Article

Elevated SNAP-25 is associated with fatty acid-induced impairment of mouse islet function.

Department of Medicine, University of Melbourne, Royal Melbourne Hospital, Parkville, Vic. 3050, Australia.
Biochemical and Biophysical Research Communications (impact factor: 2.48). 05/2004; 317(2):472-7. DOI:10.1016/j.bbrc.2004.03.067 pp.472-7
Source: PubMed

ABSTRACT The role of soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) proteins in insulin secretion following chronic exposure to non-esterified fatty acids (NEFAs) has not been extensively investigated. Here, we show that synaptosome-associated protein of 25 kDa (SNAP-25) levels were predominantly elevated in the soluble fraction of mouse islets exposed to palmitate. This coincided with an impairment of insulin secretion to glucose and non-glucose secretagogues, consistent with a defect at a distal regulatory step in exocytosis. Removal of palmitate from the media restored both SNAP-25 protein levels and insulin secretion to control levels. We conclude that increased expression of SNAP-25 is associated with NEFA-induced impairment of insulin secretion in mouse islets.

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Keywords

chronic exposure
 
control levels
 
distal regulatory step
 
exocytosis
 
insulin secretion
 
media
 
mouse islets
 
NEFA-induced impairment
 
non-esterified fatty acids
 
SNAP-25 protein levels
 
soluble N-ethylmaleimide-sensitive factor attachment protein receptor
 
synaptosome-associated protein