Scaling relations and baryonic cycling in local star-forming galaxies: I. The sample

Metallicity and gas content are intimately related in the baryonic exchange cycle of galaxies, and galaxy evolution scenarios can be constrained by quantifying this relation. To this end, we have compiled a sample of ~400 galaxies in the Local Universe, dubbed "MAGMA" (Metallicity And Gas for Mass Assembly), which covers an unprecedented range in parameter space, spanning more than 5 orders of magnitude in stellar mass (Mstar), star-formation rate (SFR), and gas mass (Mgas), and a factor of ~60 in metallicity [Z, 12+log(O/H)]. Stellar masses and SFRs have been recalculated for all the galaxies using IRAC, WISE and GALEX photometry, and 12+log(O/H) has been transformed, where necessary, to a common metallicity calibration. To assess the true dimensionality of the data, we have applied multi-dimensional principal component analyses (PCAs) to our sample. In confirmation of previous work, we find that even with the vast parameter space covered by MAGMA, the relations between Mstar, SFR, Z and Mgas (MHI+MH2) require only two dimensions to describe the hypersurface. To accommodate the curvature in the Mstar-Z relation, we have applied a piecewise 3D PCA that successfully predicts observed 12+log(O/H) to an accuracy of ~0.1dex. MAGMA is a representative sample of isolated star-forming galaxies in the Local Universe, and can be used as a benchmark for cosmological simulations and to calibrate evolutionary trends with redshift.Comment: 21 pages, 12 figures. Accepted for publication in A&A. Sample and results improved compared to previous versions. Some analysis has been removed and will be expanded in future paper

Alterations in proton leak, oxidative status and uncoupling protein 3 content in skeletal muscle subsarcolemmal and intermyofibrillar mitochondria in old rats.

BACKGROUND: We considered of interest to evaluate how aging affects mitochondrial function in skeletal muscle. METHODS: We measured mitochondrial oxidative capacity and proton leak, together with lipid oxidative damage, superoxide dismutase specific activity and uncoupling protein 3 content, in subsarcolemmal and intermyofibrillar mitochondria from adult (six months) and old (two years) rats. Body composition, resting metabolic rate and plasma non esterified fatty acid levels were also assessed. RESULTS: Old rats displayed significantly higher body energy and lipids, while body proteins were significantly lower, compared to adult rats. In addition, plasma non esterified fatty acid levels were significantly higher, while resting metabolic rates were found to be significantly lower, in old rats compared to adult ones. Significantly lower oxidative capacities in whole tissue homogenates and in intermyofibrillar and subsarcolemmal mitochondria were found in old rats compared to adult ones. Subsarcolemmal and intermyofibrillar mitochondria from old rats exhibited a significantly lower proton leak rate, while oxidative damage was found to be significantly higher only in subsarcolemmal mitochondria. Mitochondrial superoxide dismutase specific activity was not significantly affected in old rats, while significantly higher content of uncoupling protein 3 was found in both mitochondrial populations from old rats compared to adult ones, although the magnitude of the increase was lower in subsarcolemmal than in intermyofibrillar mitochondria. CONCLUSIONS: The decrease in oxidative capacity and proton leak in intermyofibrillar and subsarcolemmal mitochondria could induce a decline in energy expenditure and thus contribute to the reduced resting metabolic rate found in old rats, while oxidative damage is present only in subsarcolemmal mitochondria

A possible link between hepatic mitochondrial dysfunction and diet-induced insulin resistance

Mitochondria are the main cellular sites devoted to ATP production and lipid oxidation. Therefore, the mitochondrial dysfunction could be an important determinant of cellular fate of circulating lipids, that accumulate in the cytoplasm, if they are not oxidized. The ectopic fat accumulation is associated with the development of insulin resistance, and a link between mitochondrial dysfunction and insulin resistance has been proposed

Mitochondrial efficiency and insulin resistance

Insulin resistance, “a relative impairment in the ability of insulin to exert its effects on glucose, protein and lipid metabolism in target tissues,” has many detrimental effects on metabolism and is strongly correlated to deposition of lipids in non-adipose tissues. Mitochondria are the main cellular sites devoted to ATP production and fatty acid oxidation. Therefore, a role for mitochondrial dysfunction in the onset of skeletal muscle insulin resistance has been proposed and many studies have dealt with possible alteration in mitochondrial function in obesity and diabetes, both in humans and animal models. Data reporting evidence of mitochondrial dysfunction in type two diabetes mellitus are numerous, even though the issue that this reduced mitochondrial function is causal in the development of the disease is not yet solved, also because a variety of parameters have been used in the studies carried out on this subject. By assessing the alterations in mitochondrial efficiency as well as the impact of this parameter on metabolic homeostasis of skeletal muscle cells, we have obtained results that allow us to suggest that an increase in mitochondrial efficiency precedes and therefore can contribute to the development of high-fat-induced insulin resistance in skeletal muscle