Background: The potassium voltage-gated channel subfamily Q member 1 (KCNQ1) gene has recently received much attention as a candidate susceptibility gene for type 2 diabetes mellitus, especially in Asian populations. We previously reported that Kcnq1 mutant mice exhibit reduced insulin secretion and hyperglycemia due to a decrease in pancreatic β-cell mass. Through in vivo and in vitro analyses, we ascertained that this mechanism is the result of the downregulation of the non-coding RNA ‘Kcnq1ot1,’ which is expressed in the paternal allele of the Kcnq1 gene region, causing an increase in the expression of the cell cycle inhibitor cyclin dependent kinase inhibitor 1C (Cdkn1c). It was found that decreased Kcnq1ot1 expression resulted in pancreatic β-cell failure; however, the degree of pancreatic β-cell volume reduction was not severe. Methods: We induced obesity in Kcnq1ot1 truncation mice by feeding them a high-fat diet and evaluated pancreatic β-cell mass. Results: In the present study, we reveal that CCAAT/enhancer binding protein beta (C/EBPβ), which is expressed at higher levels in pancreatic β-cells in obese individuals, further increases the expression of Cdkn1c, which is upregulated by the Kcnq1 gene mutation. We found that simultaneous Cdkn1c hypomethylation and C/EBPβ overexpression in pancreatic β-cells causes a synergistic decrease in pancreatic β-cell mass. Conclusion This finding suggests that the synergistic effect of genetic factors such as Kcnq1 gene mutations and environmental factors such as obesity and overeating, which lead to increased expression of C/EBPβ, contribute to the regulation of pancreatic β-cell mass. This study is the first to show that the Kcnq1 gene is related to pancreatic β-cell mass through genetic-environment interactions.

The case is that of a 90-years-old man. A previous doctor performed abdominal graft replacement for an abdominal aortic aneurysm 5 years earlier and continued outpatient CT follow-up. Follow-up CT showed the right aortic arch and dilation of the thoracic aortic aneurysm, and the patient was referred to our hospital. Contrast-enhanced CT showed an aortic arch aneurysm ; the aneurysm diameter was 62 mm in major axis and 60 mm in minor axis, which was judged to be suitable for surgery. It was a rare right-sided aortic arch with no congenital heart malformation and no situs inversus. Endovascular treatment was considered because he was 90 years old and very elderly, but there were concerns about the risk of embolism, irregular manipulation and central landing. For the surgical method, we selected total arch replacement using a frozen elephant trunk technique. We succeeded in avoiding serious complications by selecting an appropriate treatment method through careful evaluation.