Key result
Type 1 diabetes in Akita mice caused tissue-specific remodeling of the mitochondrial proteome, with preserved function in kidney, brain, and liver, but mitochondrial dysfunction in the heart.
Authors
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Caution against clinical extrapolation from Akita mice; leaves open cardiac-selective mitochondrial mechanisms in human T1D.
Bugger et al. (2009) studied Type 1 diabetes. Type 1 diabetes (Akita mice) vs. Wild-type mice was evaluated on Mitochondrial proteome expression, respiration, ATP synthesis, and morphology across tissues. Type 1 diabetes in Akita mice caused tissue-specific remodeling of the mitochondrial proteome, with preserved function in kidney, brain, and liver, but mitochondrial dysfunction in the heart.
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