BibTex Citation Data :
@article{dmj53717, author = {Rendri Hansah and Kurnia Handayani and Widia Sari and Ghaniyyatul Khudri and Syandrez Putra and Roland Helmizar}, title = {VITAMIN D AND INSULIN RESPONSE IN STREPTOZOTOCIN-INDUCED DIABETIC RATS: AN IN VIVO INVESTIGATION}, journal = {Jurnal Kedokteran Diponegoro (Diponegoro Medical Journal)}, volume = {15}, number = {5}, year = {2026}, keywords = {Insulin; Rat model; Streptozotocin; Type 2 diabetes mellitus; Vitamin D; β-cell function}, abstract = { Background: Type 2 diabetes mellitus (T2DM) is a widespread global health problem, defined by increasing insulin resistance and gradual deterioration of β-cell function. Vitamin D is posited to influence glucose metabolism, although the evidence about its impact on insulin dynamics is inconsistent. Objective: This study evaluated the effect of vitamin D supplementation on insulin levels in a streptozotocin (STZ)-induced diabetic rat model. Methods: Twenty-five Sprague Dawley rats were randomly assigned to five groups: A (healthy control), B (healthy + vitamin D 415 IU/day), C (T2DM control), D (T2DM + 415 IU/day), and E (T2DM + 1,100 IU/day). Diabetes was induced using a high-fat diet followed by STZ injection. Vitamin D supplementation was given orally for 30 days. Serum insulin and vitamin D were measured by ELISA, and group differences were analyzed using one-way ANOVA with Bonferroni post hoc testing. Results: Insulin concentrations differed significantly across groups (p = 0.022). Healthy rats receiving vitamin D (Group B) exhibited higher insulin levels compared with both diabetic controls (p = 0.004) and diabetic rats supplemented with the same dose (p = 0.005). Higher-dose supplementation in diabetic rats (Group E) showed only a nonsignificant trend toward increased insulin (p = 0.224). No significant correlation was observed between serum vitamin D and insulin levels (r = 0.171, p = 0.415). Conclusion: Vitamin D supplementation markedly enhanced insulin secretion in healthy rats but did not improve insulin output in diabetic rats. These findings suggest that vitamin D’s stimulatory effects on insulin may be more pronounced in healthy or early metabolic conditions and less effective in established diabetes. }, issn = {2540-8844}, pages = {403--410} doi = {10.14710/dmj.v15i5.53717}, url = {https://ejournal3.undip.ac.id/index.php/medico/article/view/53717} }
Refworks Citation Data :
Background: Type 2 diabetes mellitus (T2DM) is a widespread global health problem, defined by increasing insulin resistance and gradual deterioration of β-cell function. Vitamin D is posited to influence glucose metabolism, although the evidence about its impact on insulin dynamics is inconsistent. Objective: This study evaluated the effect of vitamin D supplementation on insulin levels in a streptozotocin (STZ)-induced diabetic rat model. Methods: Twenty-five Sprague Dawley rats were randomly assigned to five groups: A (healthy control), B (healthy + vitamin D 415 IU/day), C (T2DM control), D (T2DM + 415 IU/day), and E (T2DM + 1,100 IU/day). Diabetes was induced using a high-fat diet followed by STZ injection. Vitamin D supplementation was given orally for 30 days. Serum insulin and vitamin D were measured by ELISA, and group differences were analyzed using one-way ANOVA with Bonferroni post hoc testing. Results: Insulin concentrations differed significantly across groups (p = 0.022). Healthy rats receiving vitamin D (Group B) exhibited higher insulin levels compared with both diabetic controls (p = 0.004) and diabetic rats supplemented with the same dose (p = 0.005). Higher-dose supplementation in diabetic rats (Group E) showed only a nonsignificant trend toward increased insulin (p = 0.224). No significant correlation was observed between serum vitamin D and insulin levels (r = 0.171, p = 0.415). Conclusion: Vitamin D supplementation markedly enhanced insulin secretion in healthy rats but did not improve insulin output in diabetic rats. These findings suggest that vitamin D’s stimulatory effects on insulin may be more pronounced in healthy or early metabolic conditions and less effective in established diabetes.
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