Oral administration of 1,25-dihydroxyvitamin D3 completely protects NOD mice from insulin-dependent diabetes mellitus

• Published in: Archives of biochemistry and biophysics Vol. 417; no. 1; pp. 77 - 80
• Main Authors: Zella, Julia B, McCary, Laura C, DeLuca, Hector F
• Format: Journal Article
• Language: English
• Published: United States 01-09-2003
• Subjects: Administration, Oral; Age of Onset; Animals; Blood Glucose - analysis; Calcitriol - administration & dosage; Calcitriol - therapeutic use; Calcium - blood; Calcium - metabolism; Diabetes Mellitus, Type 1 - genetics; Diabetes Mellitus, Type 1 - metabolism; Diabetes Mellitus, Type 1 - prevention & control; Female; Hypercalcemia - chemically induced; Incidence; Male; Mice; Mice, Inbred NOD; Vitamin D Deficiency - complications; Vitamin D Deficiency - physiopathology
• ISSN: 0003-9861
• DOI: 10.1016/s0003-9861(03)00338-2

1,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)), the biologically active form of vitamin D, is widely recognized as a modulator of the immune system as well as a regulator of mineral metabolism. The objective of this study was to determine the effects of vitamin D status and treatment with 1,25(OH)(2)D(3) on diabetes onset in non-obese diabetic (NOD) mice, a murine model of human type I diabetes. We have found that vitamin D-deficiency increases the incidence of diabetes in female mice from 46% (n=13) to 88% (n=8) and from 0% (n=10) to 44% (n=9) in male mice as of 200 days of age when compared to vitamin D-sufficient animals. Addition of 50 ng of 1,25(OH)(2)D(3)/day to the diet prevented disease onset as of 200 days and caused a significant rise in serum calcium levels, regardless of gender or vitamin D status. Our results indicate that vitamin D status is a determining factor of disease susceptibility and oral administration of 1,25(OH)(2)D(3) prevents diabetes onset in NOD mice through 200 days of age.