No abstract

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Non-alcoholic fatty liver disease (NAFLD) is a chronic liver disease characterized by an excessive accumulation of triacylglycerol in the liver. Autophagy is a lysosome-dependent degradation product recovery process, which widely occurs in eukaryotic cells, responsible for the vital maintenance of cellular energy balance. Previously published studies have demonstrated that autophagy is closely related to NAFLD occurrence and maternal obesity increases the susceptibility of offspring to non-alcoholic fatty liver disease, however, the underlying mechanism of this remains unclear. In the present study, NAFLD mouse models (offspring of an obese mother mouse via high-fat feeding) were generated, and the physiological indices of the liver were observed using total cholesterol, triglyceride, high-density lipoprotein and low-density lipoprotein serum assay kits. The morphological changes of the liver were also observed via HE, Masson and oil red O staining. Reverse transcription-quantitative-PCR and western blotting were performed to detect changes of autophagy-related genes in liver or fibrosis marker proteins (α-smooth muscle actin or TGF-β 1 ). Changes in serum inflammatory cytokine IL-6 levels were determined via ELISA. The results of the present study demonstrated that the offspring of an obese mother were more likely to develop NALFD than the offspring of a chow-fed mother, due to their increased association with liver fibrosis. When feeding continued to 17 weeks, the worst cases of NAFLD were observed and the level of autophagy decreased significantly compared with the offspring of a normal weight mouse. In addition, after 17 weeks of feeding, compared with the offspring of a chow-fed mother, the offspring of an obese mouse mother had reduced adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK) phosphorylation levels and increased mammalian target of rapamycin (mTOR) phosphorylation levels. These results suggested that a reduced level of AMPK/mTOR mediated autophagy may be of vital importance for the increased susceptibility of offspring to NAFLD caused by maternal obesity. In conclusion, the current study provided a new direction for the treatment of NAFLD in offspring caused by maternal obesity.

Soil microorganisms have been recognized as important decomposers that link above-and below-ground processes in terrestrial ecosystems. In this study, we conducted an experiment to assess the influence of canopy nitrogen deposition and understory removal in a Cunninghamia lanceolata plantation. The effects of four treatments, i.e. control (CK), understory removal (UR), nitrogen deposition (N) and nitrogen deposition plus understory removal (N × UR) on soil microbial community were investigated using phospholipid fatty acids (PLFAs). Soil samples (0-10 layer) were collected in April (spring) and October (autumn), 2016. Results showed that the total soil microbial PLFAs and the other groups (bacteria, fungi and actinomycete) of soil microbial PLFAs in autumn were significantly higher than those in spring, but fungi/bacteria ratio did not change significantly between two sampling seasons. Bacteria dominated among different PLFAs groups, followed by fungi and actinomycetes. Relative to CK treatment, UR treatment had slightly higher total PLFAs, bacterial PLFAs, gram negative bacterial PLFAs and actinomycetes PLFAs