Inflammatory bowel disease (IBD) is a chronic inflammation of the gastrointestinal tract (GIT), including Crohn’s disease (CD) and ulcerative colitis (UC), which differ in the location and lesion extensions. Both diseases are associated with microbiota dysbiosis, with a reduced population of butyrate-producing species, abnormal inflammatory response, and micronutrient deficiency (e.g., vitamin D hypovitaminosis). Vitamin D (VitD) is involved in immune cell differentiation, gut microbiota modulation, gene transcription, and barrier integrity. Vitamin D receptor (VDR) regulates the biological actions of the active VitD (1α,25-dihydroxyvitamin D3), and is involved in the genetic, environmental, immune, and microbial aspects of IBD. VitD deficiency is correlated with disease activity and its administration targeting a concentration of 30 ng/mL may have the potential to reduce disease activity. Moreover, VDR regulates functions of T cells and Paneth cells and modulates release of antimicrobial peptides in gut microbiota-host interactions. Meanwhile, beneficial microbial metabolites, e.g., butyrate, upregulate the VDR signaling. In this review, we summarize the clinical progress and mechanism studies on VitD/VDR related to gut microbiota modulation in IBD. We also discuss epigenetics in IBD and the probiotic regulation of VDR. Furthermore, we discuss the existing challenges and future directions. There is a lack of well-designed clinical trials exploring the appropriate dose and the influence of gender, age, ethnicity, genetics, microbiome, and metabolic disorders in IBD subtypes. To move forward, we need well-designed therapeutic studies to examine whether enhanced vitamin D will restore functions of VDR and microbiome in inhibiting chronic inflammation.

The increasing prevalence of type 2 diabetes mellitus (T2DM) worldwide has become a burden to healthcare systems. In 2019, around 463 million adults were living with diabetes mellitus, and T2DM accounted for 90 to 95% of cases. The relationship between the gut microbiota and T2DM has been explored with the advent of metagenomic techniques. Genome-wide association studies evaluating the microbiota of these individuals have pointed to taxonomic, functional, and microbial metabolite imbalances and represent a potential intervention in T2DM management. Several microbial metabolites and components, such as imidazole propionate, trimethylamine, and lipopolysaccharides, appear to impair insulin signaling, while short-chain fatty acids, secondary bile acids, and tryptophan metabolites may improve it. In addition, the use of probiotics with the aim of transiently restoring the microbial balance or reducing the effects of microbial metabolites that impair insulin sensitivity has been explored. Herein, we critically review the available literature on the changes in the gut microbiota in T2DM together with potential adjuvant therapies that may improve the health status of this population.