Swimming exercise activates peroxisome proliferator-activated receptor-alpha and mitigates age-related renal fibrosis in rats.

Aging results in progressive decline of renal function as well as histological alterations including glomerulosclerosis and interstitial fibrosis. The objective of current study was to test the benefits of moderate swimming exercise in aged rats on renal function and structure and investigate its molecular mechanisms. Aged rats of 21-months old were given moderate swimming exercise for 12 weeks. Swimming exercise in aged rats led to reduced plasma levels of creatinine and blood urea nitrogen. Periodic acid-Schiff staining results revealed reduced renal injury scores in aged rats after swimming exercise. Swimming exercise in aged rats mitigated renal fibrosis and downregulated the mRNA expression of Acta2, Fn, Col1a, Col4a, and Tgfb1 in kidneys. Swimming exercise in aged rats attenuated lipid accumulation and reduced levels of triglyceride in kidneys. Swimming exercise in aged rats abated oxidative stress, evidenced by reduced MDA levels and increased MnSOD activities in kidneys. Swimming exercise in aged rats inhibited NF-κB activities and reduced renal expression of pro-inflammatory cytokines including MCP-1, IL-1ß and IL-6. Mechanistically, swimming exercise restored mRNA and protein expression of PPAR-α in kidney of aged rats. Furthermore, swimming exercise in aged rats increased expression of PPAR-α-targeting microRNAs including miR-21 and miR-34a. Collectively, swimming exercise activated PPAR-α, which partly explained the benefits of moderate swimming exercise in aging kidneys.

Changes in the gut microbiota of forest musk deer (Moschus berezovskii) during ex situ conservation.

Ex situ conservation is an important technique for protecting rare and endangered wildlife, and maintaining stable individual health is crucial to its success. Gut microbiota composition is a critical indicator of animal health and should therefore be closely monitored during ex situ conservation to track impacts on animal health. Forest musk deer (Moschus berezovskii) were historically distributed in Hebei Province, China, however, they are now extinct in the region. Thus, ex situ conservation efforts were conducted in 2016 whereby approximately 50 individuals were artificially migrated from Weinan, Shaanxi to Huailai, Hebei. To monitor gut health of these migrated individuals, we used 16S rRNA high-throughput sequencing technology to examine the microbiota differences between Huailai juvenile and Weinan juvenile groups, and between Huailai adult and Weinan adult groups. Alpha diversity analysis indicated that the richness of microbiota significantly decreased after migration to the Huailai area, and the beta diversity results also showed significant dissimilarity in gut microbial communities, demonstrating the distinct microbial structure differences in the forest musk deer population from the two areas, for both juvenile and adult groups, respectively. In addition, PICRUSt functional profile prediction indicated that the functions of gut digestion and absorption, and degradation of toxic substances were significantly weakened after ex situ conservation. Differences in diet composition between the individuals of the two sites were also observed and the impact of food on gut microbiota compositions within forest musk deer during ex situ conservation was investigated. This study provides a theoretical basis for developing ex situ conservation measures, especially for the protection of forest musk deer.

Exercise training suppresses Mst1 activation and attenuates myocardial dysfunction in mice with type 1 diabetes.

Our study was to test the effects of aerobic exercise on myocardial function in mice with type 1 diabetes and investigate the underlying mechanism associated with mammalian sterile 20-like kinase 1 (Mst1). Wild-type mice and Mst1(-/-) mice were injected with streptozotocin to induce diabetes and given moderate-intensity exercise for 12 weeks. Phosphorylation of Mst1 was significantly enhanced in the left ventricles of diabetic mice, which was reversed by exercise training. Exercise training or Mst1 deficiency improved myocardial function and reduced myocardial fibrosis in diabetic mice. Exercise training or Mst1 deficiency reduced TUNEL-positive cells and caspase-3 activity in the myocardium of diabetic mice. Exercise training or Mst1 deficiency abated oxidative stress and reduced mitochondrial reactive oxygen species formation, attenuated mitochondrial swelling, and enhanced mitochondrial adenosine triphosphate formation and mitochondrial membrane potential in the myocardium of diabetic mice. Exercise training or Mst1 deficiency suppressed inflammation in the myocardium of diabetic mice. Furthermore, exercise training did not provide further protection in Mst1 knockout mice in diabetes. In conclusion, chronic exercise training attenuated myocardial dysfunction in mice with type 1 diabetes, at least in part, through suppressing Mst1 activation.