alpha-Lipoic acid prevents mild portal endotoxaemia-induced hepatic inflammation and beta cell dysfunction

doi:10.1111/j.1365-2362.2011.02630.x

CNU IR > Pharmacy and Science > Dept. of Health and Nutrition (including master's program) > Periodical Articles > Item 310902800/27645

Please use this identifier to cite or link to this item: https://ir.cnu.edu.tw/handle/310902800/27645

Title:	alpha-Lipoic acid prevents mild portal endotoxaemia-induced hepatic inflammation and beta cell dysfunction
Authors:	Tian, Yu-Feng Hsieh, Chang-Hsun Hsieh, Yen-Ju Chen, Yu-Ting Peng, Yi-Jen Hsieh, Po-Shiuan
Contributors:	保健營養系
Keywords:	A-Lipoic Acid Beta Cell Dysfunction Chronic Hepatic Inflammation Oxidative Stress Portal Endotoxaemia
Date:	2012-06
Issue Date:	2014-03-21 16:16:19 (UTC+8)
Publisher:	Wiley-Blackwell
Abstract:	Eur J Clin Invest 2012; 42 (6): 637648 Abstract Background This study was undertaken to evaluate the preventive effect of a-lipoic acid (LA) on chronic mild portal endotoxaemia-mediated subacute hepatic inflammation and pancreatic beta cell dysfunction in rats. Materials and methods Male SpragueDawley 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 a 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 beta cell dysfunction. Conclusions a-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.
Relation:	European Journal of Clinical Investigation, 42(6), 637-648
Appears in Collections:	[Dept. of Health and Nutrition (including master's program)] Periodical Articles

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