It is well known that human activities and climate change have increased steppe habitat loss and fragmentation in Northwest China. Carabid beetles are often used as bioindicators of environmental change because they are extremely sensitive to disturbance. We chose 42 landscapes (18 fragmented and 24 continuous) in both desert and typical steppes of Northwest China to examine the influence of habitat loss and fragmentation on carabid beetle communities. The results showed the largest correlation coefficient between carabid communities and landscape compositions within a 7-km spatial scale in both desert and typical steppes. Further, the response of carabid communities to habitat fragmentation was species-specific in both desert and typical steppes. Habitat fragmentation in the desert steppe had positive effects on the richness and abundance of carabid communities, while in the typical steppe, the effects were negative. Additionally, habitat fragmentation significantly decreased the abundance of two common carabid species in the desert steppe. Therefore, the effects of habitat fragmentation on carabid biodiversity differ with species characteristics and habitat traits, where plant communities, soil structure, and microclimate vary in the different steppe types. The results of this study provide experimental evidence and technical support for biodiversity conservation management in the steppes of Northwest China.

A high intake of carbohydrates, associated with obesity, is one of the major causes of fatty liver disease in humans. This study investigated how high carbohydrate intake induces fatty liver disease in Blunt snout bream (Megalobrama amblycephala). Blunt snout bream were fed a high-carbohydrate diet (HCBD) for 60 days. Their growth indices were evaluated, and the transcriptomes, metabolites, biochemistry, and histology of their blood and livers were analyzed. The final weight, weight gain, specific growth rate, and feed conversion ratio were all higher in the HCBD group than in the control group, but not significantly so (P > 0.05). The hepatosomatic index (HSI) differed significantly in the two groups (P < 0.05), and the metabolomics results showed that a high carbohydrate intake induced significant increases in plasma α/β-glucose, succinate, and tyrosine, which could increase hepatic glycogen and triglyceride. Low levels of betaine were also found in the livers of the HCBD group. The histology and blood biochemistry results suggested abnormal liver, with excessive lipid accumulation and liver damage. A transcriptome analysis and quantitative reverse transcription–PCR (RT–qPCR) indicated that the expression of the factors INSR, IRS, PI3K, PDK, AKT, ACC, IL6, AP1, ChREBP-MLX, PEPCK, and FBP in the insulin signaling pathway was significantly upregulated and that of SOCS3, GSK3β, and AMPK significantly downregulated in the HCBD. This pattern is associated with the nonalcoholic fatty liver disease (NAFLD) pathway. This study extends our understanding of how high carbohydrate causes increased fat deposition in the liver, enhanced glycolysis (α/β-glucose) in the plasma, and reduced betaine in the liver. This leads to activation of hepatocyte insulin resistance and lipogenesis by regulating the expression of genes related to fatty liver disease.