ESPE Abstracts

Introduction: Neurotensin is a 13 amino acid peptide with central and intestinal effects. It has been shown to decrease intestinal and gastric motility, increase the absorption of fat by regulating the release of pancreas and bile acid. In addition, it is reported that there is also an anorexigenic effect of the neurotensin released from the central nervous system. In the literature, conflicting results related to serum / plasma neurotensin levels were reported in experimental and adult obese studies.

Objective: In this study, we aimed to evaluate the effect of serum neurotensin level (i) on metabolic and anthropometric parameters in obese children, (ii) its role in binge eating disorder patogonesis and (iii) on food consumption / preference.

Materials and Methods: The study included adolescents with a body mass index (BMI)> 95p who presented with weight gain between 12-17 years of age and healthy adolescents with a BMI of 3 artiş85p, similar in age and gender. Anthropometric measurements and biochemical analyzes [fasting blood glucose, insulin, lipid profile, ALT, insulin resistance, serum neurotensin, ghrelin and leptin levels] were performed in all cases. Body fat analysis was evaluated with bioelectric impedance device. In all cases, the presence of binge eating disorder (TYB) and three-day food consumption were evaluated.

Results: 65 obese (32 girls, 14,6 ± 1,4 years) and 65 healthy adolescents (32 girls, 14,6 ± 1,5 years) were included in the study. In obese group, BMI, BMI standard deviation score (SDS), waist circumference, fat percentage, fat mass, fasting insulin, insulin resistance index, triglyceride, leptin and neurotensin levels were significantly higher and ghrelin level was significantly lower than the control group. When the levels of leptin, ghrelin and neurotensin were compared in terms of insulin resistance and the presence of TYB in the obese group, no statistically significant difference was found. No significant difference was found in the relation of serum neurotensin level with anthropometric, metabolic and nutritional consumption levels in obese and control groups.

Conclusion: Although the high neurotensin in obese patients has a role in the etiopathogenesis of obesity by increasing intestinal effect (by increasing lipid absorption), it is observed that its effect on TYB is not obvious. The results of this study suggest the presence of hypothalamic neurotensin resistance (increase in compensatory neurotensin) despite the high neurotensin level and no anorexigenic effect detected in obese patients