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胰腺β细胞质量的调节。

Regulation of pancreatic beta-cell mass.

作者信息

Bouwens Luc, Rooman Ilse

机构信息

Cell Differentiation Unit, Vrije Universiteit Brussel/Free University of Brussels, Laarbeeklaan 103, B-1090 Brussels, Belgium.

出版信息

Physiol Rev. 2005 Oct;85(4):1255-70. doi: 10.1152/physrev.00025.2004.

Abstract

Beta-cell mass regulation represents a critical issue for understanding diabetes, a disease characterized by a near-absolute (type 1) or relative (type 2) deficiency in the number of pancreatic beta cells. The number of islet beta cells present at birth is mainly generated by the proliferation and differentiation of pancreatic progenitor cells, a process called neogenesis. Shortly after birth, beta-cell neogenesis stops and a small proportion of cycling beta cells can still expand the cell number to compensate for increased insulin demands, albeit at a slow rate. The low capacity for self-replication in the adult is too limited to result in a significant regeneration following extensive tissue injury. Likewise, chronically increased metabolic demands can lead to beta-cell failure to compensate. Neogenesis from progenitor cells inside or outside islets represents a more potent mechanism leading to robust expansion of the beta-cell mass, but it may require external stimuli. For therapeutic purposes, advantage could be taken from the surprising differentiation plasticity of adult pancreatic cells and possibly also from stem cells. Recent studies have demonstrated that it is feasible to regenerate and expand the beta-cell mass by the application of hormones and growth factors like glucagon-like peptide-1, gastrin, epidermal growth factor, and others. Treatment with these external stimuli can restore a functional beta-cell mass in diabetic animals, but further studies are required before it can be applied to humans.

摘要

β细胞质量调节是理解糖尿病的一个关键问题,糖尿病是以胰腺β细胞数量近乎绝对(1型)或相对(2型)缺乏为特征的一种疾病。出生时存在的胰岛β细胞数量主要由胰腺祖细胞的增殖和分化产生,这一过程称为新生。出生后不久,β细胞新生停止,一小部分处于增殖周期的β细胞仍能增加细胞数量以补偿胰岛素需求的增加,尽管速度缓慢。成体中β细胞自我复制的能力很低,以至于在广泛的组织损伤后无法实现显著的再生。同样,长期增加的代谢需求会导致β细胞无法进行代偿。胰岛内外祖细胞的新生是导致β细胞质量强劲扩张的一种更有效的机制,但这可能需要外部刺激。出于治疗目的,可以利用成体胰腺细胞以及可能还有干细胞令人惊讶的分化可塑性。最近的研究表明,通过应用胰高血糖素样肽-1、胃泌素、表皮生长因子等激素和生长因子来再生和扩大β细胞质量是可行的。用这些外部刺激进行治疗可以恢复糖尿病动物的功能性β细胞质量,但在应用于人类之前还需要进一步研究。

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