Changes in islet plasma membrane calcium-ATPase activity and isoform expression induced by insulin resistance

We studied the effect of insulin resistance (IR) induced by administration of a fructose-rich diet (FRD) to normal Wistar rats for 21 days, upon islet plasma membrane calcium ATPases (PMCAs) and insulin secretion. FRD rats showed significantly higher triglyceride and insulin levels, insulin:glucose...

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Detalles Bibliográficos
Autores: Alzugaray, Maria Eugenia, Garcia, Maria Elisa, del Zotto, Hector Herminio, Raschia, Maria Agustina, Palomeque, Julieta, Rossi, Juan Pablo Francisco, Gagliardino, Juan Jose, Flores, Luis Emilio
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2009
País:Argentina
Institución:Consejo Nacional de Investigaciones Científicas y Técnicas
Repositorio:CONICET Digital (CONICET)
Idioma:inglés
OAI Identifier:oai:ri.conicet.gov.ar:11336/94431
Acceso en línea:http://hdl.handle.net/11336/94431
Access Level:acceso abierto
Palabra clave:CALCIUM PUMPS
INSULIN RESISTANCE
INSULIN SECRETION
PANCREATIC ISLETS
PMCA ISOFORMS
PMCAS
https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
Descripción
Sumario:We studied the effect of insulin resistance (IR) induced by administration of a fructose-rich diet (FRD) to normal Wistar rats for 21 days, upon islet plasma membrane calcium ATPases (PMCAs) and insulin secretion. FRD rats showed significantly higher triglyceride and insulin levels, insulin:glucose ratio and HOMA-IR index than controls. FRD islets released significantly more insulin in response to glucose and showed (a) marked changes in PMCA isoform protein content (decreased PMCA 2 and increased PMCA 3), (b) a decrease in total PMCAs activity, and (c) higher levels of cytosolic calcium [Ca2+]i. The lower PMCAs activity with the resultant increase in [Ca2+]i would favor the compensatory greater release of insulin necessary to cope with the IR state present in FRD rats and to maintain normal glucose homeostasis. Thus, changes in PMCAs activity and isoform expression play a modulatory role upon insulin secretion during long-term adaptation to an increased hormone demand.