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Protective effects of r-alpha-lipoic acid and acetyl-l-carnitine in min6 and isolated rat islet cells chronically exposed to oleic acid

文献类型:期刊论文

作者Shen, Weili2; Liu, Kai2; Tian, Chuan2,3; Yang, Lu2; Li, Xuesen2,3; Ren, Jinmin2; Packer, Lester4; Head, Elizabeth; Sharman, Edward; Liu, Jiankang1,2
刊名Journal of cellular biochemistry
出版日期2008-07-01
卷号104期号:4页码:1232-1243
关键词Acetyl-l-carnitine Insulin secretion R-alpha-lipoic acid Mitochondria Oxidative stress Uncoupling protein (ucp)-2 Beta-cell
ISSN号0730-2312
DOI10.1002/jcb.21701
通讯作者Liu, jiankang(j.liu@uci.edu)
英文摘要Mitochondrial dysfunction due to oxidative stress and concomitant impaired p-cell function may play a key role in type 2 diabetes. preventing and/or ameliorating oxidative mitochondrial dysfunction with mitochondria-specific nutrients may have preventive or therapeutic potential. in the present study, the oxidative mechanism of mitochondrial dysfunction in pancreatic beta-cells exposed to sublethal levels of oleic acid (oa) and the protective effects of mitochondrial nutrients [r-alpha-lipoic acid (la) and acetyl-l-carnitine (alc)] were investigated. chronic exposure (72 h) of insulinoma min6 cells to oa (0.2-0.8 mm) increased intracellular oxidant formation, decreased mitochondrial membrane potential (mmp), enhanced uncoupling protein-2 (ucp-2) mrna and protein expression, and consequently, decreased glucose-induced atp production and suppressed glucose-stimulated insulin secretion. pretreatment with la and/or alc reduced oxidant formation, increased mmp, regulated ucp-2 mrna and protein expression, increased glucose-induced atp production, and restored glucose-stimulated insulin secretion. the key findings on atp production and insulin secretion were verified with isolated rat islets. these results suggest that mitochondrial dysfunction is involved in oa-induced pancreatic p-cell dysfunction and that pretreatment with mitochondrial protective nutrients could be an effective strategy to prevent p-cell dysfunction.
WOS关键词PANCREATIC BETA-CELLS ; STIMULATED INSULIN-SECRETION ; FREE FATTY-ACIDS ; UNCOUPLING PROTEIN-2 ; MITOCHONDRIAL DYSFUNCTION ; INS-1 CELLS ; TRIGLYCERIDE ACCUMULATION ; METABOLIC ANTIOXIDANT ; OXIDATIVE DAMAGE ; HIGH GLUCOSE
WOS研究方向Biochemistry & Molecular Biology ; Cell Biology
WOS类目Biochemistry & Molecular Biology ; Cell Biology
语种英语
WOS记录号WOS:000257567300010
出版者WILEY-LISS
URI标识http://www.irgrid.ac.cn/handle/1471x/2390983
专题中国科学院大学
通讯作者Liu, Jiankang
作者单位1.Univ Calif Irvine, Inst Brain Aging & Dementia, Gillespie Neurosci Res Facil 1261, Irvine, CA 92697 USA
2.Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Nutr Sci, Shanghai 200031, Peoples R China
3.Chinese Acad Sci, Grad Sch, Beijing, Peoples R China
4.Univ So Calif, Dept Mol Pharmacol & Pharmaceut Sci, Sch Pharm, Los Angeles, CA 90089 USA
推荐引用方式
GB/T 7714
Shen, Weili,Liu, Kai,Tian, Chuan,et al. Protective effects of r-alpha-lipoic acid and acetyl-l-carnitine in min6 and isolated rat islet cells chronically exposed to oleic acid[J]. Journal of cellular biochemistry,2008,104(4):1232-1243.
APA Shen, Weili.,Liu, Kai.,Tian, Chuan.,Yang, Lu.,Li, Xuesen.,...&Liu, Jiankang.(2008).Protective effects of r-alpha-lipoic acid and acetyl-l-carnitine in min6 and isolated rat islet cells chronically exposed to oleic acid.Journal of cellular biochemistry,104(4),1232-1243.
MLA Shen, Weili,et al."Protective effects of r-alpha-lipoic acid and acetyl-l-carnitine in min6 and isolated rat islet cells chronically exposed to oleic acid".Journal of cellular biochemistry 104.4(2008):1232-1243.

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来源:中国科学院大学

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