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Crosstalk of glucose-induced lipid metabolism and redox homeostasis in beta-cell physiology and pathology

PhD project: Crosstalk of glucose-induced lipid metabolism and redox homeostasis in beta-cell physiology and pathology

Our newly established laboratory investigates the physiology and pathophysiology of pancreatic beta cells. Beta cells are the guardians of glucose homeostasis in the body, and their deficiency and impaired function trigger the development of diabetes. We focus on the role of redox homeostasis and lipid metabolism during glucose stimulation and subsequent signaling in beta cells. Altered redox status and modified glucose-induced lipid metabolism may affect cellular signaling i.e. insulin secretion, while in the long term they may induce cellular stress. The switching point and metabolic targets of signaling are unknown in beta cells.
The aim of this PhD project is to identify redox regulated glucose-induced lipid signaling and lipid metabolism under physiological conditions of insulin secretion on the one hand and the mechanism of its dysregulation to develop diabetes on the other hand. A unique mouse model with altered redox status in beta cells and isolated Langerhans islets/cells will be used for the study, employing novel experimental strategies in combination with omics analyses.

Candidate’s profile (requirements):
We are looking for talented and motivated biological problem solving graduates with a background in biological and biomedical sciences and computational biology. Experience with cell culture, mouse/rat models, molecular biology and biochemistry, omics data analysis and computational biology is a plus. We offer a full-time salary.

Supervisor: Lydie Plecitá (



  • Holendová B, Benáková Š, Křivonosková M, Pavluch V, Tauber J, Gabrielová E, Ježek P, Plecitá-Hlavatá L. NADPH oxidase 4 in mouse β cells participates in inflammation on chronic nutrient overload.
  • Obesity (Silver Spring). 2023 Dec 12.
  • Holendova B, Plecita-Hlavata L. Cysteine residues in signal transduction and its relevance in pancreatic beta cells. Front Endocrinol (Lausanne). 2023 Jun 29;14:1221520. doi: 10.3389/fendo.2023.1221520.
  • Benakova S, Holendova B, Plecita-Hlavata L. Redox Homeostasis in Pancreatic beta-Cells: From Development to Failure. Antioxidants (Basel). 2021;10(4).
  • Plecita-Hlavata L, Jaburek M, Holendova B, Tauber J, Pavluch V, Berkova Z, et al. Glucose-Stimulated Insulin Secretion Fundamentally Requires H2O2 Signaling by NADPH Oxidase 4. Diabetes. 2020.
  • Plecita-Hlavata L, Engstova H, Holendova B, Tauber J, Spacek T, Petraskova L, et al. Mitochondrial Superoxide Production Decreases on Glucose-Stimulated Insulin Secretion in Pancreatic beta Cells Due to Decreasing Mitochondrial Matrix NADH/NAD(+) Ratio. Antioxid Redox Signal. 2020;33(12):789-815.