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α-Lipoic acid prevents mild portal endotoxaemia-induced hepatic inflammation and β cell dysfunction.
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α-Lipoic acid prevents mild portal endotoxaemia-induced hepatic inflammation and β cell dysfunction.

Author: YF Tian Affiliation: Division of General Surgery, Department of Surgery, Yung Kung Campus, Chi-Mei Medical Center, Tainan, Taiwan.CH HsiehYJ HsiehYT ChenYJ PengAll authors
Edition/Format: Article Article : English
Publication:European journal of clinical investigation, 2012 Jun; 42(6): 637-48
Other Databases: WorldCatWorldCat
Summary:
BACKGROUND: This study was undertaken to evaluate the preventive effect of α-lipoic acid (LA) on chronic mild portal endotoxaemia-mediated subacute hepatic inflammation and pancreatic β cell dysfunction in rats. MATERIALS AND METHODS: Male Sprague-Dawley rats were randomly assigned into four groups: those with intraportal vehicle (saline) or low-dose lipopolysaccharide (LPS) (0·42 ng/kg/min) infusion, combined with  Read more...
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Details

Document Type: Article
All Authors / Contributors: YF Tian Affiliation: Division of General Surgery, Department of Surgery, Yung Kung Campus, Chi-Mei Medical Center, Tainan, Taiwan.; CH Hsieh; YJ Hsieh; YT Chen; YJ Peng; PS Hsieh
ISSN:0014-2972
Language Note: English
Unique Identifier: 796845181
Awards:

Abstract:

BACKGROUND: This study was undertaken to evaluate the preventive effect of α-lipoic acid (LA) on chronic mild portal endotoxaemia-mediated subacute hepatic inflammation and pancreatic β cell dysfunction in rats. MATERIALS AND METHODS: Male Sprague-Dawley rats were randomly assigned into four groups: those with intraportal vehicle (saline) or low-dose lipopolysaccharide (LPS) (0·42 ng/kg/min) infusion, combined with oral administration of vehicle or LA, a potent antioxidant (60 mg/kg/day) for 4 weeks. The hyperglycaemic clamp and euglycaemic clamp techniques were used to access the glucose-stimulated insulin secretion and systemic insulin sensitivity in vivo. RESULTS: Body weight, fasting plasma glucose and insulin were not different among groups. In rats with chronic intraportal LPS infusion, plasma C-reactive protein, amylase, superoxide levels, the contents of thiobarbituric acid-reactive substance, tumour necrosis factor α and interleukin 6 in liver and pancreas and also the gene expression of Toll-like receptor 4 in liver were significantly increased as compared with those with LA cotreatment. The histopathological examination showed that inflammatory changes were clearly visible in liver and pancreatic islets of LPS-infused rats and rarely observed in those cotreated with LA. In addition, low-dose intraportal LPS infusion also significantly impaired glucose-stimulated insulin secretion but not affect the systemic insulin sensitivity and metabolic clearance rate of insulin. LA administration markedly reversed LPS-induced β cell dysfunction. CONCLUSIONS: α-Lipoic acid cotreatment could significantly prevent mild portal endotoxaemia-induced chronic hepatic inflammation and impaired pancreatic insulin secretion in absence of changing systemic insulin resistance.

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    schema:description "RESULTS: Body weight, fasting plasma glucose and insulin were not different among groups. In rats with chronic intraportal LPS infusion, plasma C-reactive protein, amylase, superoxide levels, the contents of thiobarbituric acid-reactive substance, tumour necrosis factor α and interleukin 6 in liver and pancreas and also the gene expression of Toll-like receptor 4 in liver were significantly increased as compared with those with LA cotreatment. The histopathological examination showed that inflammatory changes were clearly visible in liver and pancreatic islets of LPS-infused rats and rarely observed in those cotreated with LA. In addition, low-dose intraportal LPS infusion also significantly impaired glucose-stimulated insulin secretion but not affect the systemic insulin sensitivity and metabolic clearance rate of insulin. LA administration markedly reversed LPS-induced β cell dysfunction." ;
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