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Mitochondrial respiration was assessed in isolated mitochondria from the hindlimb muscle with pyruvate or palmitoylcarnitine as substrate, as described previously (Bhattacharya et?al., 1991). (See Supplemental Experimental Procedures for more detail.) Data were analyzed using t tests or ANOVA where appropriate, with Newman-Keuls tests or pairwise comparisons (Bonferroni adjusted) used for post hoc analyses. The level of significance was set at p?GUCY1B3 are reported as mean values �� SEM. This work was supported by NIH grants DK45416 and HL58427 (D.P.K.), Neuroscience Blueprint Interdisciplinary Core Grant P30 NS057105 (D.F.W.), an American Diabetes Association Research Award (AR050429, Z.Y.), Deutsche Forschungsgemeinschaft Research Fellowship ZE 796/2-1 (C.Z.), and the Digestive Diseases Research Center (P30 DK052574) at Washington University School of Medicine (WUSM). Special thanks to Genevieve DeMaria for assistance with manuscript preparation; Sara Conyers at WUSM for assistance with the behavioral studies; Jochen K. Lennerz at WUSM for helpful discussion regarding histology; Karen Green and William Kraft for performing the electron microscopy (WUSM Research Electron Microscopy Core Facility); Julio Ayala and Emily King of the Sanford-Burnham Cardiometabolic Phenotyping Core for assistance with GTT, ITT, and insulin measurements; and Suellen PD173074 mouse Greco (WUSM) for performing the CK measurements. ""Aging and metabolic diseases Ulixertinib datasheet share certain common pathogeneses. Caloric excess results in metabolic diseases and shorter life expectancy. Conversely, caloric restriction (CR) improves metabolic parameters and increases longevity (Lee et?al., 2009?and?Murphy et?al., 2003). At the cellular level, the age-dependent decline in mitochondrial function has been implicated in aging and related metabolic disorders (Balaban et?al., 2005, Reznick et?al., 2007?and?Zid et?al., 2009). The electron transport chain drives the oxidative phosphorylation (OXPHOS) of ADP to produce ATP. An unavoidable by-product of mitochondrial respiration is the generation of reactive oxygen species (ROS). Many cellular mechanisms exist to protect the cell and its organelles from oxidative damage (Wallace and Fan, 2009). ROS scavenging proteins, including superoxide dismutase 1 (SOD1), SOD2, glutathione peroxidase (GPx), catalase, and glutathione S-transferases pi (GSTP), possess enzymatic functions that neutralize specific ROS. If uncontrolled, oxidative damage caused by ROS affects proteins, lipids, and nucleic acids, leading to enzyme and membrane dysfunctions as well as genetic mutations. These changes further reduce mitochondrial function and increase susceptibility of cells to oxidative stress, which is a hallmark of aging (Kapahi et?al., 1999?and?Kenyon, 2005).