近年研究发现，孕期营养状况对子代成年疾病的发生有重要的影响，探讨生命早期营养因素的程序性作用及作用机制成为研究的热点。本研究以Wistar大鼠为对象，将喂饲高碳水化合物饲料(HCD)、高蛋白质饲料(HPD)、高中链脂肪酸饲料(HMCFAD)和高长链脂肪酸饲料(HLCFAD)的孕鼠所产雄性大鼠分为四组，分别为HC、HP、HMCF和HLCF组，由喂饲HCD的孕鼠哺乳3w断乳，转为HCD喂饲5w后，将HC组随机分为两组：一组继续喂饲HCD (HC组)；另一组喂饲高饱和长链脂肪酸饲料(HSLCFAD),为高脂高碳水化合物(HFHC)组，同时HP、HMCF和HLCF组大鼠也喂饲HSLCFAD,高脂诱导肥胖6w后结束实验。分期处死大鼠，动态观察体重、体脂含量、血脂、肥胖相关的代谢基因和蛋白的表达，研究孕期喂饲不同构成饲料对子代肥胖的程序性影响及机制。结果如下： 一、大鼠体重和体脂含量的动态变化 喂饲不同构成饲料的孕鼠子代出生体重无显著性差异(P＞0.05)；断乳时HP组的体重和HMCF组的体重及体脂含量均低于HC组(P＜0.05)；喂饲HCD至第8w时，各组体重和体脂含量均无显著性差异(P＞0.05)；喂饲HSLCFAD后，HFHC和HLCF组的体重和体脂含量均高于HC组(P＜0.05)； HP和HMCF组的体重和体脂含量均明显低于HFHC组(P＜0.05)。 二、大鼠血脂的动态变化 喂饲不同构成饲料的孕鼠子代出生时血脂无差异；断乳时，与HC组相比，其余三组的TG均降低(P＜0.05), HMCF组的HDL升高(P＜0.05)；喂饲HCD至第8w时，HMCF组TG降低(P＜0.05)，其余各组均无显著性差异(P＞0.05)；喂饲HSLCFAD 后，HP 和 HMCF 组 TG 均降低(P＜0.05), HDL 均升高(P＜0.05)。 三、大鼠成年高脂饲料诱导肥胖的肥胖率 HSLCFAD后各组的肥胖率分别为：HP组33.33%, HMCF组30%，HFHC组70%, HLCF组63.33%。其中HP和HMCF组的肥胖率明显低于HFHC组(P＜0.05)，HLCF与HFHC组的肥胖率差异无显著性(P＞0.05)。说明喂饲HPD和HMCFAD的孕鼠子代在摄入HSLCFAD后不易发生肥胖，而喂饲HCD和HLCFAD的孕鼠子代容易发生肥胖。 四、大鼠肥胖相关的代谢基因和蛋白表达的动态变化 (一)HFHC组 与 HC 组相比，喂饲 HSLCFAD 后 HFHC 组 AMPK、ACC、FAS、HSL、CPT1、 PEPCK、UCP3 基因和 AMPK、P-AMPK、CPT1、UCP3 蛋白表达升高，PFK 基因表达降低。脂肪代谢活跃，氧化分解及合成均增加；糖异生增加，葡萄糖酵解减少；热能消耗增加，导致体脂沉积、体重和血脂增加。说明高脂饲料诱导肥胖模型成功。 (二)HP组 喂饲HPD的孕鼠子代从出生到成年高脂饲料诱导肥胖后，AMPK、P-AMPK、 HSL、CPT1、PFK、UCP3基因和蛋白表达持续升高。而且ACC、FAS、PEPCK基因在喂饲高脂饲料(母乳和HSLCFAD)时表达降低，UCP2基因表达升高，导致大鼠脂肪分解氧化、葡萄糖酵解和热能消耗持续增加，尤其是在大鼠接触高脂饲料时，脂肪合成和糖异生减少。导致该组孕鼠子代成年高脂诱导肥胖后体脂沉积、体重和血脂降低。 (三)HMCF组 喂饲HMCFAD的孕鼠子代从出生到成年高脂饲料诱导肥胖后，AMPK、 P-AMPK、PFK、CPT1、UCP3基因和蛋白表达持续升高，PEPCK基因表达持续降低。而且喂饲HSLCFAD时HSL、UCP2基因表达升高。导致脂肪氧化分解、糖酵解和能量消耗持续增加，糖异生持续减少，在成年高脂诱导肥胖后更加明显。导致该组孕鼠子代体脂含量、体重和血脂持续降低。 (四)HLCF组 喂饲HLCFAD的孕鼠子代从出生到成年高脂饲料诱导肥胖后，PEPCK基因表达持续升高，糖异生和甘油异生持续增加；HSL基因表达持续降低，脂解作用持续减弱。在喂饲HCD和HSLCFAD时PFK、AMPK、P-AMPK、CPT1基因与蛋白表达均降低，高脂饲料诱导肥胖后ACC、FAS、UCP2，3基因和蛋白表达均降低。致使葡萄糖酵解及脂肪氧化、合成降低，热能消耗减少，导致该组孕鼠子代成年高脂饲料诱导肥胖后体脂沉积、体重和血脂增加。 总之，本研究发现孕期增加蛋白质和MCFA可以程序性缓解子代成年喂饲HSLCFAD时血脂代谢紊乱和肥胖的发生。其机制是孕期不同饲料构成可影响胎儿肥胖相关的代谢基因的表达，形成特定的基因表达谱，进而程序性影响成年高脂诱导肥胖的体脂沉积、血脂及肥胖的形成。 关键词：不同饲料构成；子代；肥胖；程序性

 Maternal dietary had important effects on obesity in adult offspring.The male offsprings of wistar pregnant rats which received high-carbohydrate diet(HCD), high-protein diet (HPD),high medium-chain fatty acid diet, (HMCFAD), high long-chain fatty acid diet (HLCFAD) throughout gestation respectively were divided into HC, HP, HMCF and HLCF group. The offsprings were suckled by foster mothers fed HCD. At weaning, the offsprings fed on HCD for five weeks. Then HC group were assigned to two subgroup: HC group fed HCD; high-fat high carbohydrate (HFHC) group. HFHC and the other three group offsprings were induced obesity with high saturated long-chain fatty acid diet (HSLCFAD) for six weeks. The offsprings were killed at different stages respectively. Blood fat and abundance of related gene and protein were detected. The results were as follow. 