Dietary vitamin D3 improves postprandial hyperglycemia in aged mice

Patricio L.M. Enciso, Lixiang Wang, Yuta Kawahara, Shohei Sakamoto, Shingo Shimada, Yukina Takeichi, Ryoichi Takayanagi, Masatoshi Nomura

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

Type 2 Diabetes is closely associated with our daily diets and has become a global health problem with an increasing number of patients. Recent observational and randomized studies on vitamin D3 suggested that higher plasma 25-hydroxyvitamin D3 [25(OH)D3] concentrations and more vitamin D3 intake are associated with lower risk of type 2 diabetes, which is characterized by postprandial hyperglycemia due to inappropriate glucose stimulated insulin secretion (GSIS) and its age-dependent increase of onset. However, rapid action of dietary vitamin D3 on the postprandial glucose profile has not been analyzed. When vitamin D3 is orally ingested in mice aged 12-14 weeks during an oral glucose tolerance test (OGTT), the serum glucose profile was not changed. In contrast, when OGTT was performed with old mice aged 30-34 weeks, the glucose profile was dramatically improved with increased insulin secretion, suggesting that orally ingested vitamin D3 potentiated GSIS in aged mice. Interestingly, there was also a significant increase in plasma GLP-1 in these aged mice. Our results suggest that orally ingested dietary vitamin D3 in aged mice improves glucose metabolism as a GLP-1 enhancer.

Original languageEnglish
Pages (from-to)165-171
Number of pages7
JournalBiochemical and Biophysical Research Communications
Volume461
Issue number1
DOIs
Publication statusPublished - May 22 2015

All Science Journal Classification (ASJC) codes

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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    Enciso, P. L. M., Wang, L., Kawahara, Y., Sakamoto, S., Shimada, S., Takeichi, Y., Takayanagi, R., & Nomura, M. (2015). Dietary vitamin D3 improves postprandial hyperglycemia in aged mice. Biochemical and Biophysical Research Communications, 461(1), 165-171. https://doi.org/10.1016/j.bbrc.2015.04.008