Phytic Acid Improves Hepatic Steatosis, Inflammation, and Oxidative Stress in High-Fat Diet (HFD)-Fed Mice by Modulating the Gut-Liver Axis.

Nonalcoholic fatty liver disease (NAFLD) induced by obesity is a grave threat to human health. Phytic acid (PA) is a natural compound found in high-fiber diets, such as soybeans. This study investigated the effects and mechanisms of PA on obesity, hepatic lipid metabolism, and gut-liver axis homeostasis in high-fat diet (HFD)-fed mice. PA was observed to significantly inhibit obesity and alleviate liver steatosis in mice. PA improved HFD-induced liver inflammation, oxidative stress and fibrosis. Moreover, PA improved HFD-induced colonic inflammation, gut barrier damage and systemic inflammation in mice. Furthermore, PA effectively ameliorated the decreased diversity and gut microbiota composition in HFD-fed mice. Additionally, PA decreased the abundance of harmful bacteria Proteobacteria and Desulfovibrionaceae and increased the abundance of probiotic bacteria Muribaculaceae and Lachnospiraceae. Thus, PA is effective in restoring the homeostasis of the gut-liver axis. It further provides a theoretical basis for the prevention and treatment of NAFLD in patients with obesity by the rational intake of foods containing PA.

Phytic Acid Maintains the Integrity of the Blood-Milk Barrier by Regulating Inflammatory Response and Intestinal Flora Structure.

The destruction of the blood-milk barrier (BMB) caused by the mammary inflammatory response (MIR) is one of the main reasons that hinders breastfeeding. To relieve the inflammatory response and maintain BMB, we found that phytic acid (PA) has good anti-inflammatory activity. Therefore, we focused on researching the influence and mechanism of PA on BMB and MIR. We constructed a mammary inflammatory response model using lipopolysaccharide (LPS) in vivo, and we used mammary epithelial cells (mMECs) to construct a cell inflammatory response model in vitro. The results showed that PA alleviated mammary tissue damage and reduced the production of inflammatory mediators (such as IL-1ß and iNOS) in mammary tissue and mMECs. PA also maintained the integrity of the BMB in mice by increasing the expression of tight junction proteins. 16S rDNA high-throughput sequencing showed that PA significantly ameliorated the intestinal flora of model mice. Mechanism studies showed that PA exerted an anti-MIR effect by inhibiting the AKT/NF-κB signaling pathway. In summary, our study found that PA maintains the integrity of BMB by regulating the inflammatory response and intestinal flora structure.