目的　探讨瘦素在男性青春期发育中的作用及其与胰岛素、生长激素、睾酮和雌二醇的相互关系。方法　筛选7-17岁单纯性肥胖男生150人,以相互身高相差不超过2cm，年龄相差不超过3个月进行配比，选择正常组和营养不良组各150人。结果　肥胖组血清瘦素水平显著高于正常组，正常组显著高于营养不良组。不论组别，男生血清瘦素水平均随年龄增长先升高再下降，肥胖组峰值为16-96μg/ L (10-11 岁)，正常组和营养不良组分别为10.25μg/ L 和5.08μg/ L (11-12岁)。男生血清瘦素水平从Tanner G1期到G2期显著上升,之后G2-4期出现逐步下降, G5期再次升高。7-17岁血清胰岛素水平随年龄增长而升高，生长激素、睾酮和雌二醇水平于10-11岁开始随年龄增长而升高。瘦素与胰岛素呈正相关，与生长激素呈负相关,与睾酮呈强负相关，与雌二醇无相关性。结论　瘦素可能有加速男性青春期发育的作用，而在启动和维持男性青春期发育中是非决定性因素。G5 期瘦素水平再次增长具有抑制生长激素分泌作用,预示青春期发育结束。

目的　探讨不同饲料构成对大鼠褐色脂肪组织、白色脂肪组织与骨骼肌解偶联蛋白- 2基因表达的影响。方法　利用不同的饲料(包括基础饲料、高蛋白、高脂肪饲料、高能饲料1与高能饲料2) 喂养雄性Wistar大鼠2个月，观察不同饲料构成对大鼠体重、脂体比与游离脂肪酸的影响，并应用RT-PCR方法则定大鼠褐色脂肪组织、白色脂肪组织与骨骼肌UCP2mRNA 表达水平。结果　高能饲料1组与高能饲料2组的体重、脂体比与游离脂肪酸均显著高于基础组、高蛋白组与高脂肪组( P<0.05)，而后三者的体重、脂体比与游离脂肪酸无显著性差异( P>0.05)。高能饲料1 与高能饲料2组白色脂肪组织UCP2基因表达增强，而能量相同的基础组、高蛋白组与高脂肪组没有明显差异。各组褐色脂肪组织与骨骼肌UCP2 mRNA 水平相近。结论　能量能诱导大鼠白色脂肪组织UCP2 mRNA 表达，表达的强弱与体内的储存能量多少有关。褐色脂肪组织与骨骼肌UCP2 mRAN 表达不受饲料成分的影响。

The aim of this study was to investigate the effects of a post-weaning isocaloric hyper-soybean oil diet on later obesity and explore the underlying mechanisms. In the present study, newborn male Wistar rats were weaned on d 24, divided into CON (control), HC and HSO groups. CON was assigned to AIN-93G diet (a hypercarbohydrate diet, for short HC diet) during the entire experiment. HC and HSO were fed with HC and isocaloric hyper-soybean oil (HSO) diet for 3 wk respectively, fed with HC diet for 2 wk successively, finally administrated high fat diet (HF) for 6 wk to induce obesity. On 3,5,11wk, the body weight, body fat content, blood glucose, blood lipid, serum insulin and leptin levels and obesity-related gene (CPT-1, FAS, UCP2, UCP3) expression levels in rats were detected. It was shown that body weight, body fat content, blood glucose and blood lipid, serum insulin and leptin levels in HSO were down-regulated on 3 and 5wk, therefore were significantly reduced on 11wk vs. HC. The CPT-1, UCP2, UCP3 gene expressions were up-regulated but FAS were down-regulated persistently in HSO. The study indicated that an early isocaloric HSO diet may reduce later obesity risk and reduce blood lipid and glucose abnormalities in adulthood via persistently influencing insulin and leptin sensitivity and permanent regulation of obesity-related gene expressions.

目的　探讨肥胖抵抗大鼠摄食量减少的原因。方法　采用50只健康雄性SD大鼠，分为对照组10只和高脂组40只，分别用基础饲料和高脂饲料喂养13周，然后根据体重和能量摄入量筛选出饮食诱导肥胖抵抗(DD-R)大鼠9只和饮食诱导肥胖(DD)大鼠10只，观察总摄食量的变化，放免法测定血清瘦素和血浆神经肽Y水平，免疫印迹法测定大鼠脑组织中黑色素皮质激素受体-4 (MCR24)蛋白含量。结果　DD-R大鼠总摄食量为(1679.1±146.8)g，明显低于DD大鼠的总摄食量(1818.4±148.9)g。DD-R大鼠血浆神经肽Y含量为(795.24±83.59)ng/L,显著低于DD大鼠(1007.14±172.83) ng/L；基础组大鼠血清瘦素含量为(4.80±0.75)μg/L, DD-R组为(9.17±1.19)μg/L， DD组为(9.32±1.04)μg/L,提示高脂饲料使大鼠血清瘦素水平明显增加，但DD-R与DD大鼠间无明显差别；基础组大鼠脑组织中MCR-4含量峰面积分析表明基础组为(342±31)mm2，DD-R组为(455±33)mm2，DD组为(355±30) mm2，说明高脂饲料使DD-R大鼠脑组织中MCR24含量增加。结论　DD-R大鼠通过增加ob基因的表达降低神经肽Y途径活性并激活MCR-4途径来减少进食量,从而抑制体重的增加。