On February 10, Maria S. Remedi, PhD and colleagues had their abstract titled “Hyperexcitability reduces TRPM5 in pancreatic β-cells: Insights into disruption of insulin secretion in chronically stimulated islets,” published in Biophysical Journal.
“Acute inhibition of ATP-sensitive K+ (KATP) channels in pancreatic β-cells result in depolarization, Ca2+ influx, and insulin secretion.” Throughout their research, the authors look to determine the counterintuitive mechanisms which cause congenital hyperinsulinism associated with KATP loss, to gradually remit or progress into a diabetic state, and KATP lacking adult mice to display lower insulin secretion and glucose-intolerance.
In search of contributors to reduced insulin secretion in KATP KO, Remedi and colleagues examine “gene expression using whole islet, single cell RNAseq and qPCR in several different mouse models of loss of β-cell KATP activity.”
Their findings suggest “that loss of TRPM5 may contribute to reduced levels of stimulatory [Ca2+]i and to reduced insulin secretion following KATP loss.” Drawing crucial new insight to an unexplained phenomenon, in which they state “is critical to understand, given the potentially profound clinical consequences.”
York, N. W., Yan, Z., Tate, A. L., Remedi, M. S., & Nichols, C. G. (2023). Hyperexcitability reduces TRPM5 in pancreatic β-cells: Insights into disruption of insulin secretion in chronically stimulated islets. Biophysical Journal, 122(3S1), 111a. https://doi.org/10.1016/j.bpj.2022.11.779