On February 23, Maria S. Remedi, PhD and collaborators had their findings published in “Diabetes,” titled “ATP-Sensitive Potassium Channels in Hyperinsulinism and Type 2 Diabetes: Inconvenient Paradox or New Paradigm?”
The article is meant to assess if adenosine triphosphate-sensitive potassium (KATP) channels are a new and effective way of thinking, in regard to hyperinsulinism and type 2 diabetes (T2D). Adenosine triphosphates are energy carrying molecules found within the cells of living things.
Remedi and collaborators review multiple key findings and how they do not align within the simple paradigm of how “mice with complete absence of β-cell KATP activity are not hyper-insulinemic,” and are instead “paradoxically glucose intolerant and prone to diabetes.”
They conclude that despite advances, “there has been little insight into any role of KATP channel activity changes in the development of T2D. Intriguingly, congenital hyperinsulinism (CHI) progression from hypersecretion to under-secretion mirrors the classical response to insulin resistance in the progression of T2D. In seeking to explain the progression of CHI, multiple lines of evidence lead us to propose that underlying mechanisms are also similar and that development of T2D may involve loss of KATP activity.”