Source: Thailand Medical News Dec 24, 2019 4 years, 10 months, 4 weeks, 3 hours, 12 minutes ago
Medical researchers at Karolinska Institutet in Sweden have deciphered the diabetogenic role of a certain type of
calcium channel in insulin-secreting beta cells. The researchers believe that blockade of these channels could be a potential new treatment strategy for
diabetes.
The recent study is published in the scientific journal
PNAS.
The
CaV3.1 channels have a marginal role in healthy insulin-secreting beta cells in the endocrine pancreas but become hyperactive along with the occurrence of
diabetes. This raises a critical question of whether the hyperactivation of these
calcium channels is a cause or consequence of
diabetes. Now, researchers at Karolinska Institutet have found that increased expression of
CaV3.1 leads to excessive calcium influx, impairing the genomic expression of exocytotic proteins in beta cells.
Dr. Jia Yu, first author of the study and Senior researcher at the Department of Molecular Medicine and Surgery, Karolinska Institutet explained to
Thailand Medical News, "This leads to a reduced insulin-secretion capacity of beta cells and aberrant glucose homeostasis."
The detrimental role of
CaV3.1 in the development of
diabetes was investigated with a series of approaches, including experiments on rat and human pancreatic islets and
diabetic rats. The experimental models used suggest that the results apply to both type 1 and type 2
diabetes, but more studies are needed to verify this.
Dr. Shao-Nian Yang, Associate professor at the Department of Molecular Medicine and Surgery, Karolinska Institutet, and senior author of the study commented, "Over a long period of time, the pathological role of beta cell
CaV3.1 channels in the development of
diabetes and its complications has been neglected. Our work pinpoints an increased expression of these channels as a critical pathogenic mechanism in
diabetes, meaning that
CaV3.1 channels should not be neglected in
diabetes research."
The researchers now want to work out if increased expression of
CaV3.1 also alter transcriptomic profiles in other types of cells, such as vascular smooth muscle cells and T cells of the immune system to contribute to the development of
diabetes and its complications.
Professor Dr Per-Olof Berggren, Director of the Rolf Luft Research Center, Karolinska Institutet, and senior author of the study added, "The selective blockade of
CaV3.1 channels may have potential as a new mechanism-based treatment strategy," "Clinical trials with
CaV3.1 channel blockers in patients with
diabetes will be one of our future study priorities."
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Reference : Jia Yu el al., "Enhanced expression of β cell CaV3.1 channels impairs insulin release and glucose homeostasis," PNAS (2019). www.pnas.org/cgi/doi/10.1073/pnas.1908691117
