Laparoscopic Roux-en-Y gastric bypass (LRYGB) and laparoscopic sleeve gastrectomy (LSG) are two most common weight loss procedures; our meta-analysis aims to compare these two in the treatment of morbid obesity and its related comorbidities. An electronic literature research of published studies concerning LRYGB and LSG was performed from inception to October 2013. Percentage of excess weight loss (%EWL), resolution or improvement rate of comorbidities, and adverse events were all pooled and compared by the software Review Manager 5.1. As a result, a total of 21 studies involving 18,766 morbidly obese patients were eventually selected according to the inclusion criteria. No significant difference was found in %EWL during 0.5- to 1.5-year follow-up (P > 0.05), but after that, LRYGB achieved higher %EWL than LSG (P < 0.05). Except for type 2 diabetes mellitus (T2DM) (P < 0.001), the difference between these two procedures in the resolution or improvement rate of other comorbidities did not reach a statistical significance (P > 0.05). There were more adverse events in LRYGB compared with LSG (P < 0.01). In conclusion, LRYGB is superior to LSG in efficacy but inferior to LSG in safety.
Background
Sepsis-associated acute lung injury remains the major cause of mortality in critically ill patients and is characterized by marked oxidative stress and mitochondrial dysfunction. Mitochondrial dynamics are indispensable for functional integrity. Additionally, heme oxygenase (HO)-1/carbon monoxide conferred cytoprotection against end-organ damage during endotoxic shock. Herein, we tested the hypothesis that HO-1/carbon monoxide played a critical role in maintaining the dynamic process of mitochondrial fusion/fission to mitigate lung injury in Sprague-Dawley rats or RAW 264.7 macrophages exposed to endotoxin.
Methods
The production of reactive oxygen species, the respiratory control ratio (RCR), and the expressions of HO-1 and mitochondrial dynamic markers were determined in macrophages. Concurrently, alterations in the pathology of lung tissue, lipid peroxidation, and the expressions of the crucial dynamic proteins were detected in rats.
Results
Endotoxin caused a 31% increase in reactive oxygen species and a 41% decrease in RCR levels (n = 5 per group). In parallel, the increased expression of HO-1 was observed in lipopolysaccharide-stimulated macrophages, concomitantly with excessive mitochondrial fission. Furthermore, carbon monoxide-releasing molecule-2 or hemin normalized mitochondrial dynamics, which were abrogated by zinc protoporphyrin IX. Additionally, impaired mitochondrial dynamic balance was shown in Sprague-Dawley rats that received lipopolysaccharide, accompanied by pathologic injury, elevated malondialdehyde contents, decreased manganese superoxide dismutase activities, and lowered RCR levels in rat lung mitochondria. However, the above parameters were augmented by zinc protoporphyrin IX and were in turn reversed by hemin.
Conclusions
The HO-1/carbon monoxide system modulated the imbalance of the dynamic mitochondrial fusion/fission process evoked by lipopolysaccharide and efficiently ameliorated endotoxin-induced lung injury in vivo and in vitro.
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