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Purpose: Obstructive Sleep Apnea (OSA) is associated with the presence and severity of Non-Alcoholic Fatty Liver Disease (NAFLD). We aimed to investigate the relationship between the severity of OSA and NAFLD and to recognize a polysomnographic parameter correlated with progression of fibrosis, determined by a non-invasive score of liver fibrosis, FIBrosis-4 index (FIB-4), in patients affected by severe obesity and OSA. Methods: We enrolled 334 patients (Body Mass Index, BMI 44.78 ± 8.99 kg/m2), divided into classes according to severity of OSA evaluated with Apnea Hypopnea Index (AHI): OSAS 0 or absent (17%), mild OSA (26%), moderate OSA (20%), severe OSAS (37%). We studied anthropometric, polysomnographic, biochemical data and FIB-4. A multiple regression model was computed to identify a polysomnographic independent predictor of FIB-4 among those parameters previously simple correlated with FIB-4. Results: The severity of OSA was associated with a decrease in High-Density Lipoprotein–cholesterol (HDL) and an increase in BMI, triglycerides, Homeostasis model assessment insulin-resistance index (HOMA), transaminases and FIB-4. FIB-4 correlated with sex, age, BMI, AHI, mean percentage oxyhaemoglobin (meanSaO2%), number of desaturations, platelets, transaminases, HDL, triglycerides and HOMA. The only variables independently related to FIB-4 were sex, BMI, triglycerides and meanSpO2 (r= 0.47, AdjRsqr = 0.197). Conclusion: MeanSpO2% represented an independent determinant for the worsening of FIB-4 in patients with severe obesity and OSA. Hence, it could hypothesize a clinical role of meanSaO2% in recognizing patients with obesity and OSA and higher risk of developing advanced fibrosis and, thus, to undergo further investigation. Level III: Evidence obtained from well-designed cohort analytic studies.

AbstractSatellite cells (SCs) are undifferentiated skeletal muscle cells that allow muscular growth and regeneration. Since their first description, SCs were simply considered myogenic precursors, but now it is widely accepted that SCs are a heterogeneous stem cell population characterized by plasticity and self-renewal. In this report we focus on SCs capacity to undergo adipogenic differentiation both spontaneous and induced by adipogenic factors. Understanding SC behavior is especially important because their adipogenic potential could represent a pathophysiological explanation for the intramuscular fat depots and associated insulin resistance that characterize many metabolic diseases and age-related sarcopenia. Moreover, SC are a therapeutic promise for neuromuscular diseases in the context of tissue engineering, representing an interesting cell source for implantation.