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祖细胞可能有助于代谢健康的肥胖个体成功实现胰岛代偿。

Progenitor cells may aid successful islet compensation in metabolically healthy obese individuals.

作者信息

Singh Himadri, Parthasarathy Vikram, Farouk Mohammed, Venkatesan Vijayalakshmi

机构信息

Biochemistry/Stem Cell Research, National Institute of Nutrition (ICMR), Tarnaka, Hyderabad, Andhra Pradesh, India.

Department of Biochemistry, Sri BM Patil Medical College Hospital and Research Centre, BLDE University, Bijapur, Karnataka, India.

出版信息

Med Hypotheses. 2016 Jan;86:97-9. doi: 10.1016/j.mehy.2015.10.027. Epub 2015 Oct 28.

Abstract

Obesity is associated with insulin resistance and type 2 diabetes. Fortunately most obese, insulin-resistant individuals do not develop type 2 diabetes as they can overcome reduced efficiency of insulin action by increasing the functional β-cell mass. Compelling evidences suggest β-cells neogenesis through progenitor/stem cells residing in pancreatic ductal cells and islets, but the role of β-cell regeneration in obesity/insulin resistance from progenitor/stem cells is not clear. Based on many indirect evidences in human studies such as unchanged β-cell replication, apoptosis and size during compensation in insulin resistance in humans, we suggest successful β-cells mass compensation in metabolically healthy obesity is contributed by neoformation of β-cells, through expansion of progenitor cells/stem cells in synergy with β-cell replication.

摘要

肥胖与胰岛素抵抗和2型糖尿病相关。幸运的是,大多数肥胖的胰岛素抵抗个体不会发展为2型糖尿病,因为他们可以通过增加功能性β细胞量来克服胰岛素作用效率的降低。有力证据表明,通过存在于胰腺导管细胞和胰岛中的祖细胞/干细胞可实现β细胞新生,但祖细胞/干细胞在肥胖/胰岛素抵抗中β细胞再生的作用尚不清楚。基于人类研究中的许多间接证据,如人类胰岛素抵抗代偿期间β细胞复制、凋亡和大小未发生变化,我们认为代谢健康型肥胖中β细胞量的成功代偿是由β细胞新形成所致,即通过祖细胞/干细胞的扩增与β细胞复制协同作用实现。

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