Epidemiological evidence indicates that vitamin D is involved in defense against 
diabetes; however, the precise underlying mechanism remains to be elucidated. In 
the present study, the effect of vitamin D on the pathogenesis of diabetes was 
investigated, with an emphasis on its direct effect on pancreatic β‑cells. A 
streptozotocin (STZ)‑induced type 1 diabetes mellitus (T1DM) mouse model and 
MIN6 mouse insulinoma β‑cells were subjected to vitamin D treatment. 
Histopathological analysis of pancreatic islets was performed to investigate 
insulitis, and reverse transcription-quantitative polymerase chain reaction and 
western blotting were used to determine the mRNA and protein expression levels 
of markers of autophagy [microtubule-associated protein 1A/1B‑light chain 3 
(LC3) and Beclin 1] and regulation of apoptosis [B-cell lymphoma 2 (Bcl-2)]. 
Apoptosis of MIN6 cells was examined by flow cytometry following annexin 
V/propidium iodide labeling. The secretion of insulin was measured by ELISA. The 
results revealed that vitamin D reduced the incidence of T1DM, enhanced insulin 
secretion and relieved pancreatic inflammation in STZ‑treated mice. Furthermore, 
vitamin D increased the mRNA expression levels of LC3 and Beclin 1, and 
increased Bcl‑2 protein expression levels in STZ‑treated MIN6 cells, while 
decreasing the apoptosis rate. The results of the present study demonstrated, 
for the first time to the best of our knowledge, that vitamin D induces 
autophagy and suppresses apoptosis of pancreatic β‑cells, as well as preventing 
insulitis. These findings regarding vitamin D provide insights into its 
involvement in diabetes, and suggest a potential novel strategy for the 
treatment of diabetes via agents enhancing autophagy in pancreatic β-cells.