The Effects of Different Types of Exercise on Circulating Irisin Levels in Healthy Individuals and in People With Overweight, Metabolic Syndrome and Type 2 Diabetes.

Irisin is a myokine secreted during exercise. It has drawn the attention of researchers as it regulates several effects of exercise that are considered beneficial. It has also been proposed as a therapeutic tool to treat metabolic disorders. In recent years, the effect of different types of training on circulating irisin has been studied in large populations. An overall beneficial result has been shown, however, the outcome of the investigations has raised some controversy. Herein we evaluated the existing literature on the effects of different types of training on the circulating irisin levels in healthy subjects and in those displaying different metabolic condition. We conducted queries in the PubMed and Web of Science databases for literature published between January 2010 and January 2021. Thirty-seven original articles were retrieved and they were included in this review. Any letter to the editor, meta-analyses, reviews, and systematic review articles were excluded. From these 37 articles, 19 of them reported increased levels of circulating irisin. The interventions encompassed aerobic, resistance, combined, circuit, and interval training types. Such increase of circulating irisin was reported for healthy subjects and for those displaying different metabolic condition. A training that is steadily kept with a moderate to high intensity, including that characterized by brief highly intense intervals, were distinguishable from the rest. Nevertheless, the training effectiveness as evaluated by the increased circulating irisin levels depends on the subject's metabolic condition and age.

Biotin starvation with adequate glucose provision causes paradoxical changes in fuel metabolism gene expression similar in rat (Rattus norvegicus), nematode (Caenorhabditis elegans) and yeast (Saccharomyces cerevisiae).

BACKGROUND/AIM: Biotin affects the genetic expression of several glucose metabolism enzymes, besides being a cofactor of carboxylases. To explore how extensively biotin affects the expression of carbon metabolism genes, we studied the effects of biotin starvation and replenishment in 3 distantly related eukaryotes: yeast Saccharomyces cerevisiae, nematode Caenorhabditis elegans and rat Rattus norvegicus. METHODS: Biotin starvation was produced in Wistar rats, in C. elegans N2 and S. cerevisiae W303A fed with abundant glucose. High-density oligonucleotide microarrays were used to find gene expression changes. Glucose consumption, lactate and ethanol were measured by conventional tests. RESULTS: In spite of abundant glucose provision, the expression of fatty oxidation and gluconeogenic genes was augmented, and the transcripts for glucose utilization and lipogenesis were diminished in biotin starvation. These results were associated with diminished glucose consumption and glycolysis products (lactate and ethanol in yeast), which was consistent across 3 very different eukaryotes. CONCLUSION: The results point toward a strongly selected role of biotin in the control of carbon metabolism, and in adaptations to variable availability of carbon, conceivably mediated by signal transduction including soluble guanylate cyclase, cGMP and a cGMP-dependent protein kinase (PKG) and/or biotin-dependent processes.

Histiocitosis sinusal con linfadenopatía masiva o enfermedad de Rosai-Dorfman / No disponible

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Mitochondrial nitric oxide inhibits ATP synthesis. Effect of free calcium in rat heart.

Nitric oxide is a small potentially toxic molecule and a diatomic free radical. We report the interaction of L-arginine, oxygen and calcium with the synthesis of nitric oxide in heart mitochondria. Nitric oxide synthesis is increased in broken rat heart mitochondria compared with intact and permeabilized mitochondria. Intact mitochondria subjected to hypoxia-reoxygenation conditions accumulated nitric oxide that inhibits oxygen consumption and ATP synthesis. ATPase activity is not affected during this augment of nitric oxide. Physiological free calcium concentrations protected mitochondria from the damage caused by the accumulation of nitric oxide. Higher concentrations of the divalent cation increase the damage exerted by nitric oxide.

Effect of D-amino acids on some mitochondrial functions in rat liver.

We studied the role of the D-amino acids (D-aa) D-serine, D-alanine, D-methionine, D-aspartate, D-tyrosine and D-arginine on rat liver mitochondria. The stability of D-amino acids, mitochondrial swelling, transmembrane potential and oxygen consumption were studied under oxidative stress conditions in rat liver mitochondria. In the presence of glutamate-malate all D-aas salts increased mitochondrial swelling, while in the presence of succinate plus rotenone only D-ala, D-arg and D-ser, induced mitochondrial swelling. The transmembrane potential (deltapsi) was decreased in the presence of 1 microM Ca(2+). The D-aas inhibited oxygen consumption in state 3. The D-aa studied exerted effects on mitochondria via an increase of free radicals production.

Regulation of the rate of synthesis of nitric oxide by Mg(2+) and hypoxia. Studies in rat heart mitochondria.

In isolated rat heart mitochondria, L-arginine is oxidized by a nitric oxide synthase (mtNOS) achieving maximal rates at 1 mM L-arginine. The NOS inhibitor N(G)-nitro-L-arginine methyl ester (NAME) inhibits the increase in NO production. Extramitochondrial free magnesium inhibited NOS production by 59% at 3.2 mM. The mitochondrial free Mg(2+) concentration increased to different extents in the presence of L-arginine (29%), the NO donor (S-nitroso-N-acetylpenicillamine) (105%) or the NOS inhibitors L-NAME (48%) or N(G)-nitro-L-arginine methyl ester, N(G)-monomethyl-L-arginine (L-NMMA) (53%). Under hypoxic conditions, mtNOS activity was inhibited by Mg(2+) by up to 50% after 30 min of incubation. Reoxygenation restored the activity of the mtNOS to pre-hypoxia levels. The results suggest that in heart mitochondria there is an interaction between Mg(2+) levels and mtNOS activity which in turn is modified by hypoxia and reoxygenation.

Effect of Ca(2+) and Mg(2+) on the Mn-superoxide dismutase from rat liver and heart mitochondria.

The manganese superoxide dismutase (Mn-SOD) converts superoxide anions to hydrogen peroxide plus oxygen, providing the first line of defense against oxidative stress in mitochondria. Heart mitochondria exhibited higher Mn-SOD activity than liver mitochondria. In mitochondria from both tissues Mn-SOD activity decreased after incubation at low oxygen concentration (hypoxic mitochondria). The effects of free Ca(2+) ([Ca(2+)](f)) and free Mg(2+) ([Mg(2+)](f)) on normoxic and hypoxic mitochondria from either organ were tested. In normoxic mitochondria from either tissue, both [Ca(2+)](f) and [Mg(2+)](f) activated the enzyme, although [Mg(2+)](f) was less efficient as an activator and the effect was lower in heart than in liver mitochondria. When added simultaneously, high [Ca(2+)](f) and [Mg(2+)](f) exhibited additive effects which were more pronounced in heart mitochondria and were observed regardless of whether mitochondria had been incubated under normal or low oxygen. The data suggest that [Ca(2+)](f) plays a role in regulating Mn-SOD in concert with the activation of aerobic metabolism.