Effect of d-allulose feeding on the hepatic metabolomics profile in male Wistar rats

2021 ◽  
Author(s):  
Akane Kanasaki ◽  
Misato Niibo ◽  
Tetsuo Iida

d-Allulose altered hepatic metabolites, especially those related to the lipid metabolism processes, such as the fatty acid β-oxidation, cholesterol, bile acid, and glucuronic acid/xylulose pathways.

1994 ◽  
Vol 72 (3) ◽  
pp. 385-395 ◽  
Author(s):  
P. D. Overton ◽  
N. Furlonger ◽  
J. M Beety ◽  
J. Chakraborty ◽  
J. A. Tredger ◽  
...  

This study investigates the mechanisms of action for the hypocholesterolaemic effects of sugar-beet fibre (SBF) and gum gum. Four groups of ten male Wistar rats were fed ad lib. on test diets containing either 100 g SBF or guar/kg, or control diets containing 100 g cellulose or wheat bran/kg for 28 d. Food intake, weight gain and food consumption ratios were unaffected by the diets. Circulating cholesterol and hepatic cholesterol concentrations were significantly lower in both SBF- and guar-fed groups compared with either cellulose- or bran-fed animals. Circulating triacylglycerol concentrations were significantly lower in SBF- and guar-fed animals, but total hepatic lipid concentrations and hepatic and adipose tissue lipogenesis rates were unaffected by the diets. Hepatic cholesterol-7α-hydroxylase (EC1.14.13.17) activities were significantly higher in the guar-fed animals compared with cellulose or bran control groups. Hepatic 3-hydroxy-3-metbylglutaryl-CoA reductase (EC1.1.1.88) activities were unaffected. Circulating bile acid concentrations were significantly lower in SBF- and guar-fed animals and faecal bile acid output was significantly higher in the guar-fed group compared with bran- or cellulose-fed groups. This study supports the hypothesis that guar exerts its hypocholesterolaemic effect via intraluminal bile acid binding and loss of cholesterol from increased faecal bile acid excretion. The mechanism of action for the hypocholesterolaemic effect of SBF is less clear; the results of the present study point to a mechanism involving disruption of the enterohepatic bile acid circulation, possibly via changes in the rate of absorption of dietary lipid.


2017 ◽  
Vol 98 (5) ◽  
pp. 1757-1764 ◽  
Author(s):  
Arunaksharan Narayanankutty ◽  
Devika Mukundan Palliyil ◽  
Kezia Kuruvilla ◽  
Achuthan C Raghavamenon

2019 ◽  
Vol 60 (5) ◽  
pp. 1005-1019 ◽  
Author(s):  
Stephanie A. Shumar ◽  
Evan W. Kerr ◽  
Paolo Fagone ◽  
Aniello M. Infante ◽  
Roberta Leonardi

Lipid metabolism requires CoA, an essential cofactor found in multiple subcellular compartments, including the peroxisomes. In the liver, CoA levels are dynamically adjusted between the fed and fasted states. Elevated CoA levels in the fasted state are driven by increased synthesis; however, this also correlates with decreased expression of Nudix hydrolase (Nudt)7, the major CoA-degrading enzyme in the liver. Nudt7 resides in the peroxisomes, and we overexpressed this enzyme in mouse livers to determine its effect on the size and composition of the hepatic CoA pool in the fed and fasted states. Nudt7 overexpression did not change total CoA levels, but decreased the concentration of short-chain acyl-CoAs and choloyl-CoA in fasted livers, when endogenous Nudt7 activity was lowest. The effect on these acyl-CoAs correlated with a significant decrease in the hepatic bile acid content and in the rate of peroxisomal fatty acid oxidation, as estimated by targeted and untargeted metabolomics, combined with the measurement of fatty acid oxidation in intact hepatocytes. Identification of the CoA species and metabolic pathways affected by the overexpression on Nudt7 in vivo supports the conclusion that the nutritionally driven modulation of Nudt7 activity could contribute to the regulation of the peroxisomal CoA pool and peroxisomal lipid metabolism.


Diabetes ◽  
2001 ◽  
Vol 50 (10) ◽  
pp. 2316-2322 ◽  
Author(s):  
A. L. Hevener ◽  
D. Reichart ◽  
A. Janez ◽  
J. Olefsky

PLoS ONE ◽  
2019 ◽  
Vol 14 (9) ◽  
pp. e0222558
Author(s):  
Carine Lindquist ◽  
Bodil Bjørndal ◽  
Hege G. Bakke ◽  
Grete Slettom ◽  
Marie Karoliussen ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document