Alleviating the effect of quinoa and the underlying mechanism on hepatic steatosis in high-fat diet-fed rats.

BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) is considered the hepatic component of metabolic syndrome and has attracted widespread attention due to its increased prevalence. Daily dietary management is an effective strategy for the prevention of NAFLD. Quinoa, a nutritious pseudocereal, is abundant in antioxidative bioactive phytochemicals. In the present study, the effects of different amounts of quinoa on the progression of NAFLD and the related molecular mechanism were investigated. METHODS: Male SD rats were simultaneously administered a high fat diet (HF) and different amounts of quinoa (equivalent to 100 g/day and 300 g/day of human intake, respectively). After 12 weeks of the intervention, hepatic TG (triglyceride) and TC (total cholesterol) as well as serum antioxidative parameters were determined, and hematoxylin-eosin staining (H&E) staining was used to evaluate hepatic steatosis. Differential metabolites in serum and hepatic tissue were identified using UPLC-QTOF-MSE. The mRNA expression profile was investigated using RNA-Seq and further verified using real-time polymerase chain reaction (RT-PCR). RESULTS: Low amounts of quinoa (equivalent to 100 g/d of human intake) effectively controlled the weight of rats fed a high-fat diet. In addition, quinoa effectively inhibited the increase in hepatic TG and TC levels, mitigated pathological injury, promoted the increase in SOD and GSH-Px activities, and decreased MDA levels. Nontarget metabolic profile analysis showed that quinoa regulated lipid metabolites in the circulation system and liver such as LysoPC and PC. RNA-Seq and RT-PCR verification revealed that a high amount of quinoa more effectively upregulated genes related to lipid metabolism [Apoa (apolipoprotein)5, Apoa4, Apoc2] and downregulated genes related to the immune response [lrf (interferon regulatory factor)5, Tlr6 (Toll-like receptor), Tlr10, Tlr11, Tlr12]. CONCLUSION: Quinoa effectively prevented NAFLD by controlling body weight, mitigating oxidative stress, and regulating the lipid metabolic profile and the expression of genes related to lipid metabolism and the immune response.

Regulatory effects of Lactobacillus fermented black barley on intestinal microbiota of NAFLD rats.

Gut microbiota dysbiosis and oxidative stress may play important roles in the progression of nonalcoholic fatty liver disease (NAFLD). Fermented foods contain probiotics and other bioactive components that may improve gastrointestinal health and provide other health benefits. Here, we investigated the effect of Lactobacillus-fermented black barley on NAFLD rats. Adult Sprague Dawley rats were randomized into four groups: normal chow diet (NC), high-fat diet (HF), HF + fermented black barley treatment (HB) and HF + Lactobacillus treatment (HL). The rats in the HB and HL groups were continuously administered fermented black barley or Lactobacillus, respectively, for 12 weeks (1 mL/100 g·BW, containing 1 × 108 CFU/mL Lactobacillus). Compared with the HF treatment, HB treatment effectively inhibited the increase in body weight, liver and abdominal fat indexes and hepatic lipids (p < 0.01), increased hepatic SOD activity (p < 0.05), decreased thiobarbituric acid reactive substances (TBARSs) (p < 0.01) and improved liver function. Moreover, Lactobacillus-fermented black barley exhibited regulatory effect on high-fat diet-induced intestinal microbiota dysbiosis by increasing the relative microbiota abundance and diversity, increasing the relative abundance of Bacteroidetes, decreasing the Firmicutes/Bacteroidetes ratio, increasing the abundances of some intestinal probiotics (such as Akkermansia and Lactococcus), and influencing some of the fecal metabolites related to hormones and lipid metabolism. The supplementation of fermented cereal food might be a new effective and safe preventive dietary strategy against NAFLD.

Global dynamics and optimal control of a cholera transmission model with vaccination strategy and multiple pathways.

In this paper, we consider a cholera infection model with vaccination and multiple transmission pathways. Dynamical properties of the model are analyzed in detail. It is shown that the disease-free equilibrium is globally asymptotically stable if the basic reproduction number is less than unity; the endemic equilibrium exists and is globally asymptotically stable if the basic reproduction number is greater than unity. In addition, the model is successfully used to fit the real disease situation of cholera outbreak in Somalia. We consider an optimal control problem of cholera transmission with vaccination, quarantine, treatment and sanitation control strategies, and use Pontryagin's minimum principle to determine the optimal control level. The optimal control problem is solved numerically.

Fermented black barley ameliorates lung injury induced by cooking oil fumes via antioxidant activity and regulation of the intestinal microbiome in mice.

To investigate the effect of fermented black barley on cooking oil fume (COF)-induced lung injury, male ICR mice were randomized into five groups: normal control (NC), fermented black barley treatment (NF), COF exposure (O), COF + fermented black barley treatment (OF) and COF + Lactobacillus treatment (OL). The exposure of mice to COF was performed for 5 min per day and 4 days per week for a total of 9 weeks, and the mice in the OF, NF and OL groups were administered fermented black barley or Lactobacillus continuously for 9 weeks (1 mL/100 g). Our results showed that the gamma-aminobutyric acid (GABA), total phenolic, and flavonoid contents significantly increased after fermentation (P < 0.01). In addition, fermented black barley significantly increased SOD activity in the lung tissue, decreased the wet pulmonary coefficient, inhibited the reduction of microbial diversity and richness, and upregulated genes involved in cilium assembly and the cilium axoneme. These findings support the notion that fermented black barley can ameliorate COF-induced lung injury in mice.

Effects of Phytosterol Ester on the Fatty Acid Profiles in Rats with Nonalcoholic Fatty Liver Disease.

Both serum and hepatic fatty acid (FA) compositions differ among nonalcoholic hepatic steatosis, nonalcoholic steatohepatitis, and healthy subjects. The severity of the above liver disease is closely associated with the concentration and composition of FAs. Our previous study found that phytosterol ester (PSE) could alleviate hepatic steatosis in nonalcoholic fatty liver disease rats. The aims of this work were to explore the effects of PSE (0.05/100 g·body weight) on FA profiles and the mRNA levels of FA metabolism-related genes. Compared with a high-fat diet alone group, PSE treatment significantly decreased hepatic saturated fatty acid levels (P < .05) and increased monounsaturated fatty acid (especially C16:1 n-7) levels in the liver, serum, and adipose tissue and polyunsaturated fatty acid levels in the serum and liver (P < .05) after 12 weeks of intervention. In particular, PSE treatment increased the level of C22:5 n-3, an FA that was negatively correlated with the degree of hepatic steatosis in the serum, liver, and adipose tissue. The increases in some unsaturated fatty acids are probably related to the upregulation of stearoyl-coenzyme A desaturase-1 and fatty acid desaturase-1.