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Introduction
Berberine, which is an alkaloid extracted from Rhizoma coptidis, has been traditionally used in Chinese medicine to treat gastrointestinal infections, due to its antimicrobial properties. Previous clinical research and animal studies have demonstrated that berberine can regulate glucose and lipid metabolism, and attenuate insulin resistance (1–3). Several mechanisms have been proposed to explain the actions of berberine in in vitro and in vivo models; these include: The activation of AMP-activated protein kinase to downregulate the expression of lipogenesis genes and upregulate the expression of energy expenditure genes (4); the inhibition of intestinal disaccharidases and α-glucosidase (5,6); the upregulation of the hepatic low-density lipoprotein receptor (7); the inhibition of intestinal cholesterol absorption (8); and increased intestinal glucagon-like peptide-1 (GLP-1) secretion (9,10). Since berberine has been reported to have poor intestinal absorption and very low absolute bioavailability, with values ranging between 0.36 and 0.68% in rats, it may be hypothesized that berberine exerts its effects in the intestinal tract prior to its absorption (11,12).
Accumulating evidence suggests that the gut microbiome serves an important role in obesity and related metabolic abnormalities. Taking into consideration the antibacterial activity of berberine, modulation of the gut microbiota has been suggested as another possible mechanism for its actions. Xie et al (2) reported that berberine significantly increased the intestinal expression of fasting-induced adipose factor (Fiaf), which acts as a lipoprotein lipase inhibitor, thereby inhibiting triglyceride deposition in adipocytes. Furthermore, it has been reported that Lactobacillus paracasei may upregulate Fiaf expression in colonic epithelial cells (13). These findings indicate that, through modulating the gut microbiota, berberine may increase the expression of Fiaf.
The leakage of bacterial-derived lipopolysaccharide (LPS) through the damaged intestinal mucosa into the circulation is a well-established mechanism of metabolic endotoxemia that can trigger systemic inflammation. Zhang et al (14) previously reported that berberine may prevent obesity and insulin resistance in high-fat diet (HFD)-fed rats by modulating the gut microbiota, thus contributing to the alleviaton of inflammation via a reduction in serum LPS-binding protein and monocyte chemotactic protein-1 (MCP-1). However, there is currently little information available on whether berberine can modulate endotoxemia and intestinal or systemic inflammation.
Previous studies have suggested that gut microbiota may contribute to the development of obesity and related disorders by modulating the synthesis of...