Konjac glucomannans attenuate diet-induced fat accumulation on livers and its regulation pathway

[Display omitted] •KGM significantly attenuated HFD-induced fat accumulation on liver.•Lipid metabolism with KGM was improved by depressed biosynthesis of sphingolipids.•KGM increased level of hydrophilic bile acids and reduced hydrophobic ones in feces.•PI3K pathway and adipogenic regulator of LXR and PPARγ involved in KGM regulation. As one typical dietary fiber, Konjac glucomannan (KGM) is applied to investigate its influence on high-fat diet (HFD) induced liver dysbiosis. The current results indicated dietary KGM was associated with a declined accumulation of fat droplets on animal livers with significantly improved serum lipid compositions through a reduced biosynthesis of free fatty acid, ceramides, and oxidized-triacylglycerols, benefiting the attenuation of oxidative levels. This is the first study to reveal that KGM intervention led an increased level of hydrophilic bile acids and a reduced content of hydrophobic ones in feces. The associated lipid regulatory pathways of AMPK, PPAR and fatty acid metabolism were significantly enriched following KGM intervention. It highlights that the activation of the PI3K pathway and modulation of the expression of the adipogenic regulators of LXR and PPARγ might be the key manipulation patterns of KGM on the attenuation of liver dysbiosis induced by HFD.