一. Body weight and body fat content of offspring Body weight and body fat content were insignificant compared with HC group at birth and week 8. However, after wean and HSLCFAD, body weight and body fat content were significantly decreased in HMCF group.Body weight were significantly decreased too in HP group. 二.Blood fat of offspring At birth, blood fat is insignificant difference compared with HC group offspring;TG of HP,HMCF and HLCF group were significantly decreased, and HDL of HMCF group were significantly increased at wean;After HCD, TG of HMCF group were significantly decreased; After HSLCFAD, TG of HP, HMCF group were significantly decreased, but HDL were significantly increased. 三.HSLCFAD-induced obesity rate of adult offspring After HSLCFAD-induced obesity, the obesity rate of HP, HMCF, HFHC and HLCF group were 33.33%, 30%, 70% and 63.33% respectively.The obesity rate was significantly decreased in HP and HMCF group compared with HFHC group.But the obesity rate was significantly increased in HFHC and HLCF group compared with HC group. 四.Obesity-related metabolic gene and protein expression of offspring (一) HFHC group The high expression of AMPK, ACC, FAS, HSL, CPT1, PEPCK, UCP3 gene and AMPK, CPT1, UCP3 protein promoted fatty acid synthesis, lipolysis, gluconeogenesis, and heat energy expenditure.The low expression of PFK gene inhibited glycolysis. These changes resulted in high body fat content and obesity rate. (二)HP group From birth to week 14, the persistently high expression of AMPK, P-AMPK,HSL, PFK, UCP3, CPT1 gene and protein promoted lipolysis, glycolysis, energy expenditure.The low expression of ACC, FAS, PEPCK gene inhibited fatty acid synthesis and gluconeogenesis after wean and HSLCFAD. These changes resulted in low body fat content, blood fat and obesity rate. (三) HMCF group From birth to week 14,the persistently high expression of AMPK, P-AMPK,PFK, CPT1, UCP3 gene and protein promoted lipolysis, glycolysis, energy expenditure. The persistently low expression of PEPCK gene inhibited gluconeogenesis. After HSLCFAD, the high expression of HSL, UCP2 gene promoted lipolysis and energy expenditure.These changes resulted in low body fat content, blood fat and obesity rate. (四) HLCF group From birth to week 14, the persistently high expression of PEPCK gene promoted gluconeogenesis.The persistently low expression of HSL gene inhibited lipolysis. After HSLCFAD, the low expression of AMPK,P-AMPK, ACC, FAS, CPT1, PFK, UCP2 and 3 gene and protein inhibited fatty acid synthesis, lipolysis, glycolysis, energy expenditure.These changes resulted in high blood fat, body fat content and obesity rate. In conclusion, HPD and HMCFAD during gestation will inhibit HSLCFAD-induced blood lipid metabolic disorder arid obesity rate in adult offspring. The mechanism was fetal programming by different dietary composition stimuli in early life. Key Words: different dietary composition; offspring; obesity; programming