Whole grain germinated brown rice regulates intestinal immune homeostasis and gastrointestinal hormones in type 2 diabetic patients-a randomized control trial.

Background: Whole grains present distinguished benefits to a handful of metabolic syndromes (MetS). However, the preventive effects of germinated brown rice (GBR), a new type of brown rice, on patients with type 2 diabetes (T2DM) are rarely reported. Objectives: To investigate whether replacing 100 g refined white rice (RWR) with equal GBR per day is effective in T2DM and its underlying mechanisms. Methods: Ninety-nine qualified T2DM patients (64.58 ± 5.06 years old) were recruited. All patients were randomly divided into GBR group (100 g d-1 GBR for 12 weeks) and control group (keep the regular diet). Food frequency questionnaires, and fresh stool and serum samples were collected before and after the intervention, followed by various measurements. Results: Fasting blood glucose was obviously decreased after GBR intervention with an effective rate of 62%. Glycated hemoglobin (HbA1c) levels were decreased in the GBR group with no significance. In the GBR group, the abundance of beneficial bacteria in feces was increased, while harmful bacteria were decreased. The percentage of Bacteroides (57.2%) was largely increased. In addition, three types of short-chain fatty acids (SCFAs) including acetic acid, propanoic acid, and butyric acid were increased significantly by GBR (p < 0.05). The secretion of GLP and PYY in serum, two kinds of gastrointestinal hormones downstream of SCFAs, was stimulated by GBR (p < 0.01). Meanwhile, GBR intervention could balance the ratio of Treg/Th17 immune cells in PBMCs and reduce the levels of inflammatory factors including IL-6, IL-8, and LPS in serum, which improved the permeability of intestinal mucosa. Conclusions: GBR (100 g d-1 for 12 weeks) has positive improvement in the fasting blood glucose for T2DM patients, which attributed to the recovery of intestinal homeostasis.

Sulforaphane inhibits the production of Aß partially through the activation of Nrf2-regulated oxidative stress.

Sulforaphane (SFN), a potent nuclear factor erythroid 2-related factor 2 (Nrf2) activator, presents a potential role in improving Alzheimer's disease (AD)-specific symptoms. However, the regulation mechanism of SFN in AD is poorly understood. Here, we established AD models both in vitro and in vivo. Animal behaviors were tested by the Morris water maze test. The pathology of the hippocampus and the content of Aß were detected. SFN (40 mg kg-1) decreased the escape latency (24.96 ± 7.43 s) and increased the target-zone frequency (3.19 ± 1.19) in rats. SFN improved the pathological morphology and the number of neurons in the hippocampus. Additionally, SFN significantly upregulated the contents of thioredoxin and glutathione as well as the activities of antioxidant enzymes, along with the expression of the Nrf2 protein. Conversely, SFN lowered the Aß content and ROS level in N2a/APP cells. After silencing the Nrf2 by SiRNA, the inhibitory effects of SFN on ROS and Aß production were partially weakened. In conclusion, the improvement of AD by SFN was closely related with Nrf2 activation.

Lactate as a metabolite from probiotic Lactobacilli mitigates ethanol-induced gastric mucosal injury: an in vivo study.

BACKGROUND: Pre-administration of probiotic Lactobacilli attenuates ethanol-induced gastric mucosal injury (GMI). The underpinning mechanisms remain to be elucidated. We speculated that lactate, the main metabolite of Lactobacillus that can be safely used as a common food additive, mediated the gastroprotective effect. This study aimed to gain experimental evidence to support our hypothesis and to shed lights on its underlying mechanisms. METHODS: Lactate was orally administrated to mice at different doses 30 min prior to the induction of GMI. Gastric tissue samples were collected and underwent histopathological and immunohistochemical assessments, enzyme-linked immunosorbent assay, quantitative polymerase chain reaction (qPCR) and western blot analyses. RESULTS: Pretreatment with lactate at 1-3 g/kg significantly curtailed the severity of ethanol-induced GMI, as shown by morphological and histopathological examinations of gastric tissue samples. Significantly lower level of cytokines indicative of local inflammation were found in mice receiving lactate treatment prior to ethanol administration. Western-blot, immunohistochemical analysis and qPCR suggested that gastroprotective properties of lactate were mediated by its modulatory effects on the expression of the apoptosis regulator gene Bax, the apoptotic executive protein gene Casp3, and genes critical for gastric mucosal integrity, including those encoding tight junction proteins Occludin, Claudin-1, Claudin-5, and that for lactate receptor GPR81. CONCLUSION: Lactate mitigates ethanol-induced GMI by curtailing local gastric inflammatory response, down-regulating the expression of the apoptosis regulator and executor genes Bax and Casp3, and up-regulating the expression of genes encoding tight junction proteins Occludin, Claudin-1, and Claudin-5 and the lactate receptor GPR81.