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. 2017 May 10;66(8):2241–2253. doi: 10.2337/db16-1147

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© 2017 by the American Diabetes Association.

Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. More information is available at http://www.diabetesjournals.org/content/license.

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Mitochondrial H₂O₂ emission, proton leak respiration, and systemic oxidative stress in PRIM and SEC mice. Succinate-stimulated H₂O₂ emission (A) and leak respiration (B) in the liver. C: Octanoyl-carnitine–stimulated H₂O₂ emission in the liver. Succinate-stimulated H₂O₂ emission (D) and leak respiration (E) in the soleus muscle. F: Octanoyl-carnitine–stimulated H₂O₂ emission in the soleus muscle. G: Dose-response curves of succinate-stimulated H₂O₂ emission in the soleus muscle of 36-week-old mice. Plasma measurements of sORP (H) and antioxidant capacity (I). Data are presented as mean ± SEM (n = 5–6 per group). *P < 0.05, **P < 0.05 by two-way ANOVA with Bonferroni correction.