desumoylation controls insulin exocytosis in response to metabolic signals

Clicks: 329
ID: 147042
2012
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Abstract
The secretion of insulin by pancreatic islet β-cells plays a pivotal role in glucose homeostasis and diabetes. Recent work suggests an important role for SUMOylation in the control of insulin secretion from β-cells. In this paper we discuss mechanisms whereby (de)SUMOylation may control insulin release by modulating β-cell function at one or more key points; and particularly through the acute and reversible regulation of the exocytotic machinery. Furthermore, we postulate that the SUMO-specific protease SENP1 is an important mediator of insulin exocytosis in response to NADPH, a metabolic secretory signal and major determinant of β-cell redox state. Dialysis of mouse β-cells with NADPH efficiently amplifies β-cell exocytosis even when extracellular glucose is low; an effect that is lost upon knockdown of SENP1. Conversely, over-expression of SENP1 itself augments β-cell exocytosis in a redox-dependent manner. Taken together, we suggest that (de)SUMOylation represents an important mechanism that acutely regulates insulin secretion and that SENP1 can act as an amplifier of insulin exocytosis.
Reference Key
macdonald2012biomoleculesdesumoylation Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors ;Patrick E. MacDonald;Xiaoqing Dai;Elisa Vergari;Gregory Plummer
Journal international journal of middle east studies
Year 2012
DOI
10.3390/biom2020269
URL
http://www.mdpi.com/2218-273X/2/2/269
Keywords
insulin nadph exocytosis sumoylation redoxmicrobiology

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