Diabetes mellitus (DM) merupakan penyakit metabolik yang disebabkan berkurangnya sekresi hormon insulin, menurunnya sensitivitas insulin atau kombinasi keduanya. DM tipe2 merupakan salah satu jenis diabetes melitus yang paling banyak penyandangnya. Defisiensi vitamin D sering dikaitkan dengan kejadian DM tipe 2. Vitamin D merupakan salah satu vitamin yang berpotensi untuk memperbaiki sintesis dan sekresi insulin. Penelitian ini bertujuan untuk menilai pengaruh suplementasi vitamin D 5.000 IU/hari selama 3 dan 6 bulan terhadap fungsi sel beta pankreas yang dilihat dari penanda antioksidan (SOD), inflamasi (IL-6), PDX-1, HbA1c dan resistensi insulin (HOMA-IR) serta keamanan pemberian vitamin D yang dilihat dari peningkatan kadar 25-(OH)D dan ekspresi VDR.Penelitian ini menggunakan desain double blind randomized controlled trial mengikutsertakan 94 penyandang DM tipe 2 dengan usia 35‒80 tahun di Puskesmas Kecamatan Mampang Jakarta Selatan. Hasil randomisasi terdapat 47 subjek kelompok kontrol dan 47 subjek kelompok vitamin D. Kelompok kontrol mendapatkan plasebo sedangkan kelompok vitamin D mendapatkan plasebo dan vitamin D 5.000 IU selama 6 bulan. Studi dilakukan mulai bulan Januari─Desember 2022. SOD, IL-6, PDX-1, VDR, HbA1c, glukosa darah, insulin puasa, 25-(OH)D, HOMA-IR diperiksa pada awal penelitian, pascasuplementasi 3 dan 6 bulan. Analisis statistik dengan SPSS 20 menggunakan uji ANOVA general linear repeated measurement dan Mann Whitney.Karakteristik subjek penelitian pada kelompok vitamin D dan kelompok kontrol pada awal penelitian menunjukkan kedua kelompok setara baik pada karaktersitik demografis, laboratorium, dan asupan nutrien. Pascasuplementasi vitamin D selama 3 dan 6 bulan terdapat perbedaan bermakna kadar 25-(OH)D (p = 0,000), tidak terdapat perbedaan bermakna HbA1c dan glukosa darah (p = 0,360 dan p = 0,296) antara kelompok kontrol dan kelompok vitamin D. Terdapat perbedaan bermakna kadar insulin pasca suplementasi 3 dan 6 bulan (p = 0,034 dan p = 0,013) serta perbedaan bermakna HOMA-IR pasca suplementasi 3 dan 6 bulan (p = 0,033 dan p = 0,031) antara kelompok kontrol dan kelompok vitamin D. Kadar insulin pada kedua kelompok mengalami peningkatan tetapi peningkatan kadar insulin pada kelompok kontrol lebih tinggi. HOMA-IR pada kedua kelompok mengalami peningkatan tetapi peningkatan HOMA-IR pada kelompok kontrol lebih tinggi. Terdapatnya kadar insulin dan HOMA-IR yang lebih rendah pada kelompok vitamin D menunjukkan adanya perbaikan resistensi insulin.Untuk PDX-1 tidak terdapat perbedaan bermakna pasca suplementasi 3 dan 6 bulan (p = 0,464 dan p = 0,499) antara kelompok kontrol dan kelompok vitamin D. Vitamin D tidak terbukti meningkatkan SOD dan VDR serta tidak terbukti menurunkan IL-6.Simpulan: Suplementasi vitamin D 5.000 IU/hari selama 6 bulan dapat meningkatkan kadar 25-(OH)D dalam batas normal, serta dapat memperbaiki resistensi insulin melalui penurunan HOMA-IR dan penurunan sekresi insulin. Efek terhadap HbA1c, SOD, IL-6, PDX-1, dan VDR tidak terbukti.

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Diabetes mellitus (DM) is a metabolic disease that is caused by reduced insulin secretion, reduced insulin sensitivity, or a combination of the two. Type 2 DM is one of the types of diabetes mellitus with the greatest number of cases. Vitamin D deficiency is frequently associated with the incidence of type 2 DM. Vitamin D is one of the vitamins with the potential to improve insulin synthesis and secretion. This study aimed to evaluate the effect of supplementation of vitamin D at 5.000 IU/day for 3 and 6 months on pancreatic beta cell function from the perspective of antioxidant (SOD) and inflammatory (IL-6) markers, PDX-1 expression, HbA1c concentration, and insulin resistance (HOMA-IR), and the safety of vitamin D administration as shown by 25-(OH)D concentration and vitamin D receptor (VDR) expression. This study was a double blind randomized controlled trial involving 94 patients with type 2 DM aged 35‒80 years at Mampang District Public Health Center, South Jakarta. Randomization resulted in 47 subjects in the control group and 47 subjects in the vitamin D group. The control group received placebo whereas the vitamin D group received placebo and vitamin D at 5.000 IU for 6 months. The study was conducted from January‒December 2022. SOD, IL-6, PDX-1, VDR, HbA1c, blood glucose, fasting insulin, 25-(OH)D, and HOMA-IR were determined at baseline and after supplementation for 3 and 6 months. Statistical analysis by SPSS 20 used ANOVA general linear repeated measurement and Mann-Whitney tests. Characteristics of study subjects in the vitamin D and control groups at baseline showed that both groups were similar in demographic characteristics, laboratory measures, and nutrient intake. After supplementation of vitamin D for 3 and 6 months there were significant differences in 25-(OH)D concentration (p = 0.000), but no significant differences in HbA1c and blood glucose (p = 0.360 and p = 0.296) between control and vitamin D groups. There were significant differences in insulin concentration after supplementation for 3 and 6 months (p = 0.034 and p = 0.013) and significant differences in HOMA-IR after supplementation for 3 and 6 months (p = 0.033 and p = 0.031) between control and vitamin D groups. Insulin concentrations increased in both groups but the increase insulin concentrations was higher in the control group. HOMA-IR increased in both groups but the increase in HOMA-IR was higher in the control group. The lower insulin concentrations and decreased HOMA-IR in the vitamin D group indicated improve insulin resistance. With regard to PDX-1 there were no significant differences after supplementation for 3 and 6 months (p = 0.464 and p = 0.499) between control and vitamin D groups. Vitamin D was not proven to increase SOD and VDR, and was not proven to reduce IL-6.

Conclusion: Supplementation of vitamin D at 5.000 IU/day for 6 months was able to increase 25-(OH)D concentration within normal limits and was able to improve insulin resistance through reduction in HOMA-IR and decreased insulin secretion . Effects on HbA1c, SOD, IL-6, PDX-1, and VDR were not proven.