Cafeteria diet compromises natural adaptations of islet cell transdifferentiation and turnover in pregnancy.

Autor: Dubey V; Centre for Diabetes, School of Biomedical Sciences, Ulster University, Coleraine, Northern Ireland, UK., Tanday N; Centre for Diabetes, School of Biomedical Sciences, Ulster University, Coleraine, Northern Ireland, UK., Irwin N; Centre for Diabetes, School of Biomedical Sciences, Ulster University, Coleraine, Northern Ireland, UK., Tarasov AI; Centre for Diabetes, School of Biomedical Sciences, Ulster University, Coleraine, Northern Ireland, UK., Flatt PR; Centre for Diabetes, School of Biomedical Sciences, Ulster University, Coleraine, Northern Ireland, UK., Moffett RC; Centre for Diabetes, School of Biomedical Sciences, Ulster University, Coleraine, Northern Ireland, UK.
Jazyk: angličtina
Zdroj: Diabetic medicine : a journal of the British Diabetic Association [Diabet Med] 2025 Jan; Vol. 42 (1), pp. e15434. Date of Electronic Publication: 2024 Sep 10.
DOI: 10.1111/dme.15434
Abstrakt: Background: Pancreatic islet β-cell mass expands during pregnancy, but underlying mechanisms are not fully understood. This study examines the impact of pregnancy and cafeteria diet on islet morphology, associated cellular proliferation/apoptosis rates as well as β-cell lineage.
Methods: Non-pregnant and pregnant Ins1 Cre/+ ;Rosa26-eYFP transgenic mice were maintained on either normal or high-fat cafeteria diet, with pancreatic tissue obtained at 18 days gestation. Immunohistochemical changes in islet morphology, β-/α-cell proliferation and apoptosis, as well as islet cell identity, neogenesis and ductal cell transdifferentiation were assessed.
Results: Pregnant normal diet mice displayed an increase in body weight and glycaemia. Cafeteria feeding attenuated this weight gain while causing overt hyperglycaemia. Pregnant mice maintained on a normal diet exhibited typical expansion in islet and β-cell area, owing to increased β-cell proliferation and survival as well as ductal to β-cell transdifferentiation and β-cell neogenesis, alongside decreased β-cell dedifferentiation. Such pregnancy-induced islet adaptations were severely restricted by cafeteria diet. Accordingly, islets from these mice displayed high levels of β-cell apoptosis and dedifferentiation, together with diminished β-cell proliferation and lack of pregnancy-induced β-cell neogenesis and transdifferentiation, entirely opposing islet cell modifications observed in pregnant mice maintained on a normal diet.
Conclusion: Augmentation of β-cell mass during gestation arises through various mechanisms that include proliferation and survival of existing β-cells, transdifferentiation of ductal cells as well as β-cell neogenesis. Remarkably, cafeteria feeding almost entirely annuls pregnancy-induced islet adaptations, which may contribute to the development of gestational diabetes in the setting of dietary provoked metabolic stress.
(© 2024 The Author(s). Diabetic Medicine published by John Wiley & Sons Ltd on behalf of Diabetes UK.)
Databáze: MEDLINE
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