Sarcopenia is an age-related disease that mainly involves decreases in muscle mass, muscle strength and muscle function. At the same time, the body fat content increases with aging, especially the visceral fat content. Adipose tissue is an endocrine organ that secretes biologically active factors called adipokines, which act on local and distant tissues. Studies have revealed that some adipokines exert regulatory effects on muscle, such as higher serum leptin levels causing a decrease in muscle function and adiponectin inhibits the transcriptional activity of Forkhead box O3 (FoxO3) by activating peroxisome proliferators-activated receptor-γ coactivator -1α (PGC-1α) and sensitizing cells to insulin, thereby repressing atrophy-related genes (atrogin-1 and muscle RING finger 1 [MuRF1]) to prevent the loss of muscle mass. Here, we describe the effects on muscle of adipokines produced by adipose tissue, such as leptin, adiponectin, resistin, mucin and lipocalin-2, and discuss the importance of these adipokines for understanding the development of sarcopenia.
Humans ; Adipokines ; Leptin ; Adiponectin ; Sarcopenia ; Muscles

Objective    To compare the effects of transthoracic device closure and traditional surgical repair on atrial septal defect systemically. Methods    A systematic literature search was conducted using the PubMed, EMbase, The Cochrane Library, VIP, CNKI, CBM, Wanfang Database up to July 31, 2018 to identify trials according to the inclusion and exclusion criteria. Quality was assessed and data of included articles were extracted. The meta-analysis was conducted by RevMan 5.3 and Stata 12.0 software. Results    Thirty studies were identified, including 3 randomized controlled trials (RCTs) and 27 cohort studies involving 3 321 patients. For success rate, the transthoracic closure group was lower than that in the surgical repair group (CCT, OR=0.34, 95%CI 0.16 to 0.69, P=0.003). There was no statistical difference in mortality between the two groups (CCT, OR=0.43, 95%CI 0.12 to 1.52, P=0.19). Postoperative complication occurred less frequently in the transthoracic closure group than that in the surgical repair group (RCT, OR=0.30, 95%CI 0.12 to 0.77,  P=0.01; CCT, OR=0.27, 95%CI 0.17 to 0.42, P<0.000 01). The risk of postoperative arrhythmia in the transthoracic closure group was lower than that in the surgical repair group (CCT, OR=0.56, 95%CI 0.34 to 0.90, P=0.02). There was no statistical difference in the incidence of postoperative residual shunt in postoperative one month (CCT, OR=4.52, 95%CI 0.45 to 45.82, P=0.20) and in postoperative one year (CCT, OR=1.03, 95%CI 0.29 to 3.68, P=0.97) between the two groups. Although the duration of operation (RCT MD=–55.90, 95%CI –58.69 to –53.11, P<0.000 01; CCT MD=–71.68, 95%CI -– 79.70 to –63.66, P<0.000 01), hospital stay (CCT, MD=–3.31, 95%CI –4.16, –2.46, P<0.000 01) and ICU stay(CCT, MD=–10.15, 95%CI –14.38 to –5.91, P<0.000 01), mechanical ventilation (CCT, MD=–228.68, 95%CI –247.60 to – 209.77, P<0.000 01) in the transthoracic closure group were lower than those in the traditional surgical repair group, the transthoracic closure costed more than traditional surgical repair during being in the hospital (CCT, MD=1 221.42, 95%CI 1 124.70 to 1 318.14, P<0.000 01). Conclusion    Compared with traditional surgical repair, the transthoracic closure reduces the hospital stay, shortens the length of ICU stay and the duration of ventilator assisted ventilation, while has less postoperative complications. It is safe and reliable for patients with ASD within the scope of indication.