ESPE Abstracts

Introduction: Chronic inflammation is closely associated with metabolic disorders such as obesity, insulin resistance and Type 2 DM, and is dependent on abnormal cytokine production and activation of inflammatory signaling pathways. Adipose tissue is a metabolically active organ that can be a source of low-grade chronic inflammation in obese individuals. Our aim in this study; to determine whether there are changes in proinflammatory and antiinflammatory cytokine levels in obese/overweight and Type 2 diabetes mellitus children and to evaluate their relationship with clinical and laboratory findings and body fat distribution.

Materials and methods: The study included 44 (50%) obese/overweight, 16 (18.2%) Type 2 Diabetes patients and 28 (31.8%) healthy children with normal body mass index (BMI), between the ages of 10-18 who applied to the Pediatric Endocrinology Clinic. TNF-α, IL-1β, IL-6, IL-18 and IFN-γ as proinflammatory markers; TGF-β and IL-10 levels as antiinflammatory markers were studied. Subcutaneous, preperitoneal and visceral fat tissue thickness was measured by abdominal ultrasonography in the obese/overweight group and Type 2 DM group, and the presence and degree of hepatosteatosis were evaluated.

Results: Age and gender distribution was similar between the groups. While all 16 patients in the Type 2 DM group had a family history of diabetes, 31 (70.5%) of 44 obese/overweight patients had a family history of diabetes (P=0.013). While hepatosteatosis was present in all cases in the Type 2 DM group, hepatosteatosis was detected in 36 cases (81.8%) in the obese/overweight group. High density lipoprotein (HDL) cholesterol was lower in the Type 2 DM group than in the obese/overweight group (P=0.016). While visceral and preperitoneal adipose tissue thickness was similar to the obese/overweight group in the Type 2 DM group, subcutaneous adipose tissue thickness was higher than the obese/overweight group (P=0.021). Subcutaneous adipose tissue thickness and HDL cholesterol were significantly negatively correlated in the Type 2 DM group (P=0.003, r=-0.684). TGF-β level was significantly lower in the Type 2 DM group than the control group (P=0.039), and there was no difference between the groups in other cytokine levels. There was no significant correlation between TGF-β level and clinical findings and laboratory variables in the type 2 DM group.

Conclusion: TGF-β level was found to be lower than the control group in children with Type 2 DM. It was thought that the change in TGF-β level might have a role in the pathogenesis of Type 2 DM.