For years, it has been reported that Alzheimer’s disease (AD) is the most common cause of dementia. Various external and internal factors may contribute to the early onset of AD. This review highlights a contribution of the disturbances in the microbiota–gut–brain (MGB) axis to the development of AD. Alteration in the gut microbiota composition is determined by increase in the permeability of the gut barrier and immune cell activation, leading to impairment in the blood–brain barrier function that promotes neuroinflammation, neuronal loss, neural injury, and ultimately AD. Numerous studies have shown that the gut microbiota plays a crucial role in brain function and changes in the behavior of individuals and the formation of bacterial amyloids. Lipopolysaccharides and bacterial amyloids synthesized by the gut microbiota can trigger the immune cells residing in the brain and can activate the immune response leading to neuroinflammation. Growing experimental and clinical data indicate the prominent role of gut dysbiosis and microbiota–host interactions in AD. Modulation of the gut microbiota with antibiotics or probiotic supplementation may create new preventive and therapeutic options in AD. Accumulating evidences affirm that research on MGB involvement in AD is necessary for new treatment targets and therapies for AD.

Diabetes and obesity are metabolic diseases that have become alarming conditions in recent decades. Their rate of increase is becoming a growing concern worldwide. Recent studies have established that the composition and dysfunction of the gut microbiota are associated with the development of diabetes. For this reason, strategies such as the use of prebiotics to improve intestinal microbial structure and function have become popular. Consumption of prebiotics for modulating the gut microbiota results in the production of microbial metabolites such as short-chain fatty acids that play essential roles in reducing blood glucose levels, mitigating insulin resistance, reducing inflammation, and promoting the secretion of glucagon-like peptide 1 in the host, and this accounts for the observed remission of metabolic diseases. Prebiotics can be either naturally extracted from non-digestible carbohydrate materials or synthetically produced. In this review, we discussed current findings on how the gut microbiota and microbial metabolites may influence host metabolism to promote health. We provided evidence from various studies that show the ability of prebiotic consumption to alter gut microbial profile, improve gut microbial metabolism and functions, and improve host physiology to alleviate diabetes and obesity. We conclude among other things that the application of systems biology coupled with bioinformatics could be essential in ascertaining the exact mechanisms behind the prebiotic–gut microbe–host interactions required for diabetes and obesity improvement.

The global increase in prevalence of (pre-)diabetes demands immediate intervention strategies. In our earlier work, we demonstrated in vitro antidiabetic potential of a fermented beetroot product (PN39). Here, we examined the impact of PN39 on glucose tolerance and gut microbiota in C57BL/6J male mice and on prediabetic (PD) subjects’ stool microbiota. In mice, high-fat diet (HFD) consumption for 9 weeks resulted in hyperglycemia and impaired glucose tolerance (GT) while concomitant consumption of PN39 and HFD (PN39+HFD) prevented GT impairment. Meanwhile, feeding the mice with HFD for 5 weeks to induce PD and later administering them with PN39 for 4 weeks (PD + PN39) neither improved fasting blood glucose nor GT. Relative to control groups, the gut microbiota of both PD mice and humans were characterized by decreased Clostridia UCG-014 and Lactobacilli as well as significantly altered gut microbial carbohydrate metabolism. Feeding PN39 together with HFD preserved Clostridia UCG-014 and Lactobacilli, increased short chain fatty acid production relative to mice fed with HFD only. Treating gut microbiota of PD subjects with PN39 however increased Clostridia UCG-014 and Lactobacilli populations and increased short chain fatty acids concentrations in the stools. In both mice and humans, PN39 treatment rectified the altered microbial carbohydrate metabolism observed in their PD counterparts. This suggests that the gut microbial modulatory effects of PN39 coupled with its capacity to regulate gut microbial glucose metabolism, likely played a role in preventing PD in mice receiving PN39+HFD. Taken together, our results indicate that PN39 could act as a potent antidiabetic functional food for preventing diabetes and its associated dysbiosis.

This strain was isolated from traditionally (homemade) fermented Lithuanian cherry tomatoes. The genome consists of 55 contigs with a total size of 3,326,119 bp, an N50 of 170738, and a GC% of 44.3 %. According to the COG annotation, most of these proteins were divided into three categories related to transcription (K category: 307), amino acid transport and metabolism (E category: 222), and carbohydrate transport and metabolism (G category: 268). No genes associated with antimicrobial resistance or virulence factors were identified. The data presented here can be used in comparative genomics to identify antimicrobial resistance genes and virulence factors that may be present in relevant Lactobacillus species. PlasmidFinder server revealed the presence of plasmid pR18 (assessment number JN601038) in the genome that has lincomycin resistance, can be transferred from one bacterium to another, and is one of the most common plasmids in the genera Bacillus and Lactobacillus. The draft genome sequence data have been deposited with NCBI under Bioproject under accession number PRJNA947394.