Anık Ahmet, Çatlı Gönül, Abacı Ayhan, Küme Tuncay, Bober Ece
J Pediatr Endocrinol Metab. 2014 Jul;27(7-8):623-8. doi: 10.1515/jpem-2013-0475.
Nesfatin-1, a recently discovered anorexigenic peptide, is expressed in several tissues, including pancreatic islet cells and central nervous system. However, its pathophysiological role in the development of obesity and insulin resistance remains unknown.
To investigate the possible involvement of nesfatin-1 in the pathogenesis of childhood obesity, we examined the relationship between fasting and postprandial nesfatin-1 concentrations and metabolic/antropometric parameters in obese children.
The study included obese children with a body mass index >95th percentile. Fasting serum glucose, insulin, lipid profile, fasting and postprandial (120th min) nesfatin-1 levels were measured to evaluate the metabolic parameters. Different cutoff values for prepubertal and pubertal stages were used to determine the status of insulin resistance (HOMA-IR) (prepubertal >2.5, pubertal >4). The percentage of body fat was measured using bioelectric impedance analysis.
Seventy-one obese children were included in this study. There was no statistically significant difference between fasting and postprandial nesfatin-1 levels in obese subjects (0.70 ± 0.15 and 0.69 ± 0.14 ng/mL, p>0.05, respectively). Insulin resistance was observed in 58% (41/71) of the cases. There was no significant difference in either fasting or postprandial serum nesfatin-1 levels between the insulin-resistant and non-resistant groups (p>0.05). There was no correlation between fasting and postprandial serum nesfatin-1 levels and anthropometric and metabolic parameters in insulin-resistant and non-resistant groups.
In this study, there was no significant increase in the postprandial level of nesfatin-1. This observation suggested that oral glucose load in obese children may not be sufficient for nesfatin-1 response and that nesfatin-1 may not have an effect as a short-term regulator of food intake.
Nesfatin-1是一种最近发现的厌食肽，在包括胰岛细胞和中枢神经系统在内的多种组织中表达。然而，其在肥胖和胰岛素抵抗发生发展中的病理生理作用仍不清楚。
为了研究Nesfatin-1在儿童肥胖发病机制中的可能作用，我们检测了肥胖儿童空腹和餐后Nesfatin-1浓度与代谢/人体测量参数之间的关系。
研究纳入体重指数>第95百分位数的肥胖儿童。测量空腹血糖、胰岛素、血脂谱、空腹和餐后（120分钟）Nesfatin-1水平以评估代谢参数。使用青春期前和青春期的不同临界值来确定胰岛素抵抗状态（HOMA-IR）（青春期前>2.5，青春期>4）。使用生物电阻抗分析测量体脂百分比。
本研究纳入71名肥胖儿童。肥胖受试者空腹和餐后Nesfatin-1水平之间无统计学显著差异（分别为0.70±0.15和0.69±0.14 ng/mL，p>0.05）。58%（41/71）的病例存在胰岛素抵抗。胰岛素抵抗组和非抵抗组的空腹或餐后血清Nesfatin-1水平均无显著差异（p>0.05）。胰岛素抵抗组和非抵抗组的空腹和餐后血清Nesfatin-1水平与人体测量和代谢参数之间均无相关性。
在本研究中，Nesfatin-1的餐后水平没有显著升高。这一观察结果表明，肥胖儿童口服葡萄糖负荷可能不足以引起Nesfatin-1反应，并且Nesfatin-1可能不作为食物摄入的短期调节因子发挥作用。
