Insights into pancreatic β cell energy metabolism using rodent β cell models.

Autor:	Morten KJ; Nuffield Department of Obstetrics & Gynaecology, The Women's Centre, University of Oxford, John Radcliffe Hospital, Oxford, UK., Potter M; Nuffield Department of Obstetrics & Gynaecology, The Women's Centre, University of Oxford, John Radcliffe Hospital, Oxford, UK., Badder L; Nuffield Department of Obstetrics & Gynaecology, The Women's Centre, University of Oxford, John Radcliffe Hospital, Oxford, UK., Sivathondan P; Nuffield Department of Obstetrics & Gynaecology, The Women's Centre, University of Oxford, John Radcliffe Hospital, Oxford, UK., Dragovic R; Nuffield Department of Obstetrics & Gynaecology, The Women's Centre, University of Oxford, John Radcliffe Hospital, Oxford, UK., Neumann A; Nuffield Department of Obstetrics & Gynaecology, The Women's Centre, University of Oxford, John Radcliffe Hospital, Oxford, UK., Gavin J; Nuffield Department of Obstetrics & Gynaecology, The Women's Centre, University of Oxford, John Radcliffe Hospital, Oxford, UK., Shrestha R; Nuffield Department of Obstetrics & Gynaecology, The Women's Centre, University of Oxford, John Radcliffe Hospital, Oxford, UK., Reilly S; Department of Cardiovascular Medicine, John Radcliffe Hospital, Oxford, UK., Phadwal K; BRC Translational Immunology Lab, NIHR, Nuffield Department of Medicine, University of Oxford, John Radcliffe Hospital, Oxford, UK., Lodge TA; Nuffield Department of Obstetrics & Gynaecology, The Women's Centre, University of Oxford, John Radcliffe Hospital, Oxford, UK., Borzychowski A; Nuffield Department of Obstetrics & Gynaecology, The Women's Centre, University of Oxford, John Radcliffe Hospital, Oxford, UK., Cookson S; Institute of Cellular Medicine, Haematological Sciences, Medical School, Newcastle University, Newcastle upon Tyne, UK., Mitchell C; Nuffield Department of Obstetrics & Gynaecology, The Women's Centre, University of Oxford, John Radcliffe Hospital, Oxford, UK., Morovat A; Clinical Biochemistry, John Radcliffe Hospital, Oxford, UK., Simon AK; Kennedy Institute of Rheumatology, University of Oxford, Oxford, UK., Uusimaa J; Department of Paediatrics, University of Oulu, Oulu, Finland., Hynes J; Luxcel BioSciences Ltd, BioInnovation Centre, University College Cork, Cork, Ireland., Poulton J; Nuffield Department of Obstetrics & Gynaecology, The Women's Centre, University of Oxford, John Radcliffe Hospital, Oxford, UK.
Jazyk:	angličtina
Zdroj:	Wellcome open research [Wellcome Open Res] 2017 Oct 11; Vol. 2, pp. 14. Date of Electronic Publication: 2017 Oct 11 (Print Publication: 2017).
DOI:	10.12688/wellcomeopenres.10535.2
Abstrakt:	Background : Mitochondrial diabetes is primarily caused by β-cell failure, a cell type whose unique properties are important in pathogenesis. Methods : By reducing glucose, we induced energetic stress in two rodent β-cell models to assess effects on cellular function. Results : Culturing rat insulin-secreting INS-1 cells in low glucose conditions caused a rapid reduction in whole cell respiration, associated with elevated mitochondrial reactive oxygen species production, and an altered glucose-stimulated insulin secretion profile. Prolonged exposure to reduced glucose directly impaired mitochondrial function and reduced autophagy. Conclusions : Insulinoma cell lines have a very different bioenergetic profile to many other cell lines and provide a useful model of mechanisms affecting β-cell mitochondrial function. Competing Interests: Competing interests: JH is an employee of Luxcel Biosciences. None of the other authors have competing interests. (Copyright: © 2017 Morten KJ et al.)
Databáze:	MEDLINE
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