The dynamic plasticity of insulin production in β-cells

被引:138
作者
Boland, Brandon B. [1 ]
Rhodes, Christopher J. [1 ]
Grimsby, Joseph S. [1 ]
机构
[1] MedImmune, Cardiovasc & Metab Dis Res, 1 Medlmmune Way, Gaithersburg, MD 20878 USA
关键词
T2DM; Insulin production; beta-cell rest; ISLET AMYLOID POLYPEPTIDE; GENOME-WIDE ASSOCIATION; SECRETORY GRANULE BIOGENESIS; DEPENDENT DIABETES-MELLITUS; PEPTIDE-1 RECEPTOR AGONISTS; ISOLATED PANCREATIC-ISLETS; UNFOLDED PROTEIN RESPONSE; ISOLATED RAT ISLETS; PROINSULIN BIOSYNTHESIS; GROWTH-HORMONE;
D O I
10.1016/j.molmet.2017.04.010
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background: Although the insulin-producing pancreatic beta-cells are quite capable of adapting to both acute and chronic changes in metabolic demand, persistently high demand for insulin will ultimately lead to their progressive dysfunction and eventual loss. Recent and historical studies highlight the importance of 'resting' the beta-cell as a means of preserving functional beta-cell mass. Scope of Review: We provide experimental evidence to highlight the remarkable plasticity for insulin production and secretion by the pancreatic beta-cell alongside some clinical evidence that supports leveraging this unique ability to preserve beta-cell function. Major conclusions: Treatment strategies for type 2 diabetes mellitus (T2DM) targeted towards reducing the systemic metabolic burden, rather than demanding greater insulin production from an already beleaguered beta-cell, should be emphasized to maintain endogenous insulin secretory function and delay the progression of T2DM. (C) 2017 MedImmune, LLC. Published by Elsevier GmbH.
引用
收藏
页码:958 / 973
页数:16
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