Objective:To explore the interaction between pediatric sleep-disordered breathing（SDB）, the intestinal microbiota, and pediatric non-alcoholic fatty liver disease（NAFLD）. Methods:A total of 63 non-obese children（47 children with SDB in the experimental group and 16 without SDB in the control group） were enrolled in this study. The liver function and degree of SDB were assessed in both groups. High-throughput 16S rRNA sequencing was conducted to detect the composition and functional variations of the intestinal microbiota in the two groups of children. Results:Compared with children in the experimental group, serum ALT and AST levels were higher in the control group. and the relative proteobacteria abundance of intestinal flora increased, and the relative abundance of Bacteroidetes decreased significantly. Function including membrane transport, carbohydrate metabolism and lipid metabolism, were enriched in the intestinal microbiota of children with SDB. Conclusion:The composition and functional annotation of the pediatric liver functional status and gut microbiota were significantly different between the two groups of children with and without SDB. Changes in SDB-associated intestinal bacterial abundance may be related to the pathogenesis of pediatric NAFLD.
Humans ; Non-alcoholic Fatty Liver Disease/microbiology* ; Gastrointestinal Microbiome ; Child ; Male ; Sleep Apnea Syndromes/microbiology* ; Female ; RNA, Ribosomal, 16S/genetics* ; Bacteroidetes ; Proteobacteria/isolation & purification* ; Lipid Metabolism

Diabetes complications are the primary cause of disability and mortality in diabetic patients. As the center of cell energy metabolism, mitochondria dysfunction is closely related to the occurrence and development of various microvascular complications. This review focuses on common complications, including diabetic ulcers, diabetic nephropathy and diabetic retinopathy, and on the research progress of mitochondrial function and oxidative stress involving pathological mechanisms of diabetic microvascular complications. We also conclude and update the theoretical basis for targeting mitochondrial oxidative stress in the treatment of these diseases.

Mitochondrial dysfunction plays an important role in the pathogenesis of diabetic complications, and more attention has been paid to the treatment strategies targeting mitochondrial function in these diseases. Our group has been devoted to exploring the relationship between mitochondrial dysfunction such as mitochondrial oxidative stress and energy metabolism, as well as various diabetic complications. This review highlighted recent progresses in the role of mitochondrial dysfunction in the pathogenesis of diabetic ulcer, diabetic nephropathy, diabetes complicated with nonalcoholic fatty liver and their correspondent molecular pathways, tried to explore the feasibility of targeting mitochondrial dysfunction in the treatment of these diseases.