Microbe-Derived Antioxidants Alleviate Liver and Adipose Tissue Lipid Disorders and Metabolic Inflammation Induced by High Fat Diet in Mice

Abstract

Obesity induces lipodystrophy and metabolic inflammation. Microbe-derived antioxidants (MA) are novel small-molecule nutrients obtained from microbial fermentation, and have anti-oxidation, lipid-lowering and anti-inflammatory effects. Whether MA can regulate obesity-induced lipodystrophy and metabolic inflammation has not yet been investigated. The aim of this study was to investigate the effects of MA on oxidative stress, lipid disorders, and metabolic inflammation in liver and epididymal adipose tissues (EAT) of mice fed with a high-fat diet (HFD). Results showed that MA was able to reverse the HFD-induced increase in body weight, body fat rate and Lee’s index in mice; reduce the fat content in serum, liver and EAT; and regulate the INS, LEP and resistin adipokines as well as free fatty acids to their normal levels. MA also reduced de novo synthesis of fat in the liver and EAT and promoted gene expression for lipolysis, fatty acid transport and β-oxidation. MA decreased TNF-α and MCP1 content in serum, elevated SOD activity in liver and EAT, induced macrophage polarization toward the M2 type, inhibited the NLRP3 pathway, increased gene expression of the anti-inflammatory factors IL-4 and IL-13 and suppressed gene expression of the pro-inflammatory factors IL-6, TNF-α and MCP1, thereby attenuating oxidative stress and inflammation induced by HFD. In conclusion, MA can effectively reduce HFD-induced weight gain and alleviate obesity-induced oxidative stress, lipid disorders and metabolic inflammation in the liver and EAT, indicating that MA shows great promise as a functional food.

Protective Mechanisms of Various Active Substances on Cell DNA Damage and Apoptosis Induced by Deoxynivalenol

“…Quercetin also significantly restored ROS levels, inhibited growth rates, and apoptosis after exposure to DON and 15-acetyl deoxynivalenol and minimized the toxic effects of DON and 15-acetyl deoxynivalenol . Microorganisms and their byproducts are known to reduce toxicity and protect animal gut microbiota by either degrading or regulating them. , MA are novel, small-molecule nutrients obtained from microbial fermentation and have various effects, including antioxidation, lipid-lowering, and anti-inflammation . MA can also attenuate the damage of various harmful substances to animals and cells. − Specifically, Luo et al found that MA can attenuate cobalt chloride-induced mitochondrial function, autophagy, and BNIP3-dependent mitophagy pathways in BRL3A cells .…”

Microbe-Derived Antioxidants Protect IPEC-1 Cells from H2O2-Induced Oxidative Stress, Inflammation and Tight Junction Protein Disruption via Activating the Nrf2 Pathway to Inhibit the ROS/NLRP3/IL-1β Signaling Pathway

“…The UHPLC-QTOF-MS analysis revealed that MAs contain 426 metabolites, mainly including organic acids and derivatives (15.96%), organic oxygen compounds (10.80%), organoheterocyclic compounds (7.04%), lipids and lipid-like molecules (6.10%), benzenoids (4.46%), and phenylpropanoids and polyketides (4.23%) [15]. In our prior research, it was documented that MAs exhibit a commendable ability to scavenge free radicals [15], enhance hepatic antioxidant capacity in mothers and offspring [16], and regulate metabolic inflammation in mice [17], but whether MAs can mitigate oxidative stress and inflammatory responseinduced disruption of intestinal epithelial tight junction through the Nrf2-ROS-NLRP3 signaling pathway is unclear. In this study, we employed IPEC-1 cells as a cellular model and developed Nrf2 and NLRP3 knockdown IPEC-1 cells to explore the molecular pathways involved in the impact of MAs on oxidative stress, inflammatory response, and disruption of tight junction proteins.…”