Purpose: Childhood obesity is a major risk factor for chronic diseases such as type 2 diabetes (T2D) and cardiovascular disease. Elevated soluble suppression of tumorigenicity 2 (sST2) is associated with obesity, diabetes, and cardiovascular disease in adults, and is used as a biomarker of cardiometabolic disease. Such biomarkers play an important role in the management of obesity and cardiometabolic disease. In this cross-sectional study, we examined the levels of circulating sST2 in children and adolescents, as well as its association with inflammatory and metabolic markers. Methods: A total of 85 children and adolescents (aged 5-16 years) were included. Participants' characteristics included being of normal weight (body mass index, BMI <85th percentile; n=13), overweight (BMI 85-94th percentile; n=2), or obese (BMI ≥95th percentile; n=70; a total of 8 with confirmed T2D). Clinical and biochemical markers (including plasma glucose, glycated hemoglobin (HbA1c), insulin, vitamin D, and lipid, liver, and renal profiles) were assessed using established procedures on peripheral blood samples. The levels of sST2, interleukin (IL)-33, IL-6, C-reactive protein (CRP), leptin, and adiponectin, were quantified using commercially available ELISA kits. Results: sST2 level was directly correlated with body fat % (r=0.3, P=0.016, n=64) and fat to muscle ratio (r=0.37, P=0.01, n=45), but inversely correlated with muscle mass % (r=-0.34, P=0.02, n=45). sST2 level was directly correlated with insulin (r=0.29, P=0.04, n=50), HbA1c (r=0.29, P=0.04, n=51), and urea (r=-0.34, P=0.01, n=54). sST2 level was directly correlated with the inflammatory markers CRP (r=0.34, P=0.008, n=59) and IL-6 (r=0.32, P=0.0045, n=77). The data were consistent after adjustment for age and sex. Conclusion: Increased circulating levels of sST2 is associated with increased body fat, metabolic dysfunction, and inflammation in children and adolescents. Disclosure A.Hasan: None. S.P.Kochumon: None. I.D.Albasiri: None. F.Almulla: None. R.Ahmad: None. Funding The Kuwait Foundation for the Advancement of Sciences (RA2011-018)
Purpose: Circulating calprotectin is elevated in inflammatory disorders and is a biomarker of severity in inflammatory rheumatic and bowel diseases. Calprotectin has immunomodulatory properties that may influence the progression and outcome of inflammatory diseases. Calprotectin is elevated in children with obesity, but its levels in children with T1D co-morbid with obesity remain unexplored. We examined the levels of circulating calprotectin in children with T1D and obesity and compared these levels with those of children with normal weight as well as those with obesity and T2D or children with obesity only (no prediabetes or T2D). Methods: Sixty-four children (aged 5-13 years) were included. Participants' characteristics included being of normal weight (body mass index, BMI <85th percentile; n = 12), having obesity (BMI ≥95th percentile) with T1D (n = 4), obesity with T2D (n = 8), or having obesity without prediabetes or diabetes (n = 40). Clinical markers were assessed using established procedures on peripheral blood. The levels of calprotectin were quantified using commercially available ELISA kits. Results: Circulating calprotectin was significantly (P = 0.0044) higher in children with T1D and obesity, as well as in children with T2D and obesity (P = 0.02), compared to healthy children with normal weight. There was no difference in calprotectin levels between children with T1D and obesity compared to those with T2D and obesity or obesity without prediabetes or diabetes. Conclusion: Increased calprotectin in children with T1D (as well as T2D) is due to the obese state and is not further increased by having diabetes. Given the immunomodulatory properties of calprotectin, obesity in children with T1D might hasten disease progression, resulting in a worse outcome. These findings highlight the need for tailored obesity prevention in children with high risk for T1D and emphasize the importance of treatment strategies for weight management in children with T1D. Disclosure A. Hasan: None. S. P. Kochumon: None. I. D. Albasiri: None. S. Albeloushi: None. E. S. Alozairi: None. F. Almulla: None. Funding Kuwait Foundation for the Advancement of Sciences
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