups' with-obesity and without-obesity, but not with gender.ROC curves shown potential ability of the LMW-Adiponectin levels to differentiate IR from non-IR individuals, with AUC of 0.815, P<0.0001 (95%, CI: 0.726-0.903).Conclusion: The present study shown that LMW-Adiponectin-resolvinE1-chemerin serum unbalance establishes a specific relationship with adiposopathy in individuals with obesity, which could be a way to identify risk factors in early stages of IR.
No takes yet. Share an insight, caveat, or question.
PM et al. (2020) conducted a cross-sectional in Obesity and Insulin Resistance (n=230). Obesity (BMI 30.0-39.9 kg/m2) vs. Without-obesity (BMI 18.5-29.9 kg/m2) was evaluated on Differentiation of insulin resistance from non-insulin resistant individuals using LMW-Adiponectin levels (Area Under the Curve) (AUC 0.815, 95% CI 0.726-0.903, p=<0.0001). LMW-Adiponectin levels demonstrated a strong potential to differentiate insulin resistance from non-insulin resistant individuals, yielding an area under the curve of 0.815.
Synapse has enriched 10 related papers. Consider them for comparative context: