Plasma brain-derived neurotrophic factor in prepubertal obese children: results from a 2-year lifestyle intervention programme
Plasma brain-derived neurotrophic factor in prepubertal obese children: results from a 2-year lifestyle intervention programme
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DOI：
10.1111/j.1365-2265.2012.04431.x
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发表时间：
2012-11-01
影响因子：
3.2
通讯作者：
Caixas, Assumpta
中科院分区：
文献类型：
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作者：
Corripio, Raquel;Gonzalez-Clemente, Jose-Miguel;Caixas, Assumpta
脑源性神经营养因子（BDNF）是一种神经营养因子，可能参与成人肥胖和代谢综合征的病理生理过程。在儿童中，它几乎没有被研究过。目的分析青春期前肥胖人群生活方式干预2年前后血浆脑源性神经营养因子（BDNF）水平及其与代谢综合征组分的关系。设计和设置病例对照研究，在转诊的儿科内分泌门诊中心进行为期2年的前瞻性随访。患者和方法73青春期前肥胖儿童，8.03类似+/-类似1.08类似岁，和47年龄和性别匹配的瘦对照进行了研究。对人体测量参数、血压、血小板计数（PLT）、口服葡萄糖耐量试验、胰岛素抵抗稳态模型评估（HOMA-IR）、血脂、BDNF、饮食和体力活动进行评价。如果z评分体重指数（BMI）降低至少0.5 SD，则认为体重减轻。结果在基线时，青春期前肥胖儿童的BDNF水平低于瘦对照儿童（P = 0.076）。BDNF与任何代谢综合征成分无关。2年后，肥胖患者的BDNF增加。经年龄、性别、青春期、BMI、PLT和HOMA-IR校正后的回归模型分析显示，在体重减轻（P相似=相似0.036）、经常运动（P相似=相似=相似= 0.008）和碳水化合物摄入充足（P相似=相似=相似= 0.032）的受试者中，BDNF增加。结论：青春期前肥胖儿童的血浆BDNF水平往往低于瘦对照组，与代谢综合征的任何其他成分无关，并在生活方式干预计划后升高。
Context Brain-derived neurotrophic factor (BDNF) is a neurotrophin potentially involved in the pathophysiology of obesity and metabolic syndrome in adults. In children, it has scarcely been studied. Objective To analyse plasma BDNF and its relationship with metabolic syndrome components before and after 2 similar to years of a lifestyle intervention programme in a prepubertal obese cohort. Design and setting Casecontrol study with a 2-year prospective follow-up in a referral paediatric endocrine outpatient centre. Patients and methods Seventy-three prepubertal obese children, 8.03 similar to +/-similar to 1.08 similar to years old, and 47 age- and gender-matched lean controls were studied. Anthropometric parameters, blood pressure, platelet count (PLT), oral glucose tolerance test, homoeostatic model assessment for insulin resistance (HOMA-IR), lipid profile, BDNF, diet and physical activity were evaluated. Weight loss was considered if z-score body mass index (BMI) decreased at least 0.5 SD. Results At baseline, BDNF tended to be lower in prepubertal obese children compared with lean controls (P similar to=similar to 0.076). BDNF did not correlate with any metabolic syndrome component. After 2 similar to years, obese patients showed an increase in BDNF. Regression model analysis adjusted by age, sex, puberty, BMI, PLT and HOMA-IR showed that BDNF increased in subjects who lost weight (P similar to=similar to 0.036), practiced sports (P similar to=similar to 0.008) and had an adequate carbohydrate intake (P similar to=similar to 0.032). Conclusions Plasma BDNF tends to be lower in obese prepubertal children than in lean controls, is not related to any other metabolic syndrome component and increases after a lifestyle intervention programme.