학술논문

miR-124a expression contributes to the monophasic pattern of insulin secretion in islets from pregnant rats submitted to a low-protein diet.
Document Type
Article
Source
European Journal of Nutrition. Jun2018, Vol. 57 Issue 4, p1471-1483. 13p. 1 Chart, 8 Graphs.
Subject
*ANIMALS
*CALCIUM-binding proteins
*CELL physiology
*DIET in disease
*DIET therapy
*DYNAMICS
*GENE expression
*GLUCOSE
*INSULIN
*ISLANDS of Langerhans
*MEMBRANE proteins
*POLYMERASE chain reaction
*DIETARY proteins
*RATS
*SECRETION
*BIPHASIC insulin
Language
ISSN
1436-6207
Abstract
Purpose: To evaluate the role of miR-124a in the regulation of genes involved in insulin exocytosis and its effects on the kinetics of insulin secretion in pancreatic islets from pregnant rats submitted to a low-protein diet.Methods: Adult control non-pregnant (CNP) and control pregnant (CP) rats were fed a normal protein diet (17%), whereas low-protein non-pregnant (LPNP) and low-protein pregnant (LPP) rats were fed a low-protein diet (6%) from days 1 to 15 of pregnancy. Kinetics of the glucose-induced insulin release and measurement of [Ca2+]i in pancreatic islets were assessed by standard protocols. The miR-124a expression and gene transcriptions from pancreatic islets were determined by real-time polymerase chain reaction.Results: In islets from LPP rats, the first phase of insulin release was abrogated. The AUC [Ca2+]i from the LPP group was lower compared with the other groups. miR-124a expression was reduced by a low-protein diet. SNAP-25 mRNA, protein expression, and Rab3A protein content were lower in the LPP rats than in CP rats. Syntaxin 1A and Kir6.2 mRNA levels were decreased in islets from low-protein rats compared with control rats, whereas their protein content was reduced in islets from pregnant rats.Conclusions: Loss of biphasic insulin secretion in islets from LPP rats appears to have resulted from reduced [Ca2+]i due, at least in part, to Kir6.2 underexpression and from the changes in exocytotic elements that are influenced either directly or indirectly by miR-124a. [ABSTRACT FROM AUTHOR]