Abstract
Lactobacillus plantarum ZJUFB2 is a novel probiotic isolate derived from Chinese traditional sourdough that possesses promising probiotics properties. This study aimed to investigate the effects of L. plantarum ZJUFB2 (B2) on insulin sensitivity using mice fed on a high-fat diet (HFD) as well as to explore the involved mechanisms. Purposely, male C57BL/6 mice continuously received an intervention of B2 (~109 CFU/day) for 16 weeks. The results showed that B2 treatment remarkably ameliorated insulin resistance and hyperglycemia in HFD-fed mice. The B2 intervention significantly decreased the hepatic lipid accumulation, serum low-density lipoproteins cholesterol, and lipopolysaccharides, and regulated the bile acids levels as well as liver mRNA expression involved in lipid metabolism. Moreover, the B2 intervention significantly changed the gut microbiota, specifically, showed a lower abundance of obesity-related and inflammation-associated microbes, e.g., Ruminococcus and Mogibacteriaceae. Furthermore, it exhibited a higher abundance of short-chain fatty acids and bile salt hydrolas-producing bacteria, such as Bifidobacterium and F16 compared with the HFD group. The findings of this study suggested that B2 is a novel probiotic, effective in preventing insulin resistance by improving the gut microbiota and bile acids.
Highlights
Type 2 diabetes mellitus is a public pandemic that remains a challenging health issue of the 21st century which leads to the onset of plenty of health risks and economic burdens [1]
Many studies indicated that systemic inflammation and fat accumulation were the key factors in triggering abnormal cellular responses to insulin, resulting in insulin resistance (IR) [4, 5]
The mechanism regarding the interaction of the gut microbiota with the host is still not clear, few studies have demonstrated that a liver-bile acids (BAs)gut microbiome metabolic axis drives significant modifications of BAs and microbiota composition capable of triggering metabolic disorders [17]
Summary
Type 2 diabetes mellitus is a public pandemic that remains a challenging health issue of the 21st century which leads to the onset of plenty of health risks and economic burdens [1]. Many studies indicated that systemic inflammation and fat accumulation were the key factors in triggering abnormal cellular responses to insulin, resulting in IR [4, 5]. In this regard, regulating the pro-inflammatory cytokines expression and fat accumulation are the challenging concerns in preventing obesity-related inflammation and subsequently insulin sensitivity. Many studies have indicated that intestinal microflora dysbiosis may trigger the onset of diabetes and obesity-related issues [10]. Sterile rodents showed resistance to high-fat diet (HFD) induced obesity, indicating that the gut microbiota may influence the mammalian adiposity through regulation of the metabolic pathways that control the bioenergetics [11]. The small heterodimer partner (SHP), which controls the metabolic pathways, is involved in the glycolipids homeostasis and hepatic BAs production through the transcriptional repression of several other nuclear receptors [18]
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