In:
American Journal of Physiology-Endocrinology and Metabolism, American Physiological Society, Vol. 287, No. 5 ( 2004-11), p. E1008-E1018
Abstract:
A low-taurine diet during fetal or early postnatal life causes abnormal pancreatic β-cell development. Tissue and plasma taurine concentrations can also be low in diabetic patients. We examined the effect of taurine on impaired glucose responses in diabetic rat β-cells adenovirally overexpressing uncoupling protein (UCP)2, which is upregulated in obesity-related type 2 diabetes. We found that taurine pretreatment restored the ATP-to-ADP (ATP/ADP) ratio and glucose-stimulated insulin secretion in UCP2-infected islets. ATP-sensitive K + channel sensitivity to dihydroxyacetone, another insulin secretagogue, was similar in both UCP2-infected and control β-cells. In freshly isolated mitochondria from UCP2-overexpressing insulin-secreting (INS)-1 β-cells, methyl pyruvate-mediated mitochondrial Ca 2+ increase was significantly ameliorated by taurine. A mitochondrial Ca 2+ uniporter blocker, ruthenium red, inhibited the action of taurine. This study suggests that taurine enhances the glucose sensitivity of UCP2-overexpressing β-cells, probably by increasing mitochondrial Ca 2+ influx through the Ca 2+ uniporter, thereby enhancing mitochondrial metabolic function and increasing the ATP/ADP ratio.
Type of Medium:
Online Resource
ISSN:
0193-1849
,
1522-1555
DOI:
10.1152/ajpendo.00008.2004
Language:
English
Publisher:
American Physiological Society
Publication Date:
2004
detail.hit.zdb_id:
1477331-4
SSG:
12
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