Our findings suggest that low vitamin D exposure results in an inflammatory-prone status that may contribute to or be a risk factor for several diseases including inflammatory bowel disease, obesity, diabetes, and cardiovascular diseases.

Bifidobacterium bifidum MIMBb75 is a recently identified probiotic. However, its distribution along the intestine and impact on resident microbiota is unknown. Herein, we established a quantitative real-time polymerase chain reaction assay targeting the B. bifidum-specific BopA region for the quantification of B. bifidum in feces and used this assay to investigate transit of B. bifidum MIMBb75 through the murine intestine. We also analyzed the consequential impact on resident microbial cohorts. C57BL/6J mice were daily gavaged with 0.2 mL of either sterile PBS or PBS containing 10(8) colony-forming units of B. bifidum MIMBb75 for 2 weeks, after which intestinal contents and fecal samples were analyzed for microbial compositional changes. Bifidobacterium bifidum MIMBb75 was able to transiently colonize the murine intestine, with the predominant niche being the ceco-proximal colonic region. Region-specific effects on host microbiota were observed including decreased levels of Clostridium coccoides in the cecum, increased levels of bifidobacteria in the proximal and distal colon, total bacteria and Clostridium leptum in the proximal colon, and of C. coccoides in the feces. These findings suggest that probiotic properties of B. bifidum MIMBb75 may partially depend on its ability to at least transiently colonize the intestine and impact on the resident microbial communities at various intestinal loci.

Lower maternal serum 25‐hydroxyvitamin D or ultraviolet B exposure is associated with lower bone mineral in offspring during childhood. The effect of higher maternal vitamin D status on offspring bone health at adulthood is less clear. Using the CD‐1 mouse model, this study determined if dams fed supplemental (5,000 IU/kg diet) versus low (25 IU/kg diet) levels of vitamin D during pregnancy and lactation affected bone health of male offspring. At weaning, expression of osterix, osteoprotegrin, RANKL and vitamin D receptor (VDR) in the tibia growth plate was measured by immunohistochemical analyses in a subset of male mice (n=8/group). Some offspring were fed their mothers diet or the opposite diet (n=14/group) until age 3 months when bone strength, i.e. peak load, at lumbar vertebra and femur neck and midpoint was measured. At weaning, mice exposed to supplemental vitamin D had higher (p<0.05) expression of osteoprotegrin and osterix and lower (p<0.05) expression of VDR with no difference in expression of RANKL in proliferating or hypertrophic chondrocytes in the tibia growth plate. At 3 months of age, offspring of mothers fed supplemental vitamin D had lower (p<0.05) femur neck peak load with no difference in peak load at other skeletal sites regardless of post‐weaning diet. Further study is required to understand the structural changes that contribute to the lower femur neck peak load.

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