Abnormal mitochondrial function impairs calcium influx in diabetic mouse pancreatic beta cells / 中华医学杂志(英文版)
Chinese Medical Journal
;
(24): 502-510, 2012.
Artigo
em Inglês
| WPRIM
| ID: wpr-262582
ABSTRACT
<p><b>BACKGROUND</b>Abnormal insulin secretion of pancreatic beta cells is now regarded as the more primary defect than the insulin function in the etiology of type 2 diabetes. Previous studies found impaired mitochondrial function and impaired Ca(2+) influx in beta cells in diabetic patients and animal models, suggesting a role for these processes in proper insulin secretion. The aim of this study was to investigate the detailed relationship of mitochondrial function, Ca(2+) influx, and defective insulin secretion.</p><p><b>METHODS</b>We investigated mitochondrial function and morphology in pancreatic beta cell of diabetic KK-Ay mice and C57BL/6J mice. Two types of Ca(2+) channel activities, L-type and store-operated Ca(2+) (SOC), were evaluated using whole-cell patch-clamp recording. The glucose induced Ca(2+) influx was measured by a non-invasive micro-test technique (NMT).</p><p><b>RESULTS</b>Mitochondria in KK-Ay mice pancreatic beta cells were swollen with disordered cristae, and mitochondrial function decreased compared with C57BL/6J mice. Ca(2+) channel activity was increased and glucose induced Ca(2+) influx was impaired, but could be recovered by genipin.</p><p><b>CONCLUSION</b>Defective mitochondrial function in diabetic mice pancreatic beta cells is a key cause of abnormal insulin secretion by altering Ca(2+) influx, but not via Ca(2+) channel activity.</p>
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Fisiologia
/
Cálcio
/
Secreções Corporais
/
Diabetes Mellitus
/
Eletrofisiologia
/
Células Secretoras de Insulina
/
Potencial da Membrana Mitocondrial
/
Insulina
/
Metabolismo
/
Camundongos Endogâmicos C57BL
Tipo de estudo:
Estudo prognóstico
Limite:
Animais
Idioma:
Inglês
Revista:
Chinese Medical Journal
Ano de publicação:
2012
Tipo de documento:
Artigo
Similares
MEDLINE
...
LILACS
LIS