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Previous work demonstrated that hyperthermia (43°C for 2 h) results in delayed, apoptotic-like death in striatal neuronal cultures. We investigated early changes in mitochondrial function induced by this heat stress. Partial depolarization of the mitochondrial membrane potential (ΔΨ(m)) began about 1 h after the onset of hyperthermia and increased as the stress continued. When the heat stress ended, there was a partial recovery of ΔΨ(m), followed hours later by a progressive, irreversible depolarization of ΔΨ(m). During the heat stress, O(2) consumption initially increased but after 20-30 min began a progressive, irreversible decline to about one-half the initial rate by the end of the stress. The percentage of oligomycin-insensitive respiration increased during the heat stress, suggesting an increased mitochondrial leak conductance. Analysis using inhibitors and substrates for specific respiratory chain complexes indicated hyperthermia-induced dysfunction at or upstream of complex I. ATP levels remained near normal for ∼4 h after the heat stress. Mitochondrial movement along neurites was markedly slowed during and just after the heat stress. The early, persisting mitochondrial dysfunction described here likely contributes to the later (>10 h) caspase activation and neuronal death produced by this heat stress. Consistent with this idea, proton carrier-induced ΔΨ(m) depolarizations comparable in duration to those produced by the heat stress also reduced neuronal viability. Post-stress ΔΨ(m) depolarization and/or delayed neuronal death were modestly reduced/postponed by nicotinamide adenine dinucleotide, a calpain inhibitor, and increased expression of Bcl-xL.

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Aim: Recently obesity, has become the main risk for a number of conditions and metabolic syndrome including type 2 diabetes (T2DM). The aims of this study were to assess whether irisin can bring out the missing circle between increasing physical activity and weight reduction. Methods: 108 subjects were chosen to matched with 76 diabetic patients in age and BMI, both groups were divided into subgroups according to their BMI.22 healthy athlete men were also involved in the study. Results: The mean (± SD) value of serum irisin concentrations of obese healthy individuals was the highest concentration (p=0.015) in comparison with normal and overweight healthy individuals. The more recent observation which describe irisin as adipokine factor (willing myokine source), irisin levels were examine pursuant to gender, obese women group have had the highest level of serum irisin than other women studied groups (p=0.001), while in healthy men serum irisin did not differ significantly. Carful examination were searched for irisin as a myokine after adjusting age and BMI for gender depending on that women had significantly lower serum irisin (p=0.006) inspite of signficantly higher fat precentage (p=0.001) when compared with men. signficantly lower serum irisin concentration in healthy men with normal physical activity (p=0.01) than healthy athlete men pointed that irisin as myokine potentionally. Diabetic patients showed significant lower serum irisin level than healthy subjects. Conclusion: Serum irisin levels findings may reflect its protective role against developing insulin resistance. uncoupling protein (UCP1) [7]. The browning of WAT is associated with augmented mitochondrial density and oxygen consumption producing heat leading to favorable effect on [9]. Irisin discovery may raise hopes regarding the hypothesis that it may provide a new treatment for obesity and diabetes. That peptide hormone may hold additional benefits for a wide range of pathological conditions since this hormone may be therapeutically and clinically beneficial [10]. The aims of this study were 1) to assess whether irisin is the link circle between increasing physical activity and weight reduction, increasing insulin sensitivity and improvement of DM, and prevention of pre-diabetic status, 2) to show the included mechanism and 3) to evaluate its effectiveness as adipokine to myokine.