Link between omentin‐1, obesity and insulin resistance in children: Findings from a longitudinal intervention study

• Published in: Pediatric obesity 2020-05, Vol.15 (5), p.e12605-n/a
• Main Authors: Rothermel, Juliane, Lass, Nina, Barth, Andre, Reinehr, Thomas
• Format: Article
• Language: English
• Subjects: bioactive leptin; Blood pressure; Childrens health; Hormones; Insulin resistance; lifestyle intervention; Obesity; Pediatrics; Thyroid gland; Weight control; weight loss
• ISSN: 2047-6302; 2047-6310
• DOI: 10.1111/ijpo.12605

Objective The adipokine omentin‐1 has been suggested to be inversely associated with obesity and insulin resistance in humans. We studied the relationships between omentin‐1, parameters of fat mass, insulin resistance, lipids and blood pressure in children with obesity in a longitudinal study. Methods We analysed omentin‐1 concentrations in 23 normal‐weight children and in 82 children with obesity participating in a one‐year lifestyle intervention. In the children with obesity, omentin‐1, bioactive and conventional leptin, thyroid hormones (thyroid‐stimulating hormone, free thyroxine 4, free triiodothyronine), body mass index, waist circumference, body fat based on skin‐fold measurements and bioimpedance analyses, lipids, insulin resistance as homeostatic model assessment of insulin resistance (HOMA‐IR) and blood pressure were determined at baseline and 1 year later. Furthermore, we measured omentin‐1 concentrations 1 year after the end of the lifestyle intervention. Results The omentin‐1 concentrations were significantly (P = .008) lower in children with obesity compared to normal‐weight children (296 ± 108 ng ml−1 vs. 232 ± 99 ng ml−1). Omentin‐1 concentrations increased significantly (P < .001) in children with obesity and substantial weight loss (35 ± 55 ng ml−1), while omentin‐1 concentrations did not change significantly (P = .750) in children with obesity without weight loss (−5 ± 108 ng ml−1) during the intervention. Substantial weight loss after the end of intervention led to a significant (P < .001) increase of omentin‐1 concentrations (+64 ± 14 ng ml−1). Omentin‐1 was significantly and negatively associated with HOMA‐IR both in cross‐sectional (r = −.27, P = .006) and longitudinal analyses (r = −.33, P = .001). Omentin‐1 concentrations were not related to pubertal stage, sex or thyroid hormones. Conclusions Our data do support the hypothesis that omentin‐1 is reversibly decreased in obesity and is a link between obesity and insulin resistance.