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The aims of this randomized controlled double-blind clinical trial were to assess the impact of vitamin D supplementation on calcium metabolism and non-calcemic broad gene expression by relating them to the individual’s responsiveness to varying doses of vitamin D 3 . Thirty healthy adults were randomized to receive 600, 4,000 or 10,000 IU/d of vitamin D 3 for 6 months. Circulating parathyroid hormone (PTH), 25(OH)D, calcium and peripheral white blood cells broad gene expression were evaluated. We observed a dose-dependent increase in 25(OH)D concentrations, decreased PTH and no change in serum calcium. A plateau in PTH levels was achieved at 16 weeks in the 4000 and 10,000 IU/d groups. There was a dose-dependent 25(OH)D alteration in broad gene expression with 162, 320 and 1289 genes up- or down-regulated in their white blood cells, respectively. Our results clearly indicated that there is an individual’s responsiveness on broad gene expression to varying doses of vitamin D 3 . Vitamin D 3 supplementation at 10,000 IU/d produced genomic alterations several fold higher than 4,000 IU/d even without further changes in PTH levels. Our findings may help explain why there are some inconsistency in the results of different vitamin D’s clinical trials.

Background/Aim: To investigate the effects of vitamin D3 supplementation on gut microbiota. Patients and Methods: Twenty adults with vitamin D insufficiency/deficiency [25(OH)D <30 ng/ml] were enrolled and given 600, 4,000 or 10,000 IUs/day of oral vitamin D3. Stool samples were collected at baseline and 8 weeks for identifying gut microbiota using 16S rRNA gene amplification and sequencing. Results: Baseline serum 25(OH)D was associated with increased relative abundance of Akkermansia and decreased relative abundance of Porphyromonas (p<0.05). After the intervention, we observed a dose-dependent increase in relative abundance of Bacteroides with a significant difference between the 600 IUs and the 10,000 IUs groups (p=0.027), and Parabacteroides with a significant difference between the 600 IUs and the 4,000 IUs groups (p=0.039). Conclusion: Increased serum 25(OH)D was associated with increased beneficial bacteria and decreased pathogenic bacteria. A dose-dependent increase in bacteria associated with decreased inflammatory bowel disease activity was observed after vitamin D3 supplementation.

To assess the impact of vitamin D supplementation on genomic and metabolomic profiles and relate them to the individual's responsiveness to varying doses of vitamin D Patients and Methods: Healthy adults were given either 600, 4000 or 10,000 IUs vitamin D /day for 6 months. Circulating parathyroid hormone (PTH), 25-hydroxyvitamin D [25(OH)D], calcium, peripheral white blood cells broad gene expression and urine and serum metabolomic profiles were evaluated. There was a dose-dependent effect of vitamin D supplementation on serum 25(OH)D, PTH and broad gene expression. Serum calcium levels remained normal for all study subjects and no untoward toxicity was observed. The metabolomic profiles were related to the genomic expression analysis. There were significant inter-individual effects on gene expression and metabolomic profile in response to the same dose of vitamin D supplementation, despite similar changes in 25(OH)D and PTH concentrations. These results may help explain the variability observed in clinical trials regarding vitamin D's non-calcemic health benefits.

To investigate the effects of vitamin D supplementation on gut microbiota. Twenty adults with vitamin D insufficiency/deficiency [25(OH)D <30 ng/ml] were enrolled and given 600, 4,000 or 10,000 IUs/day of oral vitamin D Stool samples were collected at baseline and 8 weeks for identifying gut microbiota using 16S rRNA gene amplification and sequencing. Baseline serum 25(OH)D was associated with increased relative abundance of Akkermansia and decreased relative abundance of Porphyromonas (p<0.05). After the intervention, we observed a dose-dependent increase in relative abundance of Bacteroides with a significant difference between the 600 IUs and the 10,000 IUs groups (p=0.027), and Parabacteroides with a significant difference between the 600 IUs and the 4,000 IUs groups (p=0.039). Increased serum 25(OH)D was associated with increased beneficial bacteria and decreased pathogenic bacteria. A dose-dependent increase in bacteria associated with decreased inflammatory bowel disease activity was observed after vitamin D supplementation.

While the ventromedial hypothalamus, ventrolateral area (VMHvl) is now well-established as a critical locus of the generation of conspecific aggression, its role is complex, with populations of neurons responding during the motivational, sensory, and action phases of aggression, and also during social interactions with the opposite sex. It has been previously unclear how this brain uses the complex multidimensional signal and generates a discrete action: the attack. Here, we find that the largest posterior target of the VMHvl, the lateral periaqueductal gray (lPAG) encodes a simplified attack-selective signal during aggression. Single units in the lPAG exhibit greater selectivity for the attack action during aggression than VMHvl neurons, and a subpopulation of neurons in the PAG exhibit short-latency, time-locked spiking relative to the activity of jaw muscles for biting during attack. In addition, channelrhodopsin assisted circuit mapping reveals a preferential projection from VMHvl glutamatergic cells to lPAG glutamatergic cells. Using pathway-specific fiber photometry, we find that this excitatory projection conveys male-biased signals from the VMHvl to the downstream glutamatergic PAG neurons that integrate ongoing male-related activity over several seconds which suggests that action selectivity is generated by a combination of pre and post synaptic filtering mechanisms.