Effect of vitamin D3 on the pancreatic secretion of insulin and somatostatin
Yoshiyuki Tanaka, Yoshiki Seino, Makoto Ishida, Kanji Yamaoka, Hyakuji Yabuuchi, Hitoshi Ishida, Susumu Seino, Yutaka Seino, Hiroo Imura
Abstract
Yoshiyuki Tanaka, Yoshiki Seino, Makoto Ishida, Kanji Yamaoka, Hyakuji Yabuuchi, Hitoshi Ishida, Susumu Seino, Yutaka Seino, Hiroo Imura
Abstract
To clarify the role of vitamin D in the regulation of the endocrine pancreas, we have studied insulin and somatostatin secretion in vitamin D deficient rats (reared on a vitamin D deficient diet), D-replete rats (reared on a vitamin D deficient diet and given 160 IU of vitamin D3 sc twice a week) and control rats (reared on laboratory chow), using the isolated perfused rat pancreas. In the vitamin D deficient rats, the perfusate insulin induced by 16.7 mM glucose was only 35% of the secretion in the control rats. In the D-replete rats, the insulin release was restored to that of the controls. Similarly, the plasma insulin level in the vitamin D deficient rats was very low and the level in the D-replete rats was also restored to the level of the controls. The perfusate somatostatin response to glucose was not significantly different in any of the three groups. In addition, since the plasma calcium level in the vitamin D deficient rats was very low and in the D-replete rats was still lower, compared to normal rats, we suggest that vitamin D acts not only via the plasma calcium level but possibly also directly on the B cell.
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To clarify the role of vitamin D in the regulation of the endocrine pancreas, we have studied insulin and somatostatin secretion in vitamin D deficient rats (reared on a vitamin D deficient diet), D-replete rats (reared on a vitamin D deficient diet and given 160 IU of vitamin D3 sc twice a week) and control rats (reared on laboratory chow), using the isolated perfused rat pancreas. In the vitamin D deficient rats, the perfusate insulin induced by 16.7 mM glucose was only 35% of the secretion in the control rats. In the D-replete rats, the insulin release was restored to that of the controls. Similarly, the plasma insulin level in the vitamin D deficient rats was very low and the level in the D-replete rats was also restored to the level of the controls. The perfusate somatostatin response to glucose was not significantly different in any of the three groups. In addition, since the plasma calcium level in the vitamin D deficient rats was very low and in the D-replete rats was still lower, compared to normal rats, we suggest that vitamin D acts not only via the plasma calcium level but possibly also directly on the B cell.
Key concepts: Internal medicine, Endocrinology, Somatostatin, Insulin, Pancreas, Vitamin, Vitamin D and neurology, Calcium