Adiponectin overexpression in C2C12 myocytes increases lipid oxidation and myofiber transition

Metabolic syndrome and obesity have detrimental effects on the metabolic function of the skeletal muscle. Mounting evidence indicates that patients with those conditions may present an increased ratio of glycolytic to oxidative fibers associated with a decrease in oxidative capacity. In this regard, adiponectin, a hormone mainly secreted by adipocytes that regulates glucose and lipid metabolism, has emerged as a myokine that could play an important role in this process. We aimed to investigate whether adiponectin overexpression in skeletal muscle might be a local protective mechanism, favoring fatty acid utilization. To that end, we generated an in vitro model of myocytes with upregulated endogenous adiponectin using a lentiviral carrier. We demonstrated that the adiponectin-transduced myocytes were able to produce and secrete fully functional adiponectin complexes. Adiponectin overexpression remarkably upregulated the mRNA level of myogenic regulatory factors as well as genes implicated in lipolysis (HSL, ATGL) and cellular and mitochondrial fatty acid transport (LPL, CD36, CPT1B). This was accompanied by increased isoproterenol-induced lipolysis and β-oxidation and reduced lipogenesis, whereas insulin-stimulated glucose uptake was unaltered in transduced myocytes. Lastly, the relative expression of the more glycolytic myofibers (MyHC IIb) compared to the more oxidative ones (MyHC I) was notably reduced. Our results showed that the released adiponectin acted in an autocrine/paracrine manner, increasing lipid oxidation in myocytes and leading to a transition of myofibers from the glycolytic to the oxidative type. In conclusion, muscle adiponectin overexpression might be a way to relieve muscle diseases caused by oxidative muscle fiber deficiency. (AU)

Significant new quantitative EGG patterns in fibromyalgia

Background and Objectives: We analyzed the EEG recordings of a sample of fibromyalgia patients, with the goal of looking for new, more objective indicators on the diagnosis and severity assessment of this pathology, and looking also to establish the relationship of these new indicators with different psychological and neuropsychiatric tests. Methods: We compared the EEG recordings of a group of 13 fibromyalgia patients with a normalized database built into the software of the equipment used (Neuronic), and also with a control group of 13 individuals; both groups were selected under the same criteria of inclusion-exclusion. Patients and controls underwent quantitative EEG (eyes closed), according to international 10-20 EEG system and were specifically evaluated throughout various neuropsychiatric and psychological questionnaires. Results: We obtained the absolute powers of QEEG (quantitative) for the different electrode sites and frequency bands, we determined the corresponding values of the deviation from normal (Z-scores), and estimated various indicators and ratios, as well as correlations with the results of psychological tests. Interestingly, the ratios of theta and beta frequencies in relation with alpha appear as one of the most relevant indicators of the severity of the pathology; significant differences were also found in the peak frequency (maximum power per Hz) of the alpha band, and in the frequency peak of the total spectrum. Conclusions: The consistency of the abnormal EEG patterns of fibromyalgia patients revealed the presence of systemic dysfunction at the central nervous system level, beyond possible peripheral anomalies and specific tissue pathologies. Among the indicators and benchmarks achieved, the most important changes concern the frequencies theta, alpha and beta, and still more significant were the values of their ratios in the comparison between patients and controls. The relative values of peak frequencies are also of interest. The promising results achieved suggest that it is necessary to continue the investigation to validate these new diagnostic indicators (AU)

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