Impaired beta-cell regeneration in perinatally malnourished rats: a study with STZ.
Impaired beta-cell regeneration in perinatally malnourished rats: a study with STZ.
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围产期营养不良大鼠的 β 细胞再生受损：STZ 的研究。
DOI：
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发表时间：
2000
期刊：
影响因子：
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通讯作者：
B. Bréant
中科院分区：
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作者：
A. Garofano;P. Czernichow;B. Bréant
我们研究了在大鼠胎儿晚期和出生后早期营养不良期间观察到的β细胞质量减少的机制。研究了链脲佐菌素（STZ）破坏新生儿β细胞后β细胞的再生，包括增殖和新生。出生时注射STZ，母亲的食物限制一直持续到断奶。β-细胞质量，增殖和胰岛数量进行了定量的形态计量学测量胰腺切片STZ注射正常（C-STZ）和营养不良（R-STZ）的大鼠，与非注射C和R大鼠作为对照。在第4天，只有20%的β细胞质量留在C-STZ大鼠。它再生到未注射对照组的50%，主要是通过活跃的新生，如胰岛数/cm 2的完全恢复所示，也通过适度增加的β细胞增殖。相比之下，尽管β细胞增殖显著增加，但来自R-STZ动物的β细胞团再生不良，因为胰岛数/cm（2）恢复不足。总之，围产期营养不良损害新生和新生β细胞再生的能力，但保留β细胞增殖，这仍然是增加β细胞质量的选择。这些结果为营养不良的动物在衰老或妊娠期间适应其β细胞质量的能力受损提供了解释，这加剧了葡萄糖耐量。
We investigated the mechanisms implicated in beta-cell mass reduction observed during late fetal and early postnatal malnutrition in the rat. Beta-cell regeneration, including proliferation and neogenesis, was studied after neonatal beta-cell destruction by streptozotocin (STZ). STZ was injected at birth and maternal food restriction was continued until weaning. Beta-cell mass, proliferation, and islet number were quantified by morphometrical measurements on pancreatic sections in STZ-injected normal (C-STZ) and malnourished (R-STZ) rats, with noninjected C and R rats as controls. At day 4, only 20% of the beta cell-mass remained in C-STZ rats. It regenerated to 50% that of noninjected controls, mainly through active neogenesis, as shown by the entire recovery of islet number/cm(2), and also through moderately increased beta-cell proliferation. In contrast, beta-cell mass from R-STZ animals poorly regenerated, despite a dramatic increase of beta-cell proliferation, because islet number/cm(2) recovered insufficiently. In conclusion, perinatal malnutrition impairs neogenesis and the capacity of beta-cell regeneration by neogenesis but preserves beta-cell proliferation, which remains the elective choice to increase beta-cell mass. These results provide an explanation for the impaired capacity of malnourished animals to adapt their beta-cell mass during aging or pregnancy, which aggravate glucose tolerance.