The pancreatic β cell response to secretory demands and adaptation to stress
In this medfyle
Understanding β cell triggering and amplification can lead to novel therapies.
This Medfyle was published more than two years ago. More recent Medfyle on this topic may now be available.
About the Expert
Raghu G. Mirmira, MD, PhD
University of Chicago, Chicago, IL, USA
Dr. Mirmira is a physician scientist and endocrinologist. He obtained his MD and PhD degrees from the University of Chicago, completed his residency and endocrinology training at the University of California, San Francisco, then held faculty appointments at the University of Virginia, Indiana University, and the University of Chicago (where he is now). He is the Director of the Translational Research Center, an NIH funded investigator, and conducts a research program focused on the role of the islet in diabetes pathogenesis. He serves as Deputy Editor of the Journal of Clinical Endocrinology and Metabolism.
Disclosures: Dr Mirmira serves on the Scientific Advisory Boards for Veralox Therapeutics, HiberCell, and Sigilon Therapeutics.
Acknowledgements
This summary is based upon an article appearing in the journal entitled Endocrinology published by Oxford University Press and was created by GlobalPort. Oxford University Press takes no responsibility for its accuracy or for the use of any content therein by those reading or downloading such content.
The summary content was prepared by Marie Farrow for Medfyle, reviewed & approved by Raghu G. Mirmira, MD, PhD.
Original article:
Kalwat MA, Scheuner D, Rodrigues Dos Santos K, Eizirik DL, Cobb MH. The pancreatic β cell response to secretory demands and adaption to stress. Endocrinology. 2021 Aug 18:bqab173. doi: 10.1210/endocr/bqab173. Epub ahead of print. PMID: 34407177.
The authors of the original article had no part in the creation of the summary.
All Medfyle content, summaries, expert commentaries and slides are owned by GlobalPort (International) Limited. The original journal articles are an exclusive copyright of Endocrine Society/Oxford University Press.
This activity is supported by an educational grant from Lilly.
References
1. Henquin JC. Regulation of insulin secretion: a matter of phase control and amplitude modulation. Diabetologia 2009;52(5):739–51.
2. Lewandowski SL, Cardone RL, Foster HR, et al. Pyruvate Kinase Controls Signal Strength in the Insulin Secretory Pathway. Cell Metab 2020;32(5):736–50 e735.
3. Zhang GF, Jensen MV, Gray SM, et al. Reductive TCA cycle metabolism fuels glutamine- and glucose-stimulated insulin secretion. Cell Metab 2021;33(4):804–17.
4. Luczkowska K, Stekelenburg C, Sloan-Béna F, et al. Hyperinsulinism associated with GLUD1 mutation: allosteric regulation and functional characterization of p.G446V glutamate dehydrogenase. Hum Genomics 2020;14(1):9.
5. Prentki M, Peyot ML, Masiello P, Madiraju SRM. Nutrient-Induced Metabolic Stress, Adaptation, Detoxification, and Toxicity in the Pancreatic beta-Cell. Diabetes 2020;69(3):279–90.
6. Kaufman RJ, Back SH, Song B, et al. The unfolded protein response is required to maintain the integrity of the endoplasmic reticulum, prevent oxidative stress and preserve differentiation in beta-cells. Diabetes Obese Metab 2020;12 Suppl 2:99–107.
7. Abdulreda MH, Rodriguez-Diaz R, Caicedo A, Berggren PO. Liraglutide Compromises Pancreatic beta Cell Function in a Humanized Mouse Model. Cell Metab 2016;23(3):541–6.
8. Remedi MS, Nichols CG. Chronic antidiabetic sulfonylureas in vivo: reversible effects on mouse pancreatic beta-cells. PLoS Med 2008;5(10):e206.
9. Donath MY, Ehses JA, Maedler K, et al. Mechanisms of beta-cell death in type 2 diabetes. Diabetes 2005;54 Suppl 2:S108–13.
