Journal article
Life Science Alliance, 2024
APA
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Karampelias, C., Băloiu, B., Rathkolb, B., da Silva-Buttkus, P., Bachar-Wikström, E., Marschall, S., … Andersson, O. (2024). Examining the liver–pancreas crosstalk reveals a role for the molybdenum cofactor in β-cell regeneration. Life Science Alliance.
Chicago/Turabian
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Karampelias, Christos, Bianca Băloiu, B. Rathkolb, P. da Silva-Buttkus, Etty Bachar-Wikström, S. Marschall, H. Fuchs, et al. “Examining the Liver–Pancreas Crosstalk Reveals a Role for the Molybdenum Cofactor in β-Cell Regeneration.” Life Science Alliance (2024).
MLA
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Karampelias, Christos, et al. “Examining the Liver–Pancreas Crosstalk Reveals a Role for the Molybdenum Cofactor in β-Cell Regeneration.” Life Science Alliance, 2024.
BibTeX Click to copy
@article{christos2024a,
title = {Examining the liver–pancreas crosstalk reveals a role for the molybdenum cofactor in β-cell regeneration},
year = {2024},
journal = {Life Science Alliance},
author = {Karampelias, Christos and Băloiu, Bianca and Rathkolb, B. and da Silva-Buttkus, P. and Bachar-Wikström, Etty and Marschall, S. and Fuchs, H. and Gailus-Durner, V. and Chu, Lianhe and de Angelis, M. Hrabě and Andersson, Olov}
}
Investigation of the inter-organ, pancreas–liver, crosstalk reveals a potential role of the molybdenum biosynthetic pathway in β-cell regeneration. Regeneration of insulin-producing β-cells is an alternative avenue to manage diabetes, and it is crucial to unravel this process in vivo during physiological responses to the lack of β-cells. Here, we aimed to characterize how hepatocytes can contribute to β-cell regeneration, either directly or indirectly via secreted proteins or metabolites, in a zebrafish model of β-cell loss. Using lineage tracing, we show that hepatocytes do not directly convert into β-cells even under extreme β-cell ablation conditions. A transcriptomic analysis of isolated hepatocytes after β-cell ablation displayed altered lipid- and glucose-related processes. Based on the transcriptomics, we performed a genetic screen that uncovers a potential role of the molybdenum cofactor (Moco) biosynthetic pathway in β-cell regeneration and glucose metabolism in zebrafish. Consistently, molybdenum cofactor synthesis 2 (Mocs2) haploinsufficiency in mice indicated dysregulated glucose metabolism and liver function. Together, our study sheds light on the liver–pancreas crosstalk and suggests that the molybdenum cofactor biosynthesis pathway should be further studied in relation to glucose metabolism and diabetes.