Regulation of β-cell mass by hormones and growth factors
Regulation of β-cell mass by hormones and growth factors
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DOI：
10.2337/diabetes.50.2007.s25
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发表时间：
2001-02-01
期刊：
影响因子：
7.7
通讯作者：
Carlsson, C
中科院分区：
文献类型：
--
作者：
Nielsen, JH;Galsgaard, ED;Carlsson, C
在胰腺发育的分子机制、β细胞基因表达的调控以及生长因子在β细胞分化、生长和再生中的作用等方面积累了大量的新信息。本文综述了近年来生长激素（GH）和催乳素（PRL）等细胞因子在β细胞增殖和基因表达中的作用机制，特别是信号转导和转录激活因子（STAT）蛋白的作用。细胞因子信号传导抑制因子（SOCS）蛋白的发现对刺激和抑制细胞因子（包括生长激素、PRL、瘦素、促炎细胞因子白介素-1和干扰素- γ）之间的相互作用在β细胞存活中的意义尚不清楚。最近的研究表明，细胞粘附分子和δ样蛋白前脂肪细胞因子1/胎儿抗原1 （Pref-1/ fa -1）在细胞因子诱导的β -细胞生长和发育中的作用。令人惊讶的是，最近发现胰高血糖素样肽-1 （GLP-1）不仅可以刺激胰岛素分泌，还可以刺激β细胞的复制和分化，这可能为2型糖尿病的治疗提供新的视角。随着关于胰岛素对β细胞生长和功能的积极作用的有趣报道，一个信号事件的综合网络正在出现，这些信号事件协同作用，控制β细胞对胰岛素需求的适应。
Substantial new information has accumulated on molecular mechanisms of pancreas development, regulation of beta -cell gene expression, and the role of growth factors in the differentiation, growth, and regeneration of beta -cells. The present review focuses on some recent studies on the mechanism of action of cytokines such as growth hormone (GH) and prolactin (PRL) in beta -cell proliferation and gene expression-in particular, the role of signal transducers and activators of transcription (STAT) proteins. The implication of the discovery of suppressors of cytokine signaling (SOCS) proteins for the interaction between stimulatory and inhibitory cytokines, including GH, PRL, leptin, and the proinflammatory cytokines interleukin-1 and interferon-gamma, in beta -cell survival is not yet clear. Recent studies indicate a role of cell adhesion molecules and the delta-like protein preadipocyte factor 1/fetal antigen 1 (Pref-1/FA-l) in cytokine-induced beta -cell growth and development. Surprisingly, glucagon-like peptide-1 (GLP-1) was recently found to stimulate not only insulin secretion but also beta -cell replication and differentiation, which may present a new perspective in treatment of type 2 diabetes. Together with the intriguing reports on positive effects of insulin on both beta -cell growth and function, a picture is emerging of an integrated network of signaling events acting in concert to control beta -cell mass adaptation to insulin demand.