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目的探讨孕鼠营养异常对子鼠成年后胰岛素、瘦素抵抗的影响。方法 36只孕鼠随机分成低蛋白组(低蛋白饲料喂养)、高营养组(高营养饲料喂养)及正常营养组(普通饲料喂养),每组12只,各组孕鼠均足月自然分娩。正常营养组子鼠为正常体重组,低蛋白组子鼠体重小于孕龄(SGA)为 SGA 组(体重小于正常体重组子鼠平均体重2 s 以下),高营养组子鼠体重大于孕龄(LGA)为 LGA 组(体重高于正常营养组子鼠平均体重2 s 以上),每组子鼠36只。于子鼠出生后4周、12周龄时采用酶联免疫吸附试验测定其胰岛素、瘦素水平及胰岛素敏感指数(ISI)。结果(1)低蛋白组子鼠体重明显低于正常体重组(P<0.01),69%的子鼠为 SGA。高营养组子鼠体重明显高于正常体重组(P<0.01),38%的子鼠为 LGA。(2)子鼠出生4周时,SGA 组子鼠与正常体重组比较,体重已无显著差异,肾脏周围脂肪重量(FW)、FW 与体重(BW)比值分别为(0.36±0.14)g、6.5±0.3,显著高于正常体重组的(0.19±0.13)g、3.4±0.3(P<0.01,P<0.05);LGA 组子鼠 FW/BW 比值与正常体重组比较,差异无统计学意义(P>0.05)。子鼠出生12周时,SGA 组子鼠体重为(222±19)g,LGA 组子鼠体重为(257±24)g,均明显高于正常体重组的(215±25)g(P<0.05,P<0.01)。SGA 组子鼠FW/BW 比值为10.5±5.1,LGA 组子鼠为11.8±3.6,均明显高于正常体重组的7.2±3.6(P<0.01)。(3)SGA 组子鼠在出生4周时,胰岛素、瘦素水平分别为(5.5±0.9)μg/L、(6.1±0.7)μg/L,ISI 为3.4±0.3,与正常体重组比较,差异有统计学意义(P<0.05);出生12周时,胰岛素、瘦素水平及 ISI 的变化与正常体重组比较,差异有统计学意义(P<0.01)。LGA 组子鼠在出生4周时,胰岛素、瘦素水平及 ISI 分别为(4.0±1.0)μg/L、(5.0±0.3)μg/L 及4.1±0.5,与正常体重组比较,差异无统计学意义(P>0.05);出生12周时的胰岛素、瘦素水平及 ISI 与正常体重组比较,差异有统计学意义(P<0.01)。结论孕鼠营养异常将导致子鼠出生体重异常,体重异常子鼠在成年后可发生腹型肥胖以及胰岛素、瘦素抵抗。
Objective To investigate the effects of abnormal pregnant rats on insulin and leptin resistance after adult mice. Methods Thirty-six pregnant rats were randomly divided into low protein group (low protein diet), high nutrition group (high nutrition group) and normal nutrition group (12 groups) . Normal nutrition group rats were normal weight group, low protein group rats weight less than gestational age (SGA) for the SGA group (body weight less than the normal body weight of rats in the average body weight of 2 s or less), high nutrition group rats heavier than gestational age LGA) was LGA group (body weight was higher than that of normal nutrition group rats over 2 s), 36 rats in each group. At 4 weeks and 12 weeks after birth, the insulin and leptin levels and insulin sensitivity index (ISI) were measured by enzyme-linked immunosorbent assay. Results (1) The weight of hypoproteinemia mice was significantly lower than that of normal weight (P <0.01), and 69% of the mice were SGA. The body weight of high nutrition group mice was significantly higher than that of normal weight group (P <0.01), and 38% of the mice were LGA. (2) There was no significant difference in body weight between SGA group and normal weight group at 4 weeks after birth. The ratio of weight of fat (FW) to weight of body weight (BW) in kidney of SGA group was (0.36 ± 0.14) g, 6.5 ± 0.3, which was significantly higher than that in normal weight group (0.19 ± 0.13g, 3.4 ± 0.3, P <0.01, P <0.05). There was no significant difference in FW / BW ratio between LGA group and normal weight group (P> 0.05). At 12 weeks of birth, the body weight of SGA rats was (222 ± 19) g and that of LGA rats was (257 ± 24) g, which were significantly higher than that of normal weight rats (215 ± 25 g) (P < 0.05, P <0.01). The FW / BW ratio of SGA group was 10.5 ± 5.1, while that of LGA group was 11.8 ± 3.6, which was significantly higher than that of the normal group (7.2 ± 3.6, P <0.01). (3) The levels of insulin and leptin in SGA group were (5.5 ± 0.9) μg / L and (6.1 ± 0.7) μg / L and ISI were 3.4 ± 0.3 at 4 weeks of birth, respectively. Compared with normal weight group, (P <0.05). At 12 weeks of birth, the changes of insulin, leptin and ISI were significantly different from those of normal weight group (P <0.01). At 4 weeks after birth, insulin, leptin levels and ISI were (4.0 ± 1.0) μg / L, (5.0 ± 0.3) μg / L and 4.1 ± 0.5, respectively, in LGA group. Compared with normal weight group, the difference was not statistically significant Significance (P> 0.05). The levels of insulin, leptin and ISI at 12 weeks of birth were significantly different from those of normal weight group (P <0.01). Conclusion Abnormal nutrition in pregnant rats will lead to birth weight abnormalities. Abdominal obesity, insulin resistance and leptin resistance may occur in adult mice with abnormal weight.