摘要
目的观察追赶生长模型中摄食相关激素生长激素(GH)、胰岛素样生长因子-1(IGF-1)、胃饥饿素(ghrelin)、胆囊收缩素(CCK)和瘦素(leptin)的变化,探讨其在追赶生长发生中的作用。方法 48只5周龄雄性SD大鼠适应性喂养1周后,随机分为对照组(NC)和限食后追赶生长组(CUGRF)。NC组给予自由进食,CUGRF组给予同龄NC组进食量的60%,6周后开放自由进食。开放进食0、8、12周和16周时以酶联免疫吸附法(ELISA)测定GH、IGF-1、ghrelin、leptin、CCK等指标。结果从开放进食第14周开始CUGFR组体重追赶上NC组,差异无统计学意义(P>0.05)。两组间血清IGF-1、ghrelin、CCK浓度在各检测时间点差异均无统计学意义(均P>0.05);CUGFR组GH在限食6周后显著升高[CUGFR vs NC,(30.96±4.42)μg/L vs(21.07±4.81)μg/L,P<0.05],而leptin在限食6周后显著降低[(CUGFR vs NC,(2.63±0.57)μg/L vs(4.45±0.40)μg/L,P<0.05]。结论大鼠限食后追赶生长模型属完全追赶生长,在追赶生长大鼠模型中GH、leptin分泌水平有显著变化,并可能与CCK等能量平衡调节因子共同参与了脂肪沉积、胰岛素抵抗状态的形成以及糖代谢障碍。
Objective To observe the change of the feeding related hormone growth hormone（GH）,insulin-like growth factor-1（IGF-1）,ghrelin,cholecystokinin（CCK）and leptin in the rat model of catch-up growth after food restriction,and explore the effects of such hormones in the catch-up phenomenon. Methods After fed on normal chow for 1 week,48 5-week male SD rats were divided into normal control group（NC）and catch-up growth after food restriction group（CUGFR）.CUGFR rats were given a 60% food-restricted diet determined by quantification of normal intake in the ad libitum-fed rats for 6 weeks,and then re-fed for 0,8,12,16 weeks respectively.Serum GH,IGF-1,ghrelin,leptin and CCK were quantitatively estimated by sandwich enzyme-linked immunoabsorbent assay（ELISA）. Results There was no statistically significant difference in the body weight between CUGFR group and NC group after re-feeding for 14 weeks.There were no statistically significant differences in IGF-1,ghrelin and CCK between the two groups.However,the GH was increased[CUGFR group vs NC group,（30.96±4.42） vs（21.07±4.81） μg/L,P0.05] and leptin decreased [CUGFR group vs NC group,（2.63±0.57） vs（4.45±0.40） μg/L,P0.05] after food restriction for 6 weeks. Conclusion The CUGFR model shows a completed catch-up growth.GH and leptin are significantly changed in the CUGFR model and they maybe work together with other energy regulatory factors such as CCK in increasing body fat,decreasing insulin sensitivity,which may lead to the disturbances of glucose metabolism.
出处
《华中科技大学学报（医学版）》
CAS
CSCD
北大核心
2011年第5期537-541,共5页
Acta Medicinae Universitatis Scientiae et Technologiae Huazhong
基金
国家自然科学基金资助项目(No.30771035
No.30800531)
