Here, we examined the functionality of Lactobacillus fermentum strain JDFM216, a newly isolated probiotic bacterium, using a Caenorhabditis elegans model. We determined bacterial colonization in the intestinal tract of C. elegans by plate counting and transmission electron microscopy and examined the survival of C. elegans using a solid killing assay. In addition, we employed DNA microarray analysis, quantitative real time-polymerase chain reaction, and immunoblotting assays to explore health-promoting pathways induced by probiotic bacteria in C. elegans. Initially, we found that the probiotic bacterium L. fermentum strain JDFM216 was not harmful to the C. elegans host. Conditioning with JDFM216 led to its colonization in the nematode intestine and enhanced resistance in nematodes exposed to food-borne pathogens, including Staphylococcus aureus and Escherichia coli O157:H7. Interestingly, this probiotic strain significantly prolonged the life span of C. elegans. Whole-transcriptome analysis and transgenic worm assays revealed that the health-promoting effects of JDFM216 were mediated by a nuclear hormone receptor (NHR) family and PMK-1 signaling. Taken together, we described a new C. elegans-based system to screen novel probiotic activity and demonstrated that preconditioning with the probiotic L. fermentum strain JDFM216 may positively stimulate the longevity of the C. elegans host via specific pathway.

Black carrots (Daucus carota L.) are rich in anthocyanins which contribute many health benefits, but are limited by bioavailability and instability when exposed to oxygen, heat and light. Fermenting black carrots may improve the stability, absorption and bioactivity of its anthocyanins. Here, we examined whether and by what mechanisms the long-term consumption of unfermented black carrot extract (BC) and its extracts fermented with Lactobacillus plantarum (BCLP) or Aspergillus oryzae (BCAO) might prevent menopausal symptoms including impaired energy, glucose and lipid metabolism in estrogen-deficient animals with diet-induced obesity. Ovariectomized (OVX) rats were fed four different high-fat diets containing 2 % dextrin (OVX-control), 2 % BC, 2 % BCLP, or 2 % BCAO for 12 weeks. Sham rats were fed high-fat diets containing 2 % dextrin. The contents of total anthocyanins increased in BCAO compared to BC and BCLP, whereas the contents of cyanidin-3-rutinosides, malvidin-3,5-diglycosides and delphine-3-glucoside were lower and cyanidin and malvidin were much higher in BCLP and BCAO than BC. Fat mass and weight gain were lower in descending order of OVX-control [ BC and BCLP [ BCAO due to increased energy expenditure and fat oxidation. However, BC, BCLP and especially BCAO all normalized HOMA-IR, an indicator of insulin resistance and glucose intolerance, in OVX rats. OVX increased serum total and LDL cholesterol and triglycerides, but BC, BCLP and BCAO significantly prevented the increases. BCAO markedly decreased hepatic triglyceride levels by increasing gene expressions of CPT-1 and PPAR-a, which are involved in fatty acid oxidation, and decreasing mRNA expressions of FAS and SREBP-1c, which are associated with fatty acid synthesis. This was related to increased pAMPK ? pACC signaling and improved hepatic insulin signaling (pAkt ? pFOXO-1). Cyanidin and malvidin markedly decreased fat accumulation in 3T3-L1 adipocytes by increasing CPT-1 and decreasing FAS and SREBP-1c expression in comparison with cyanidin-3-rutinoside and malvidin-3,5-diglycosides. In conclusion, with increasing cyanidin and malvidin, BCAO prevented the exacerbation of lipid and glucose metabolism by activating hepatic insulin signaling and AMPK activation by in OVX rats.

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We determined that consuming chungkookjang fermented by Bacillus subtilis (BS) or Bacillus amyloliquefaciens (BA) alleviated hyperglycemia in partially pancreatectomized (Px) rats, an Asian type 2 diabetic (T2D) animal model. Px rats had deteriorated glucose metabolism with decreased glucose-stimulated insulin secretion and insulin sensitivity. Insulin secretion capacity was improved in the ascending order of the Px-control, positive control (3 mg of metformin/kg of body weight), BS (4.5% BS diet), BA (4.5% BA diet), and normal-control (sham-operated rats). BA and BS increased β-cell mass and decreased malondialdehyde contents and tumor necrosis factor α expression in the islets. BA increased hepatic peroxisome proliferator-activated receptor (PPAR)-α and PPAR-β similar to the positive control. Bacillales, Lactobacillales, and Verrucomicrobiales (Akkermensia muciniphila) increased and Enterobacteriales decreased in the BA and BS compared to the Px-control. BA prevented the decrease in the villi area and the number of goblet cells in intestinal tissues. In conclusion, BA improved glucose regulation by potentiating insulin secretion and reducing insulin resistance while maintaining gut mucin contents by improving gut microbiota in lean T2D rats.

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