Beta cells of the pancreatic islet express many different types of ion channels. These channels reside in the β-cell plasma membrane as well as subcellular organelles and their coordinated activity and sensitivity to metabolism regulate glucose-dependent insulin secretion. Here, we review the molecular nature, expression patterns, and functional roles of many β-cell channels, with an eye toward explaining the ionic basis of glucose-induced insulin secretion. Our primary focus is on K and voltage-gated Ca channels as these primarily regulate insulin secretion; other channels in our view primarily help to sculpt the electrical patterns generated by activated β-cells or indirectly regulate metabolism. Lastly, we discuss why understanding the physiological roles played by ion channels is important for understanding the secretory defects that occur in type 2 diabetes. © 2021 American Physiological Society. Compr Physiol 11:1-21, 2021.
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http://dx.doi.org/10.1002/cphy.c210004 | DOI Listing |
J Clin Endocrinol Metab
January 2025
Division of Endocrinology, Diabetes & Metabolism, Mayo Clinic College of Medicine, Rochester, Minnesota, USA.
Context: Defects in insulin secretion and action contribute to the progression of prediabetes to diabetes. However, the contribution of α-cell dysfunction to this process has been unclear.
Objective: Understand the relative contributions of α-cell and β-cell dysfunction to declining glucose tolerance.
Diabetes Technol Ther
January 2025
University of Minnesota School of Medicine, Minneapolis, Minnesota, USA.
We assessed whether there is an impactful glucose fraction independent of insulin secretion in autoantibody-positive individuals. Baseline 2-h oral glucose tolerance test data from the TrialNet Pathway to Prevention (TNPTP; = 6190) and Diabetes Prevention Trial-Type 1 (DPT-1; = 705) studies were used. Linear regression of area under the curve (AUC) glucose versus Index60 was performed to identify two fractions: dependent (dAUCGLU) or independent (iAUCGLU) of insulin secretion.
View Article and Find Full Text PDFPhytother Res
January 2025
Engineering Research Center of Applied Technology of Pharmacogenomics (Ministry of Education, China), Hunan Key Laboratory of Pharmacomicrobiomics, Department of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, China.
Ginsenoside compound K (GCK) has been proved to have great hypoglycemic effect pertinent to gut microbiota. However, the improvement of high-fat-diet (HFD)-induced type 2 diabetes (T2D) as well as the mechanism of GCK mediated by gut microbiota is not well-known. This study aimed to investigate the hypoglycemic effects and mechanism of GCK on a HFD-induced diabetic mouse model.
View Article and Find Full Text PDFBiochem Biophys Res Commun
December 2024
Department of Endocrinology and Metabolism, The Second Hospital & Clinical Medical School, Lanzhou University, Lanzhou, People's Republic of China; The Second Clinical Medical College, Lanzhou University, Lanzhou, People's Republic of China. Electronic address:
Previous studies have shown that nickel sulfate (NiSO) increases autophagy in thyroid cells and tissues. As an important organ of the endocrine system, the pancreas not only contributes to the exocrine function of digestion but also has the endocrine function of regulating blood sugar. However, it remains unknown whether NiSO increases pancreatic autophagy.
View Article and Find Full Text PDFFEBS J
January 2025
Department of Drug Design and Pharmacology, University of Copenhagen, Denmark.
The glucagon-like peptide-1 receptor (GLP-1R) plays an important role in regulating insulin secretion and reducing body weight, making it a prominent target in the treatment of type 2 diabetes and obesity. Extensive research on GLP-1R signaling has provided insights into the connection between receptor function and physiological outcomes, such as the correlation between Gs signaling and insulin secretion, yet the exact mechanisms regulating signaling remain unclear. Here, we explore the internalization pathway of GLP-1R, which is crucial for controlling insulin release and maintaining pancreatic beta-cell function.
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