Novel ι-Carrageenan Tetrasaccharide Alleviates Liver Lipid Accumulation via the Bile Acid–FXR–SHP/PXR Pathway to Regulate Cholesterol Conversion and Fatty Acid Metabolism in Insulin-Resistant Mice

Author(s):  
Yanqi Li ◽  
Yingying Tian ◽  
Weizhen Cai ◽  
Qinghui Wang ◽  
Yaoguang Chang ◽  
...  
2019 ◽  
Vol 10 (10) ◽  
pp. 6675-6689 ◽  
Author(s):  
Fan Wang ◽  
Jia Xu ◽  
Ivan Jakovlić ◽  
Wei-Min Wang ◽  
Yu-Hua Zhao

Dietary betaine decreased liver lipid accumulation caused by dietary carbohydrate through changes of TMA formation and TMAO and bile acid metabolism.


2012 ◽  
Vol 303 (7) ◽  
pp. F1070-F1079 ◽  
Author(s):  
Yoshikazu Muroya ◽  
Osamu Ito ◽  
Rong Rong ◽  
Kenta Takashima ◽  
Daisuke Ito ◽  
...  

Proteinuria is considered to play an essential role in the progression of tubulointerstitial damage, which causes end-stage renal disease. Fatty acid-binding albumins are filtered through glomeruli and reabsorbed into proximal tubular epithelial cells (PTECs). However, the role of fatty acid metabolism associated with albuminuria in the development of tubulointerstitial damage remains unclear. Thus, the present study was designed to determine the changes of fatty acid metabolism in the nephrotic kidney. To induce nephrotic syndrome, Sprague-Dawley rats (SDRs) and Nagase analbuminemic rats (NARs) with inherited hypoalbuminemia were treated with a single injection of puromycin aminonucleoside (PAN). In SDRs, PAN treatment induced massive proteinuria and albuminuria and caused tubular damage, apoptosis, and lipid accumulation in PTECs. Among the enzymes of fatty acid metabolism, expressions of medium-chain acyl-CoA dehydrogenase (MCAD) and cytochrome P-450 (CYP)4A significantly decreased in PTECs of PAN-treated SDRs. Expressions of peroxisome proliferator-activated receptor (PPAR)-γ coactivator (PGC)-1α and estrogen-related receptor (ERR)α also significantly decreased, without changes in the expression of PPAR-α. In NARs, PAN treatment induced proteinuria but not albuminuria and did not cause tubular damage, apoptosis, or lipid accumulation. Expressions of MCAD, PGC-1α, or ERRα did not change in the kidney cortex of PAN-treated NARs, but the expression of CYP4A significantly decreased. These results indicate that massive albuminuria causes tubular damage and lipid accumulation with the reduction of MCAD, CYP4A, PGC-1α, and ERRα in PTECs.


2007 ◽  
Vol 97 (1) ◽  
pp. 85-95 ◽  
Author(s):  
Jin Seon Lim ◽  
Yoshikazu Adachi ◽  
Yoko Takahashi ◽  
Takashi Ide

Effects of sesamin and sesamolin (sesame lignans) on hepatic fatty acid metabolism were compared in rats. Rats were fed either a lignan-free diet, a diet containing 0·6 or 2 g/kg lignan (sesamin or sesamolin), or a diet containing both sesamin (1·4 g/kg) and sesamolin (0·6 g/kg), for 10 d. Sesamin and sesamolin dose-dependently increased the activity and mRNA abundance of various enzymes involved in hepatic fatty acid oxidation. The increase was much greater with sesamolin than with sesamin. These lignans increased parameters of hepatic fatty acid oxidation in an additive manner when added simultaneously to an experimental diet. In contrast, they decreased the activity and mRNA abundance of hepatic lipogenic enzymes despite dose-dependent effects not being necessarily obvious. Sesamin and sesamolin were equally effective in lowering parameters of lipogenesis. Sesamolin accumulated in serum at 33- and 46-fold the level of sesamin at dietary concentrations of 0·6 and 2 g/kg, respectively. The amount of sesamolin accumulated in liver was 10- and 7-fold that of sesamin at the respective dietary levels. Sesamolin rather than sesamin can account for the potent physiological effect of sesame seeds in increasing hepatic fatty acid oxidation observed previously. Differences in bio-availability may contribute to the divergent effects of sesamin and sesamolin on hepatic fatty acid oxidation. Sesamin compared to sesamolin was more effective in reducing serum and liver lipid levels despite sesamolin more strongly increasing hepatic fatty acid oxidation.


2005 ◽  
Vol 50 (7) ◽  
pp. 1361-1371 ◽  
Author(s):  
Atsushi Yamaguchi ◽  
Susumu Tazuma ◽  
Tomoji Nishioka ◽  
Waka Ohishi ◽  
Hideyuki Hyogo ◽  
...  

2021 ◽  
Author(s):  
Zuyin Li ◽  
Gang Wu ◽  
Chen Qiu ◽  
Zhijie Zhou ◽  
Yupeng Wang ◽  
...  

Abstract Background and aims : Lack of effective pharmacotherapies for nonalcoholic fatty liver disease (NAFLD) is mainly attributed to an insufficient research on its pathogenesis. In this paper, we investigated the role of TM6SF2 on fatty acid metabolism in the background of fatty liver, and proposed the possible therapeutic strategies of NAFLD caused by TM6SF2 deficiency. Methods Liver samples collected from both NAFLD mouse models and human subjects, and RNA-seq data retrieved from GEO database were used to evaluate the expression of TM6SF2 in NAFLD. Knockdown of TM6SF2 was performed for clarifying the mechanistic basis of hepatic lipid accumulation in NAFLD. After confirming that TM6SF2 deficiency would cause an abnormality in fatty acid metabolism, MK-4074 administration served as the therapeutic intervention to evaluate its effect on NAFLD caused by TM6SF2 deficiency. Results Hepatic TM6SF2 levels are elevated in both NAFLD patients and mouse NAFLD models. In vivo and in vitro experiments confirmed that TM6SF2 knockdown increases intracellular lipid deposition due to dysregulated fatty acid metabolism in the context of TM6SF2 deficiency, being characterized by enhanced fatty acid uptake and synthesis, accompanied by impaired fatty acid oxidation. Moreover, MK-4074 treatment could reverse the NAFLD phenotypes caused by TM6SF2 deficiency. Conclusions TM6SF2 deficiency enhanced hepatic lipid accumulation through dysregulated fatty acid metabolism and MK-4074 treatment could alleviate the NAFLD phenotypes caused by TM6SF2 deficiency.


Diabetes ◽  
2001 ◽  
Vol 50 (6) ◽  
pp. 1389-1396 ◽  
Author(s):  
Lorraine Patricia Turcotte ◽  
Jason Richard Swenberger ◽  
Michelle Zavitz Tucker ◽  
Alice Jane Yee

Diabetologia ◽  
2008 ◽  
Vol 51 (10) ◽  
pp. 1936-1936 ◽  
Author(s):  
A. S. T. Bickerton ◽  
R. Roberts ◽  
B. A. Fielding ◽  
H. Tornqvist ◽  
E. E. Blaak ◽  
...  

Diabetologia ◽  
2008 ◽  
Vol 51 (8) ◽  
pp. 1466-1474 ◽  
Author(s):  
A. S. T. Bickerton ◽  
R. Roberts ◽  
B. A. Fielding ◽  
H. Tornqvist ◽  
E. E. Blaak ◽  
...  

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