In:
Hormone Research in Paediatrics, S. Karger AG, Vol. 70, No. 3 ( 2008), p. 165-173
Abstract:
〈 i 〉 Aim: 〈 /i 〉 We investigated whether rosiglitazone protects β-cells from glucolipotoxicity directly. 〈 i 〉 Methods: 〈 /i 〉 INS-1 cells were incubated with 25 m 〈 i 〉 M 〈 /i 〉 glucose and 0.5 m 〈 i 〉 M 〈 /i 〉 palmitate in the absence or presence of 2.5 µ 〈 i 〉 M 〈 /i 〉 rosiglitazone. We evaluated caspase-3 expression and nuclear DAPI staining. An in vivo study was performed, in which 18-week-old Otsuka Long-Evans Tokushima Fatty (OLETF) rats were treated with rosiglitazone (4 mg/kg/day, n = 6) and with placebo (n = 6) for 10 weeks. At 28 weeks of age, an oral glucose tolerance test, insulin sensitivity test, TUNEL assay and histologic examination were performed. 〈 i 〉 Results: 〈 /i 〉 Rosiglitazone attenuated glucolipotoxicity-induced nuclear change and caspase-3 expression for 8 h after treatment, but this effect was not observed at 12 h in INS-1 cells. Rosiglitazone treatment decreased β-cell apoptosis, preserved β-cell mass and improved glucose tolerance in OLETF rats. 〈 i 〉 Conclusion: 〈 /i 〉 The present in vitro findings suggest that rosiglitazone can inhibit the early stage of glucolipotoxicity-induced β-cell apoptosis. Our results suggest that the antidiabetic action of rosiglitazone is, at least in part, related to a direct effect on β-cells rather than simply an indirect effect of improving insulin sensitivity.
Type of Medium:
Online Resource
ISSN:
1663-2818
,
1663-2826
Language:
English
Publisher:
S. Karger AG
Publication Date:
2008
detail.hit.zdb_id:
2540224-9
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