Lipid Metabolism and Nutrigenomics – Impact of Sesame Lignans on Gene Expression Profiles and Fatty Acid Oxidation in Rat Liver

Author(s):  
Takashi Ide ◽  
Yasutaka Nakashima ◽  
Hiroshi Iida ◽  
Satoko Yasumoto ◽  
Masumi Katsuta
2002 ◽  
Vol 13 (5) ◽  
pp. 289-295 ◽  
Author(s):  
Masayo Kushiro ◽  
Takeshi Masaoka ◽  
Shinji Hageshita ◽  
Yoko Takahashi ◽  
Takashi Ide ◽  
...  

Author(s):  
Takashi Ide ◽  
Hideyuki Kobayashi ◽  
Lakshmikuttyamma Ashakumary ◽  
Isabelle A. Rouyer ◽  
Yoko Takahashi ◽  
...  

2013 ◽  
Vol 304 (1) ◽  
pp. G72-G86 ◽  
Author(s):  
Haiyan Zhang ◽  
Wen-Jun Shen ◽  
Yuan Cortez ◽  
Fredric B. Kraemer ◽  
Salman Azhar

Creosote bush-derived nordihydroguaiaretic acid (NDGA), a lipoxygenase inhibitor, possesses antioxidant properties and functions as a potent antihyperlipidemic agent in rodent models. Here, we examined the effect of chronic NDGA treatment of ob/ob mice on plasma dyslipidemia, hepatic steatosis, and changes in hepatic gene expression. Feeding ob/ ob mice a chow diet supplemented with either low (0.83 g/kg diet) or high-dose (2.5 g/kg diet) NDGA for 16 wk significantly improved plasma triglyceride (TG), inflammatory chemokine levels, hyperinsulinemia, insulin sensitivity, and glucose intolerance. NDGA treatment caused a marked reduction in liver weight and TG content, while enhancing rates of fatty acid oxidation. Microarray analysis of hepatic gene expression demonstrated that NDGA treatment altered genes for lipid metabolism, with genes involved in fatty acid catabolism most significantly increased. NDGA upregulated the mRNA and nuclear protein levels of peroxisome proliferator-activated receptor α (PPARα), and the activated (phosphorylated) form of AMP-activated kinase. NDGA increased PPARα promoter activity in AML12 hepatocytes and also prevented the fatty acid suppression of PPARα expression. In contrast, PPARα siRNA abrogated the stimulatory effect of NDGA on fatty acid catabolism. Likewise, no stimulatory effect of NDGA on hepatic fatty acid oxidation was observed in the livers of PPARα-deficient mice, but the ability of NDGA to reverse fatty liver conditions was unaffected. In conclusion, the beneficial actions of NDGA on dyslipidemia and hepatic steatosis in ob/ob mice are exerted primarily through enhanced fatty acid oxidation via PPARα-dependent pathways. However, PPARα-independent pathways also contribute to NDGA's action to ameliorate hepatic steatosis.


1989 ◽  
Vol 257 (4) ◽  
pp. R822-R828 ◽  
Author(s):  
M. J. Azain ◽  
J. A. Ontko

These studies were undertaken to further characterize and explain the differences in hepatic fatty acid metabolism between lean and obese Zucker rats. It was shown that the rate of palmitate or octanoate oxidation and the inhibition of palmitate oxidation by malonyl CoA in mitochondria isolated from lean and obese Zucker rats were similar. Cytochrome oxidase activity was similar in lean and obese rat livers. It was found that the addition of cytosol from the obese rat liver inhibited palmitate oxidation by 20-30% in mitochondria isolated from lean or obese rat livers and thus reproduced the conditions observed in the intact cell. Increased concentrations of metabolites such as malonyl CoA and glycerophosphate in the liver of the obese rat are likely contributors to this inhibitory effect. These results are extrapolated to the intact cell and suggest that decreased hepatic fatty acid oxidation in the obese rat can be accounted for by cytosolic influences on the mitochondria. The decreased rate of fatty acid oxidation observed in the intact hepatocyte or perfused liver cannot be explained by a defect in the capacity of mitochondria to oxidize substrate or by a decrease in mitochondrial number in the obese rat liver.


2009 ◽  
Vol 37 (2) ◽  
pp. 79-87 ◽  
Author(s):  
Keiko Motoyama ◽  
Yuji Nakai ◽  
Tomoya Miyashita ◽  
Yuichiro Fukui ◽  
Maki Morita ◽  
...  

To elucidate the physiological responses to a social stressor, we exposed mice to an isolation stress and analyzed their hepatic gene expression profiles using a DNA microarray. Male BALB/c mice were exposed to isolation stress for 30 days, and then hepatic RNA was sampled and subjected to DNA microarray analysis. The isolation stress altered the expression of 420 genes (after considering the false discovery rate). Gene Ontology analysis of these differentially expressed genes indicated that the stress remarkably downregulated the lipid metabolism-related pathway through peroxisome proliferator-activated receptor-α, while the lipid biosynthesis pathway controlled by sterol regulatory element binding factor 1, Golgi vesicle transport, and secretory pathway-related genes were significantly upregulated. These results suggest that isolation for 30 days with a mild and consecutive social stress regulates the systems for lipid metabolism and also causes endoplasmic reticulum stress in mouse liver.


PLoS ONE ◽  
2015 ◽  
Vol 10 (4) ◽  
pp. e0122024 ◽  
Author(s):  
Linyi Li ◽  
Hisae Yoshitomi ◽  
Ying Wei ◽  
Lingling Qin ◽  
Jingxin Zhou ◽  
...  

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