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The Mitochondrial Atp8 Mutation Induces Mitochondrial ROS Generation, Secretory Dysfunction, and β-Cell Mass Adaptation in Conplastic B6-mtFVB Mice

Weiss, Heike, Wester-Rosenloef, Lena, Koch, Christiane, Koch, Franziska, Baltrusch, Simone, Tiedge, Markus, Ibrahim, Saleh·2012·Endocrinology
DOI 10.1210/en.2012-1296
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Abstract

Mutations in mitochondrial DNA (mtDNA) cause a variety of pathologic phenotypes. In this study, we used conplastic mouse strains to characterize the impact of a mtDNA mutation in the Atp8 gene on β-cell function, reactive oxygen species (ROS) generation, β-cell mass, and glucose metabolism in response to high-fat diet (HFD). In comparison with B6-mt(AKR) controls, the B6-mt(FVB) strain carries a point mutation of the mtDNA-coded Atp8 gene (ATP synthase), leading to a fragmentated mitochondrial phenotype. Isolated pancreatic islets from 3-month-old B6-mt(FVB) mice showed increased mitochondrial generation of ROS, reduced cellular ATP levels, reduced glucose-induced insulin secretion, higher susceptibility to palmitate stress, and pathological morphology of mitochondria. ROS generation in β-cells was not affected by changes of the ambient glucose concentrations. Feeding a HFD for 3 months resulted in impaired glucose tolerance in B6-mt(FVB) mice but not in B6-mt(AKR) controls. In B6-mt(FVB) animals, glucose intolerance positively correlated with gain of body weight. Serum insulin levels and β-cell mass significantly increased in B6-mt(FVB) mice after a 3-month HFD. The data indicate that the mutation in the Atp8 gene induces mitochondrial dysfunction in β-cells with concomitant impairment of secretory responsiveness. This mitochondrial dysfunction induced a higher susceptibility to metabolic stressors, although this effect appeared not strictly linked to nutrient-induced ROS ge…

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  • Available systems for studying mitochondrial disease include naturally occurring mild mutations with less severe phenotypes, such as missense mutations in ATP8 and ND6.

    “Available systems therefore include the study of naturally occurring mild mutations with less severe phenotypes, such as those observed due to missense mutations in the ATP8 [149] and ND6 genes [150].”

    From The Mitochondrial Genome in Aging and Disease and the Future of Mitochondrial Therapeutics (2022) · cites this paper as [149]

  • C57/BL6(mtFVB) mice demonstrate measurable phenotypes and their cells in vitro have subtle deficits indicative of disrupted Complex V function.

    “C57/BL6(mtFVB) mice demonstrate measurable phenotypes and cells in vitro have subtle deficits indicative of disrupted CV function [90,91]”

    From Codon optimization is an essential parameter for the efficient allotopic expression of mtDNA genes (2020) · cites this paper as [91]

  • The C57/BL6(mtFVB) mutation has been shown to cause various defects in inbred mice including anxiety and inflammation-related arthritis.

    “The C57/BL6(mtFVB) mutation has been shown to cause various defects in inbred mice including anxiety and inflammation-related arthritis [91,92].”

    From Codon optimization is an essential parameter for the efficient allotopic expression of mtDNA genes (2020) · cites this paper as [91]

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Metadata

Authors
Weiss, H., Wester-Rosenloef, L., Koch, C., Koch, F., Baltrusch, S., Tiedge, M., & Ibrahim, S.
Affiliations
  • Institute of Medical Biochemistry and Molecular Biology (H.W., L.W.-R., C.K., F.K., S.B., M.T.), University of Rostock, 18057 Rostock, Germany
  • Genetics Group, Department of Dermatology (S.I.), University of Lübeck, 23538 Lübeck, Germany
Venue
Endocrinology
Publisher
The Endocrine Society
Published
2012-10-01
Volume
153
Issue
10
Pages
4666-4676
ISSN
  • 0013-7227
  • 1945-7170
DOI
10.1210/en.2012-1296
Cited by
52
References
3
Language
en

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