Potential modulation pancreas gland activity in hyperprolactimic male Rats ( Rattus norvegicus) by vitamin D3 treatment
Abstract
Hyperprolactinemia status is commonly known as abnormal levels of prolactin hormone in
the blood due to endocrine disorder. So far, there is no evidence explaining whether
hyperprolactinemia affected Pancreas gland and vitamin D level in male. Therefore, this study aimed
to eliminate hyperprolactinemia affecting the Pancreas gland by treating it with vitamin D
supplements. Eighteen male rats were equally divide into three groups: The first group (6 rats):
received normal saline for 42 days. The second group (6 rats): rats were given 5 mg/kg
metoclopramide by intraperitoneal injection for hyperprolactinemia induction for 14 days. The third
group (6 rats): hyperprolactinemic rats received 2.5 mg/kg vitamin D3 for 28 days.
After the end of experimental) 42days(,hormonal parameters (prolactin, insulin, and vitamin D3)
were measure, and the Pancreas gland was remove for routine paraffin-embedded section staining
with hematoxylin and eosin staining. The result of the study revealed a significant decrease (P≤0. 01)
in prolactin hormone concentration and a significant increase (P≤0. 01) in D3 concentration and
insulin hormone Group 3compared with Group2. Histological examination of parts of the pancreas
gland treated with vitamin D showed a remarkable recovery in the size and number of cells, and the
cells became abundant in the cytoplasm. It was also noted that the nuclei returned to a size close to
normal and took on a regular, spherical shape and central location compared to the
hyperprolactinemia group. The study concluded that vitamin D had a protective effect on Pancreas
gland by stabilizing insulin hormone level and restoration histological architectures throughout
pancreas gland.
References
Halperin Rabinovich, I., Cámara Gómez, R., García Mouriz, M., & Ollero García-Agulló, D.
(2013). Clinical guidelines for diagnosis and treatment of prolactinoma and
hyperprolactinemia. Endocrinología y Nutrición (English Edition), 60(6), 308–319.
Hoskova, K., Bryant, N. K., Chen, M. E., Nachtigall, L. B., Lippincott, M. F.,
Balasubramanian, R., & Seminara, S. B. (2022). Kisspeptin Overcomes GnRH Neuronal
Suppression Secondary to Hyperprolactinemia in Humans. Journal of Clinical Endocrinology
and Metabolism, 107(8), E3515–E3525.
Zeng, Y., Huang, Q., Zou, Y., Tan, J., Zhou, W., & Li, M. (2023). The efficacy and safety of
quinagolide in hyperprolactinemia treatment: A systematic review and meta-analysis.
Frontiers in Endocrinology, 14(January).
Tomova, N., & Pharmacist, C. (2016). Guidance on the Treatment of Antipsychotic Induced
Hyperprolactinaemia in Adults Version 1. NHS Foundation Trust, 623349, 2–9.
Vilar, L., Vilar, C. F., Lyra, R., & Da Conceição Freitas, M. (2019). Pitfalls in the Diagnostic
Evaluation of Hyperprolactinemia. Neuroendocrinology, 109(1), 7–19.
McCallum, R. W., Sowers, J. R., Hershman, J. M., & Sturdevant, R. A. L. (1976).
Metoclopramide stimulates prolactin secretion in man. Journal of Clinical Endocrinology and
Metabolism, 42(6), 1148–1152.
Molitch, M. E. (2005). Medication-induced hyperprolactinemia. Mayo Clinic Proceedings,
(8), 1050–1057.
Pirchio, R., Graziadio, C., Colao, A., Pivonello, R., & Auriemma, R. S. (2022). Metabolic
effects of prolactin. Frontiers in Endocrinology, 13(September), 1–11.
Kim, D. (2017). The role of vitamin D in thyroid diseases. International Journal of Molecular
Sciences, 18(9), 1–19.
Chen, C., Luo, Y., Su, Y., & Teng, L. (2019). The vitamin D receptor (VDR) protects
pancreatic beta cells against Forkhead box class O1 (FOXO1)-induced mitochondrial
dysfunction and cell apoptosis. Biomedicine and Pharmacotherapy, 117(June), 109170.
Gierach, M., Bruska-Sikorska, M., Rojek, M., & Junik, R. (2022). Hyperprolactinemia and
insulin resistance. Endokrynologia Polska, 73(6), 959–967.
Słuczanowska-Głabowska, S., Laszczyńska, M., Wylot, M., Głabowski, W., Piasecka, M., &
Gacarzewicz, D.(2010). Morphological and immunohistochemical compare of three rat
prostate lobes (lateral, dorsal and ventral) in experimental hyperprolactinemia. Folia
Histochemica et Cytobiologica, 48(3), 447–454
Yin, Y., Yu, Z., Xia, M., Luo, X., Lu, X., & Ling, W. (2012). Vitamin D attenuates high fat
diet-induced hepatic steatosis in rats by modulating lipid metabolism. European Journal of
Clinical Investigation, 42(11), 1189–1196.
Bancroft, J, D. and Gamble, M. (2008). Theory and practices of histological technique. 2 and
ed. Churchill Elseirier. London., Pp: 56.
Inche, A. G., and La Thangue, N. B. (2006). Keynote review: Chromatin control and cancerdrug
discovery: realizing the promise. Drug discovery today, 11(3-4): pp. 97-109.
Bornstedt, M. E., Gjerlaugsen, N., Olstad, O. K., Berg, J. P., Bredahl, M. K., & Thorsby, P.
M. (2020). Vitamin D metabolites influence expression of genes concerning cellular viability
and function in insulin producing β-cells (INS1E). Gene, 746(March 2020), 144649.
Ramos-Martínez, E., Ramos-Martínez, I., Valencia, J., Ramos-Martínez, J. C., Hernández-
Zimbrón, L., Rico-Luna, A., Pérez-Campos, E., Pérez-Campos Mayoral, L., & Cerbón, M.
(2022). Modulatory role of prolactin in type 1 diabetes. Hormone Molecular Biology and
Clinical Investigation, 1–10.
Mohd Ghozali, N., Giribabu, N., & Salleh, N. (2022). Mechanisms Linking Vitamin D
Deficiency to Impaired Metabolism: An Overview. International Journal of Endocrinology,
Murdoch, G. H., & Rosenfeld, M. G. (1981). Regulation of pituitary function and prolactin
production in the GH4 cell line by vitamin D. Journal of Biological Chemistry, 256(8), 4050–
Miteva, M. Z., Nonchev, B. I., Orbetzova, M. M., & Stoencheva, S. D. (2020). Vitamin D and
Autoimmune Thyroid Diseases - a Review. Folia Medica, 62(2), 223–229.
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