早期营养干预对小于胎龄儿大鼠胰岛β细胞功能和形态的影响

The long-term functional and morphological effects of early nutrition interference on pancreatic β cells in the SGA rats

目的:探讨早期营养干预对小于胎龄儿(SGA)大鼠在4周(婴幼儿期)和12周(成年期)周龄时胰岛β细胞功能和形态的远期影响。方法:在SGA大鼠出生后早期给予30%高蛋白等热卡饮食的营养干预措施4周,然后恢复正常基础饮食,纵向观察营养干预对SGA大鼠在4、12周龄时体格发育、空腹血糖、胰岛素和胰岛素抵抗指数(HOMA-IR)、β细胞胰岛素分泌指数(HBCI)以及胰岛β细胞形态结构的变化。结果:SGA早期高蛋白营养干预组(A组)体质量、身长呈现合理的生长追赶,直至成年期无体质量超重的情况出现;SGA对照组(B组)无早期营养干预,在12周成年期出现明显的胰岛素抵抗(IR),血清胰岛素水平(9.31±0.72)和HOMA-IR(2.34±0.46)显著高于C组(7.30±0.58和1.77±0.36),P均<0.01;A组在4、12周时均无胰岛素抵抗的出现,其胰岛大小、胰岛β细胞比例,以及空腹血糖、胰岛素和HOMA-IR、HBCI与C组比较均无显著性差异(P>0.05)。结论:出生后早期(窗口期)给予高蛋白等热卡饮食营养干预,然后在非发育敏感时期恢复基础饮食,这既能满足SGA的生长需要,又能促进SGA胎儿期胰岛β细胞发育受损的恢复,避免或延缓成年期IR的发生,是改善SGA群体远期预后的有效措施。

Objective： To investigate the functional and morphological effect of early nutrition interference on pancreatic β cells in SGA rats at 4 weeks old （in the infancy） and 12 weeks old （in the adulthood）. Methods： Calorie diets were given neonatal SGA rats for four weeks. Longitudinal observation was carried out on the physical development, fasting blood glucose, insulin and insulin resistance index （HOMA-IR） , β cell insulin secretion index （HBCI） and morphological changes of the pancreatic β cells when the rats were 4 and 12 weeks old. Results： The weight and height of the SGA rats in the early protein interference group （Group A） developed in reasonable way, no overweight appeared; while insulin resistance was Observed in the SGA rats in the control group （Group B） without early nutrition interference, in which serum insulin level （9.31 ±0. 72） and HOMA-IR （2.34 ±0.46） were significantly higher than those in Group C （7.30 ±0.58 and 1.77 ±0.36, respectively, P 〈0.01）. There was no significant difference revealed islet size, pancreatic β cell proportion, fasting blood glucose, insulin, HOMA-IR or HBCI between Group A and Group C （P 〉 0. 05 ）. Conclusion： Provision of calorie diets like high protein as nutrition interference in the early period （ the window period） and basic diets during non-development period not only meets the need of growing but also promote the recovery of the fetal impaired pancreatic β cells, avoiding or delaying the IR in the adulthood.