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Quinoa Reduces High-Fat Diet-Induced Obesity in Mice via Potential Microbiota-Gut-Brain-Liver Interaction Mechanisms.

ABSTRACT: The gut microbiota is important in the occurrence and development of obesity. It can not only via its metabolites, but also through microbiota-gut-brain-liver interactions, directly or indirectly, influence obesity. Quinoa, known as one kind of pseudocereals and weight loss food supplements, has been high-profile for its high nutritional value and broad applications. In this context, we produced high-fat diet-induced (HFD) obese mouse models and assessed the efficacy of quinoa with saponin and quinoa without saponin on obesity. We explored the potential therapeutic mechanisms of quinoa using methods such as 16S rRNA, Western blotting, Immunohistochemical (IHC). Our results indicated that quinoa can improve the obese symptoms significantly on HFD mice, as well as aberrant glucose and lipid metabolism. Further analyses suggest that quinoa can regulate microbiota in the colon and have predominantly regulation on Bacteroidetes, Actinobacteria and Desulfovibrio, meanwhile can decrease the F/B ratio and the abundance of Blautia. Contemporaneously, quinoa can upregulate the expression of TGR5 in the colon and brain, as well as GLP-1 in the colon, liver and brain. while downregulate the expression of TLR4 in the colon and liver, as well as markers of ER stress and oxidative stress in livers and serums. Beyond this, tight junctional proteins in colons and brains are also increased in response to quinoa. Therefore, quinoa can effectively reduce obesity and may possibly exert through microbiota-gut-brain-liver interaction mechanisms. IMPORTANCE Gut microbiota has been investigated extensively, as a driver of obesity as well as a therapeutic target. Studies of its mechanisms are predominantly microbiota-gut-brain axis or microbiota-gut-liver axis. Recent studies have shown that there is an important correlation between the gut-brain-liver axis and the energy balance of the body. Our research focus on microbiota-gut-brain-liver axis, as well as influences of quinoa in intestinal microbiota. We extend this study to the interaction between microbiota and brains, and the result shows obvious differences in the composition of the microbiome between the HFD group and others. These observations infer that besides the neurotransmitter and related receptors, microbiota itself may be a mediator for regulating bidirectional communication, along the gut-brain-liver axis. Taken together, these results also provide strong evidence for widening the domain of applicability of quinoa.

SUBMITTER: Wang TY

PROVIDER: S-EPMC9241864 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:ObjectiveGut microbiota may promote positive energy balance; however, germfree mice can be either resistant or susceptible to diet-induced obesity (DIO) depending on the type of dietary intervention. We here sought to identify the dietary constituents that determine the susceptibility to body fat accretion in germfree (GF) mice.MethodsGF and specific pathogen free (SPF) male C57BL/6N mice were fed high-fat diets either based on lard or palm oil for 4 wks. Mice were metabolically characterized at the end of the feeding trial. FT-ICR-MS and UPLC-TOF-MS were used for cecal as well as hepatic metabolite profiling and cecal bile acids quantification, respectively. Hepatic gene expression was examined by qRT-PCR and cecal gut microbiota of SPF mice was analyzed by high-throughput 16S rRNA gene sequencing.ResultsGF mice, but not SPF mice, were completely DIO resistant when fed a cholesterol-rich lard-based high-fat diet, whereas on a cholesterol-free palm oil-based high-fat diet, DIO was independent of gut microbiota. In GF lard-fed mice, DIO resistance was conveyed by increased energy expenditure, preferential carbohydrate oxidation, and increased fecal fat and energy excretion. Cecal metabolite profiling revealed a shift in bile acid and steroid metabolites in these lean mice, with a significant rise in 17?-estradiol, which is known to stimulate energy expenditure and interfere with bile acid metabolism. Decreased cecal bile acid levels were associated with decreased hepatic expression of genes involved in bile acid synthesis. These metabolic adaptations were largely attenuated in GF mice fed the palm-oil based high-fat diet. We propose that an interaction of gut microbiota and cholesterol metabolism is essential for fat accretion in normal SPF mice fed cholesterol-rich lard as the main dietary fat source. This is supported by a positive correlation between bile acid levels and specific bacteria of the order Clostridiales (phylum Firmicutes) as a characteristic feature of normal SPF mice fed lard.ConclusionsIn conclusion, our study identified dietary cholesterol as a candidate ingredient affecting the crosstalk between gut microbiota and host metabolism.

Project description:BackgroundObesity has become a global epidemic recognized by the World Health Organization. Probiotics supplementation has been shown to contribute to improve lipid metabolism. However, mechanisms of action of probiotics against obesity are still not clear. Lactobacillus plantarum FRT4, a probiotic previously isolated from a kind of local yogurt, had good acid and bile salt tolerance and lowered cholesterol in vitro.ObjectiveThis study aimed to evaluate the effect of L. plantarum FRT4 on serum and liver lipid profile, liver metabolomics, and gut microbiota in mice fed with a high-fat diet (HFD).DesignMice were fed with either normal diet or HFD for 16 weeks and administered 0.2 mL of 1 × 109 or 1 × 1010 CFU/mL dosage of L. plantarum FRT4 during the last 8 weeks of the diet. Cecal contents were analyzed by 16S rRNA sequencing. Hepatic gene expression and metabolites were detected by real-time quantitative polymerase chain reaction (PCR) and metabolomics, respectively.ResultsL. plantarum FRT4 intervention significantly reduced the HFD-induced body weight gain, liver weight, fat weight, serum cholesterol, triglyceride, and alanine aminotransferase (ALT) levels in the liver (P < 0.05). Liver metabolomics demonstrated that the HFD increased choline, glycerophosphocholine, and phosphorylcholine involved in the glycerophospholipid metabolism pathway. All these changes were reversed by FRT4 treatment, bringing the levels close to those in the control group. Further mechanisms showed that FRT4 favorably regulated gut barrier function and pro-inflammatory biomediators. Furthermore, FRT4 intervention altered the gut microbiota profiles and increased microbial diversity. The relative abundances of Bacteroides, Parabateroides, Anaerotruncus, Alistipes, Intestinimonas, Butyicicoccus, and Butyricimonas were significantly upregulated. Finally, Spearman's correlation analysis revealed that several specific genera were strongly correlated with glycerophospholipid metabolites (P < 0.05).ConclusionsThese findings suggested that L. plantarum FRT4 had beneficial effects against obesity in HFD-induced obese mice and can be used as a potential functional food for the prevention of obesity.

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Quinoa Reduces High-Fat Diet-Induced Obesity in Mice via Potential Microbiota-Gut-Brain-Liver Interaction Mechanisms.

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