Sex-Specific effects of vitamin D on autistic behavior and gastrointestinal symptoms in rats via the regulation of serotonin metabolism.

Scientists studied vitamin D's effects on autism-like behaviors in rats. They found that vitamin D deficiency during pregnancy and early life caused autism-like symptoms and stomach problems in male rats, but not females. When given vitamin D supplements, male rats showed improvement in both behaviors and digestion. The researchers think vitamin D helps by increasing serotonin (a brain chemical) levels, but this only happened in males.

This animal study investigated vitamin D's role in autism-like behaviors using a valproic acid-induced rat model. Researchers examined how vitamin D deficiency during pregnancy and early development affected autism symptoms and gastrointestinal function. The study found sex-specific effects: male rats with vitamin D deficiency showed autism-like behaviors and gastrointestinal dysfunction, along with decreased serotonin levels and related enzyme activity in brain and intestinal tissues. Vitamin D supplementation improved these symptoms in male rats by enhancing serotonin metabolism through vitamin D receptor activity.

Female rats showed no significant changes. The research suggests vitamin D influences autism symptoms through serotonin pathway regulation, but only in males.

Findings suggest vitamin D supplementation may benefit males with autism through serotonin pathway regulation. However, human studies are needed to confirm these sex-specific effects and optimal dosing strategies before clinical application.

Animal model may not fully represent human autism. Sample size not reported. Sex-specific effects found in rats may not translate to humans. Single intervention approach limits broader applicability.

Vitamin D (VitD) deficiency (VDD) during prenatal and early brain development may be an environmental risk factor for autism spectrum disorder (ASD). While supplementation with high-dose VitD can improve core ASD symptoms, its mechanism is unclear. In addition, VitD regulates the serotonin (5-HT) pathway, which has been shown to be closely related to ASD. To explore the relationships among VitD levels, 5-HT levels and ASD symptoms, a valproic acid (VPA)-induced ASD rat model was constructed.

From pregnancy to early postnatal life, VitD levels were modulated. Both VDD and ASD male rats exhibited ASD core symptoms and gastrointestinal dysfunction, with decreased 5-HT, VitD receptor (Vdr), and tryptophan hydroxylase (Tph) activity in intestinal and brain tissues. VitD supplementation alleviated ASD symptoms, improved gastrointestinal function, and increased 5-HT levels, Vdr, and Tph activity in male rats. Female rats in VDD and ASD groups showed no significant changes.

Our findings suggest that 1,25(OH)Denhances Tph1/2 mRNA levels via Vdr activity, increasing 5-HT levels. This study provides insights into VitD, 5-HT metabolism, and ASD, offering potential directions for subtype analysis and therapeutic interventions.