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

Abstract

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.

The “Adipo-Cerebral” Dialogue in Childhood Obesity: Focus on Growth and Puberty. Physiopathological and Nutritional Aspects

“…Therefore, it is clearly linked to LGI and indexes of inflammations, as demonstrated in children [75]. It is involved in adipogenesis, both in adult and children obesity, and its levels are elevated [31,32], particularly when visceral adipose tissue is predominant; it is positively correlated with leptin and negatively with adiponectin [33]; children with low Vitamin D levels exhibited higher chemerin concentrations [76]. Chemerin has been recently shown to be a marker of NAFLD in children [77].…”

“…Therefore, it is clearly linked to LGI and indexes of inflammations, as demonstrated in children [75]. It is involved in adipogenesis, both in adult and children obesity, and its levels are elevated [31,32], particularly when visceral…”

Bird evolution by insulin resistance

“…Four genes that supposedly maintain insulin sensitivity are missing in the bird genome [42][43][44][45] and encode the following: (i) omentin [37], (ii) GLUT4 [38,39], (iii) uncoupling protein 1 (UCP1)/UCP2 [40], and (iv) plasminogen receptor [41]. The loss of these four genes may have contributed to insulin resistance in the Triassic period, the development of which may have transformed theropods to become hyperathletic.…”

“…Omentin, secreted from adipocytes, is supposed to suppress insulin resistance and can restore insulin sensitivity [42][43][44][45]. Dakovic et al [37] reported that omentin as well as resistin, tumor necrosis factor-α (TNF-α), and plasminogen activator inhibitor are missing in the bird genome.…”

“…Dakovic et al [37] reported that omentin as well as resistin, tumor necrosis factor-α (TNF-α), and plasminogen activator inhibitor are missing in the bird genome. In mammals, insulin sensitivity is notably regulated by the actions of omentin secreted by adipose tissue, which can modulate the activity of the insulin receptor [42][43][44][45]. .…”