Public Defence: Mette Eskild Bornstedt

Cand.med. Mette Eskild Bornstedt at Institute of Clinical Medicine will be defending the thesis “The effect of vitamin D metabolites on glucose-stimulated insulin secretion (GSIS) and gene expression in murine insulin producing β-cells and pancreatic islets – an experimental study” for the degree of PhD (Philosophiae Doctor).

Due to copyright issues, an electronic copy of the thesis must be ordered from the faculty. For the faculty to have time to process the order, the order must be received by the faculty at the latest 2 days before the public defence. Orders received later than 2 days before the defence will not be processed. After the public defence, please address any inquiries regarding the thesis to the candidate.

Trial Lecture – time and place

See Trial Lecture.

Adjudication committee

  • First opponent: Professor Per Bendix Jeppesen, Aarhus University Hospital, Denmark
  • Second opponent: Professor Jørn Vegard Sagen, Haukeland University Hospital and University of Bergen
  • Third member and chair of the evaluation committee: Associate Professor Mari Mohn Paulsen, University of Oslo

Chair of the Defence

Professor Kristin Austlid Tasken, University of Oslo

Principal Supervisor

Associate Professor Per Medbøe Thorsby, University of Oslo

Summary

Insulin is secreted from β-cells at rising serum-glucose thereby lowering its level. In diabetes, there is an absolute or relative lack of insulin, leading to elevated s-glucose, which can cause organ damage. Diabetes can be treated, but still many patients suffer from complications. Previous studies have shown a correlation between poor vitamin D status and reduced β-cell function. However, the mechanisms are still unknown.

The aim of our study was to investigate whether vitamin D metabolites, 1,25(OH)2 vitamin D and 25(OH) vitamin D, could increase the amount of insulin secreted and whether vitamin D metabolites affected expression of genes important for insulin secretion.

In vitro experiments were carried out in rat insulin producing β-cells (INS1E) and mouse islets. Results showed a significant increase of insulin (43%, p < 0.05) when INS1E cells were treated with 1,25(OH)2 vitamin D, compared to control cells. Analysis showed differential expression of genes after treatment with either 1,25(OH)2 vitamin D and 25(OH) vitamin D, including genes affecting insulin secretion, cellular viability, and inhibition of inflammation.

 Similarly in mouse islets, results showed a clear trend towards increased insulin secretion after treatment with 1,25(OH)2 vitamin D. Gene expression analysis revealed differentially expressed genes after treatment with either both 1,25(OH)2 vitamin D and 25(OH) vitamin D, including genes involved in regulation of immune response and genes associated with insulin secretion and diabetes.

The study has shed light on the effect of vitamin D on insulin secretion and gene expression in β-cells and islets. The altered expression of genes may be part of the explanation for the observed increase in insulin secretion. Future studies in humans will bring more knowledge to this field and may contribute to uncover the role of vitamin D in β-cell health and disease.

Additional information

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Published Nov. 28, 2022 11:37 AM - Last modified Dec. 8, 2022 3:00 PM