AI Article Synopsis
- Early weaning (EW) in rats leads to developmental issues and obesity in adulthood, correlated with higher 25-hydroxyvitamin D (25(OH)D) levels, which can potentially be improved with calcium supplementation.
- The study involved comparing obesity and vitamin D status in rats weaned early and treated with calcium versus those who had free access to milk, revealing significant differences in vitamin D metabolism and adiposity.
- The findings suggest that calcium therapy could effectively aid in weight management and combat obesity-related metabolic disorders by addressing vitamin D resistance in fat cells.
Article Abstract
Scope: Early weaning (EW) is associated with an impairment of offspring development and leads to overweight and higher 25-hydroxyvitamin D (25(OH)D) levels in adulthood, which can be corrected by calcium supplementation, potentially via vitamin D regulation of adipogenesis.
Methods And Results: We examined vitamin D status in adipose tissue in EW obese rats, treated with calcium. Dams were separated into: EW- dams were wrapped with a bandage to interrupt lactation (last 3 days), and C- pups with free access to milk. At PN120, EW pups were divided in: EW- standard diet, and EWCa- calcium supplementation (10 g of calcium carbonate/kg of chow). On PN21, EW group has hypocalcemia. On PN180, EW group showed lower intestinal calbidin, higher adiposity, and 25(OH)D. In adipose tissue, Cyp27b1/1alpha-Hydroxylase, C/EBPB, PPAR-γ, IL6, TNF-A, and MCP1 were increased, while VDR and IL10 were decreased. Calcium increased calbidin, VDR and prevented adipose tissue dysfunction. EW group has a long-term effect of vitamin D on adipocyte, contributing to pro-inflammatory status and obesity.
Conclusion: We propose that in obese rat adipocytes, 1,25(OH)2 D down-regulates VDR, resulting in vitamin D resistance, characterized by higher Cyp27b1/1α-Hydroxylase and adipogenesis. Calcium therapy appears to be an outstanding strategy for weight loss and improving endocrine metabolic disorders that are obesity associated.
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| http://dx.doi.org/10.1002/mnfr.201500735 | DOI Listing |
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