大鼠哺乳期营养过剩对脂代谢及成年肥胖的影响及其机制研究  

Effects and mechanism of overnutrition in rats during lactation on lipid metabolism and adult obesity

作　　者：于广娜[1] 陈玲 林亚梅 韩云峰 于清 崔莉莉 张方 董艳梅[3] YU Guang-na;CHEN Ling;LIN Ya-mei;HAN Yun-feng;YU Qing;CUI Li-li;ZHANG Fang;DONG Yan-mei(The Third Affiliated Hospital of Qiqihar Medical University,Qiqihar,Heilongjiang 161006,China;不详)

机构地区：[1]齐齐哈尔医学院附属三院,黑龙江齐齐哈尔161006 [2]齐齐哈尔市妇幼保健院 [3]齐齐哈尔医学院公共卫生学院,黑龙江齐齐哈尔161006

出　　处：《现代预防医学》2021年第14期2617-2621,共5页Modern Preventive Medicine

基　　金：齐齐哈尔医学科学院临床科研基金资助项目(QMSI2020L-12);国家卫生健康委能力建设和继续教育中心2019年度立项课题(GWJJ2019100308)。

摘　　要：目的阐明哺乳期过量喂养对脂代谢基因、蛋白和成年肥胖的影响,明确成年肥胖的发育源机制及早期防治策略。方法109只Wistar新生雄性大鼠,通过调整哺乳期母亲哺乳子代的数目形成正常喂养(对照组)和高能喂养(高能组),干预3周后断乳,断乳后各组均基础膳食喂养至成年,高脂膳食诱导肥胖。在不同生长发育阶段各组各处死8只鼠以动态观察,酶法测量血脂,计算体脂质量,FQ-PCR法和WB法检测ACC1、FAS、CPT1、UCP3基因和/或蛋白的含量。结果与对照组相比,高能组大鼠在成年高脂诱导肥胖后的体脂质量(F=11.840,P=0.008,P=0.009)、体重(F=11.913,P=0.008,P=0.008)增加;血清TG(F=9.871,P=0.013,P=0.011)、血清TC增加(F=7.436,P=0.024,P=0.022),HDL-C减少(F=9.407,P=0.014,P=0.013);ACC1(F=121.782,P<0.001,P<0.001)、FAS基因(F=92.354,P<0.001,P<0.001)的含量增加,UCP3(F=36.236,P<0.001,P<0.001)、CPT1基因(F=21.427,P=0.002,P=0.001)和UCP3(F=29.016,P=0.001,P=0.001)、CPT1蛋白(F=41.222,P<0.001,P<0.001)的含量减少。结论大鼠哺乳期营养过剩可通过持续降低脂肪分解,增加脂肪合成而导致脂代谢紊乱、体脂质量增加和成年肥胖。Objective To elucidate the effects of lactational overfeeding on lipid metabolism genes, proteins and adult obesity,and to clarify the developmental source mechanisms and early prevention strategies of adult obesity. Methods A total of 109 Wistar neonatal male rats were given normal feeding(control group) and high energy feeding(high energy group) by adjusting the number of mothers nursing their offspring during lactation, weaned after 3 weeks of intervention, and all groups were fed basal diets until adulthood after weaning, and high-fat diets induced obesity. Eight rats were executed in each group at different growth and developmental stages for dynamic observation, enzymatic measurement of blood lipids and calculation of body fat mass, and FQ-PCR and western blotting(WB) methods were used to detect the content of ACC1, FAS, CPT1, UCP3 genes and/or proteins. Results At 14 weeks, the high energy diet increased the body weight(F=11.913, P=0.008, P=0.008),serum TG(F=9.871, P=0.013, P=0.011), TC(F=7.436, P=0.024, P=0.022), body fat mass(F=11.840, P=0.008, P= 0.009) and FAS(F=92.354, P<0.001, P<0.001), and ACC1 gene expression(F=121.782, P<0.001, P<0.001), but decreased serum HDLC(F= 9.407, P=0.014, P=0.013) and the gene and protein expression of CPT1(F=21.427, P=0.002, P=0.001;F=41.222, P<0.001, P<0.001) and UCP3(F=29.016, P=0.001, P=0.001;F=29.016, P=0.001, P=0.001) compared with the control group.Conclusion Nutritional excess during lactation in rats can lead to disorders of lipid metabolism, increased body fat mass, and adult obesity by consistently decreasing lipolysis and increasing lipid synthesis.

关 键 词：肥胖 基因 哺乳期 CPT1 营养过剩 

分 类 号：R589.2[医药卫生—内分泌] R15[医药卫生—内科学]