N-3long-chain PUFA supplementation prevents high fat diet induced mouse liver steatosis and inflammation in relation to PPAR-α upregulation and NF-κB DNA binding abrogation

Abstract

Data presented indicate that n-3 LCPUFAs supplementation prevents liver steatosis and inflammation induced by HFD, with underlying mechanisms involving enhanced PPAR-α signaling and diminished NF-κB activation.

Palmitoleic Acid (N-7) Attenuates the Immunometabolic Disturbances Caused by a High-Fat Diet Independently of PPARα

“…The activation of PPAR α seems to be a promising target in the treatment of NAFLD because PPAR α is also a key regulator of the genes involved in fatty acid oxidation [33–36] and anti-inflammatory effects [37, 38]. Indeed, it has been previously shown that the lack of PPAR α may cause an important hepatic steatosis and liver inflammation [34, 39].…”

Ameliorative effects of lutein on non-alcoholic fatty liver disease in rats

“…Some studies have demonstrated that PPAR-α plays an important role in the regulation of hepatic lipid metabolism [15,32] and that the inhibition of PPAR-α might induce hepatic steatosis [33] . Thus, we tested the protein level of PPAR-α and found that HFD feeding significantly inhibited the expression of PPAR-α, and that lutein supplementation reversed such inhibition effectively.…”

A high-fish-oil diet prevents adiposity and modulates white adipose tissue inflammation pathways in mice

“…Under stimulation (e.g., presence of cytokines), IκBα is phosphorylated, and NFκB can, therefore, translocate to the nucleus, where it induces the gene expression of inflammatory mediators, creating a vicious cycle of inflammation [10]. Feeding mice with an HF diet leads to the activation of NFκB [32], and inhibiting NFκB suppresses the release of proinflammatory cytokines in human adipocytes [33].…”

“…PPARα not only increases the expression of IκBα but also inhibits its degradation, blocking NFκB translocation into the nucleus and binding to DNA [32]. PPARβ/δ can inhibit inflammation by inhibiting the activation of NFκB through a mechanism related to ERK1/2 [2].…”