REGULATION OF ISLET BETA-CELL PROLIFERATION BY PROLACTIN IN RAT ISLETS
REGULATION OF ISLET BETA-CELL PROLIFERATION BY PROLACTIN IN RAT ISLETS
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DOI：
10.2337/diabetes.43.2.263
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发表时间：
1994-02-01
期刊：
影响因子：
7.7
通讯作者：
SORENSON, RL
中科院分区：
文献类型：
--
作者：
BRELJE, TC;PARSONS, JA;SORENSON, RL
本研究探讨了催乳素对朗格汉斯胰岛β细胞增殖的影响。在绵羊催乳素(OPRL)或大鼠催乳素(RPRL)存在下，培养4d的新生大鼠胰岛可显著增加胰岛素分泌和β细胞增殖。这些影响可以通过在培养液中加入抗oPRL血清来预防。虽然胰岛素分泌和β细胞增殖在rPRL暴露的前24小时略有增加，但胰岛素分泌和β细胞增殖的反应在4天后达到最大，6-10天后达到最大。β细胞对rPRL的最初促有丝分裂反应是由未分裂的β细胞有限地募集到细胞周期中以及大多数子细胞直接进入额外的细胞分裂周期而发生的。随后，rPRL对β细胞增殖的最大影响被维持在较高的募集率，以前未分裂的β细胞进入细胞周期，只有四分之一的子代细胞继续分裂。这些观察结果很难与胰岛中存在能够进行细胞分裂的有限的β细胞池的说法相一致。相反，这些观察表明，单个β细胞正在短暂地重新进入细胞周期，并对rPRL做出反应，不太频繁地分裂。在这种情况下，大多数β细胞不会处于不可逆的G(O)期。我们还证明，rPRL对β细胞增殖的影响发生在正常的血糖浓度，并受到多胺代谢抑制剂的影响。关于rPRL对胰岛β细胞影响的进一步研究应该会为胰岛素需求增加时调控胰岛细胞增殖提供重要信息。
This study examined the effects of prolactin on beta-cell proliferation in pancreatic islet of Langerhans. Insulin secretion and beta-cell proliferation were significantly increased from neonatal rat Islets cultured for 4 days in the presence of either 500 ng/ml ovine prolactin (oPRL) or rat prolactin (rPRL). These effects could be prevented by including anti-oPRL serum in the culture media. Although insulin secretion and beta-cell proliferation were slightly higher during the first 24 h of exposure to rPRL, maximal response was observed after 4 days for Insulin secretion and 6-10 days for beta-cell proliferation. The initial mitogenic response of beta-cell to rPRL occurred by the limited recruitment of nondividing beta-cells into the cell cycle and by most daughter cells proceeding directly into additional cell division cycles. Subsequently, the maximal effect of rPRL on beta-cell proliferation was maintained by a higher rate of recruitment of previously nondividing beta-cells into cell cycle with only one fourth of the daughter cells continuing to divide. These observations are difficult to reconcile with the proposal that a limited pool of beta-cells capable of undergoing cell division exists in islets. Instead, these observations suggest that individual beta-cells are transiently re-entering the cell cycle and dividing infrequently in response to rPRL. In this case, the majority of the beta-cells would not be expected to be in an irreversible G(o) phase. We also demonstrated that the effects of rPRL on beta-cell proliferation occur at normal serum glucose concentrations and are affected by inhibitors of polyamine metabolism. Additional studies on the effects of rPRL on beta-cells should provide important information on the regulation of beta-cell proliferation during conditions of increased insulin demand.