Laboratory of Pancreatic Islet Research
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About the Laboratory
Proper function of pancreatic β-cells as glucose sensors throughout life is critical for maintaining glucose homeostasis in the body. Deterioration in the function and quantity of β-cells is fundamental to the development of diabetes. The activity of β-cells is also closely related to the function of other endocrine cells in the pancreatic islets. Although insulin was discovered 100 years ago (1922) and the major signaling pathway leading to insulin secretion has since been described, we still lack many details about the mechanisms of action of pancreatic β-cells and islet cells that would help us prevent and control diabetes, one of the world’s major health problems.
To improve our understanding of how diabetes develops, our lab is studying the details of glucose metabolism in β-cell signaling. We are focusing on:
1. The role of redox signaling and lipid metabolism in β-cells upon glucose stimulation under physiological and pathophysiological conditions.
2. The interplay between β-cells and other endocrine cells in pancreatic islets in response to altered redox status of β-cells.
Our research is performed in a variety of models with diverse level of complexity, ranging from cell cultures to isolated mouse pancreatic islets to whole animals (mice). We use novel experimental strategies in combination with modern omics analyzes.
Fluorescent insulin injected into a mouse pancreatic islet
Publication
Holendová B, Benáková Š, Křivonosková M, Plecitá-Hlavatá L. Redox Status as a Key Driver of Healthy Pancreatic Beta-Cells. Physiol Res. 2024 Apr 22. Epub ahead of print. PMID: 38647167. IF = 2.103
Holendová, B., Benáková, Š., Křivonosková, M., Pavluch, V., Tauber, J., Gabrielová, E., Ježek, P., & Plecitá-Hlavatá, L. (2024). NADPH oxidase 4 in mouse β cells participates in inflammation on chronic nutrient overload. Obesity (Silver Spring, Md.), 32(2), 339–351. IF = 4.2
Benak, D., Benakova, S., Plecita-Hlavata, L., & Hlavackova, M. (2023). The role of m6A and m6Am RNA modifications in the pathogenesis of diabetes mellitus. Frontiers in endocrinology, 14, 1223583. IF 3.9
Holendova, B., & Plecita-Hlavata, L. (2023). Cysteine residues in signal transduction and its relevance in pancreatic beta cells. Frontiers in endocrinology, 14, 1221520. IF 3.9
Ježek P, Holendová B, Jabůrek M, Dlasková A, Plecitá-Hlavatá L. Contribution of Mitochondria to Insulin Secretion by Various Secretagogues. Antioxid Redox Signal. 2022 May, 36(13-15): 920–952. IF 7.468
Benáková Š, Holendová B, Plecitá-Hlavatá L. Redox Homeostasis in Pancreatic β-Cells: From Development to Failure. Antioxidants (Basel). 2021 Mar 27;10(4):526. IF 7.675
Ježek P, Holendová B, Jabůrek M, Tauber J, Dlasková A, Plecitá-Hlavatá L. The Pancreatic β-Cell: The Perfect Redox System. Antioxidants (Basel). 2021 Jan 29;10(2):197. IF 7.675
Plecitá-Hlavatá L, Jabůrek M, Holendová B, Tauber J, Pavluch V, Berková Z, Cahová M, Schroeder K, Brandes RP, Siemen D, Ježek P.Glucose-stimulated insulin secretion fundamentally requires H2O2 signaling by NADPH oxidase 4. Diabetes. 2020 Jul;69(7):1341-1354. IF 9.461
Plecitá-Hlavatá L, Engstová H, Holendová B, Tauber J, Špaček T, Petrásková L, Křen V, Špačková J, Gotvaldová K, Ježek J, Dlasková A, Smolková K, Ježek P. Mitochondrial Superoxide Production Decreases on Glucose-Stimulated Insulin Secretion in Pancreatic β Cells Due to Decreasing Mitochondrial Matrix NADH/NAD+ Ratio. Antioxid Redox Signal. 2020 Oct 20;33(12):789-815. IF 8.401
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