Synbiotic Intervention with an Adlay-Based Prebiotic and Probiotics Improved Diet-Induced Metabolic Disturbance in Mice by Modulation of the Gut Microbiota.

Metabolic syndrome and its associated conditions, such as obesity and type 2 diabetes mellitus (T2DM), are a major public health issue in modern societies. Dietary interventions, including microbiota-directed foods which effectively modulate the gut microbiome, may influence the regulation of obesity and associated comorbidities. Although research on probiotics and prebiotics has been conducted extensively in recent years, diets with the use of synbiotics remain relatively unexplored. Here, we investigated the effects of a novel synbiotic intervention, consisting of an adlay seed extrusion cooked (ASEC)-based prebiotic and probiotic (Lactobacillus paracasei and Bacillus coagulans) on metabolic disorders and microbial dysbiosis in high-fat diet (HFD)-induced obese mice. The ASEC-based synbiotic intervention helped improve HFD-induced body weight gain, hyperlipidemia, impaired glucose tolerance, insulin resistance, and inflammation of the adipose and liver tissues. In addition, data from fecal metagenomics indicated that the ASEC-based synbiotic intervention fostered reconstitution of gut bacterial diversity and composition in HFD-induced obese mice. In particular, the ASEC-based synbiotic intervention increased the relative abundance of families Ruminococcaceae and Muribaculaceae and order Bacteroidales and reduced that of families Lactobacillaceae, Erysipelotrichaceae, and Streptococcaceae in HFD-induced obese mice. Collectively, our results suggest that delayed dietary intervention with the novel ASEC-based synbiotic ameliorates HFD-induced obesity, metabolic disorders, and dysbiosis.

Adlay Seed (Coix lacryma-jobi L.) Extracts Exhibit a Prophylactic Effect on Diet-Induced Metabolic Dysfunction and Nonalcoholic Fatty Liver Disease in Mice.

Nonalcoholic fatty liver disease (NAFLD) is common worldwide and closely associated with metabolic dysfunction. NAFLD leads to a higher risk of development of severe liver diseases, such as nonalcoholic steatohepatitis (NASH), liver cirrhosis, and hepatocellular carcinoma (HCC). To date, no pharmacotherapy targeting NAFLD has received general approval. Adlay is a plant that has been used as traditional herbal medicine in Asia and is a promising candidate to solve this global issue. We have established a mouse model of NAFLD by feeding a high-fat diet (HFD) for 10 weeks. Here, ethanolic or water extracts of adlay seed (ASE and ASW, respectively), mixed with HFD, were fed to the mice for 10 weeks. The ASE and ASW treatment ameliorated hyperglycemia and improved the glucose tolerance and insulin resistance in the HFD mice. Hyperlipidemia in HFD mice was prevented by the ASE and ASW diet. In addition, the ASE and ASW supplementation attenuated hepatic steatosis and inflammation, improved liver function, and caused no harm to the kidneys. Moreover, the mechanism of the effect of ASE and ASW on inhibiting hepatic lipogenesis and inducing fatty acid ß-oxidation was certified by the simulated human fatty liver cell model. Our study showed the regulatory potential of the extracts of adlay seeds for alleviating NAFLD, as well as related liver and metabolic diseases.

Ginseng-plus-Bai-Hu-Tang ameliorates diet-induced obesity, hepatic steatosis, and insulin resistance in mice.

BACKGROUND: Dietary fat has been suggested to be the cause of various health issues. Obesity, hypertension, cardiovascular disease, diabetes, dyslipidemia, and kidney disease are known to be associated with a high-fat diet (HFD). Obesity and associated conditions, such as type 2 diabetes mellitus and nonalcoholic fatty liver disease (NAFLD), are currently a worldwide health problem. Few prospective pharmaceutical therapies that directly target NAFLD are available at present. A Traditional Chinese Medicine, ginseng-plus-Bai-Hu-Tang (GBHT), is widely used by diabetic patients to control glucose level or thirst. However, whether it has therapeutic effects on fat-induced hepatic steatosis and metabolic syndrome remains unclear. METHODS: This study was conducted to examine the therapeutic effect of GBHT on fat-induced obesity, hepatic steatosis, and insulin resistance in mice. RESULTS: GBHT protected mice against HFD-induced body weight gain, hyperlipidemia, and hyperglycemia compared with mice that were not treated. GBHT inhibited the expansion of adipose tissue and adipocyte hypertrophy. No ectopic fat deposition was found in the livers of HFD mice treated with GBHT. In addition, glucose intolerance and insulin sensitivity in HFD mice was also improved by GBHT. CONCLUSION: GBHT prevents changes in lipid and carbohydrate metabolism in a HFD mouse model. Our findings provide evidence for the traditional use of GBHT as therapy for the management of metabolic syndrome.