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Karampelias, C. ; Băloiu, B.* ; Rathkolb, B. ; da Silva Buttkus, P. ; Bachar-Wikström, E.* ; Marschall, S. ; Fuchs, H. ; Gailus-Durner, V. ; Chu, L.W.* ; Hrabě de Angelis, M. ; Andersson, O.*

Examining the liver-pancreas crosstalk reveals a role for the molybdenum cofactor in β-cell regeneration.

Life Sci. All. 7:e202402771 (2024)

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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.

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