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1.
Environ Pollut ; 343: 123217, 2024 Feb 15.
Artigo em Inglês | MEDLINE | ID: mdl-38154771

RESUMO

Green tide, a typical marine environmental disaster that profoundly influenced the coastal areas, has been occurred consecutively in the South Yellow Sea of China since 2007. Herein, the active microbial community structure and metabolic pathways in Qingdao offshore during an Ulva prolifera green tide were investigated by using metatranscriptomic approach. The dominant active microbial taxa at the outbreak phase were primarily a functional group that can utilize organic matters derived from U. prolifera, such as Lentibacter, Polaribacter and Planktomarina. While the taxa involved in biogeochemical cycles, including Phaeobacter, Pseudomonas and Marinobacterium, dominated the active microbial communities at the decline phase. The expression level of enzymes involved in U. prolifera polysaccharides degradation was significantly higher at the outbreak phase compared to the decline phase. At the same time, the main players Glaciecola and Polarbacter showed similar trends, suggesting that the low competitiveness for nutrients of related microorganisms at this phase made them degrade more U. prolifera polysaccharides to meet their own nutrient needs, thereby accelerating the degradation of U. prolifera. According to KEGG annotation, the biogeochemical pathways including nitrogen cycle, sulfur cycle and methane oxidation altered during the green tide, with thiosulfate oxidation and methane oxidation probably being the crucial pathways at the outbreak and the decline phase respectively. The coupling of sulfide oxidation and denitrification was also observed in this study. Furthermore, the green tide in Qingdao offshore might impact the greenhouse effects induced by CH4 and N2O through influencing the related microbial processes.


Assuntos
Algas Comestíveis , Eutrofização , Ulva , China , Metano/metabolismo , Polissacarídeos/metabolismo
2.
Front Endocrinol (Lausanne) ; 14: 1190827, 2023.
Artigo em Inglês | MEDLINE | ID: mdl-38053727

RESUMO

Objective: Intestinal flora homeostasis in rats with type 2 diabetes mellitus (T2DM) was evaluated to explore the effects of total Astragalus saponins (TAS) on hepatic insulin resistance (IR). Methods: Six-week-old male Sprague-Dawley rats were fed high-fat and high-sugar diet for 4 weeks and intraperitoneally injected with streptozotocin to induce T2DM, and they were then randomly divided into control, model, metformin, and TAS groups. Stool, serum, colon, and liver samples were collected after 8 weeks of drug administration for relevant analyses. Results: TAS reduced fasting blood glucose, 2-hour postprandial blood glucose, area under the curve of oral glucose tolerance test, glycated serum protein, homeostasis model assessment of insulin resistance, total cholesterol, triglyceride, and low-density lipoprotein cholesterol levels in T2DM rats but increased insulin, C-peptide, and high-density lipoprotein cholesterol levels. Moreover, TAS improved the morphology and structure of liver and colon tissues and improved the composition of the intestinal microbiome and bacterial community structure at different taxonomic levels. In addition, TAS increased the protein expression of hepatic IRS-1, PI3K, PDK1, and p-AKT and decreased the protein expression of p-GSK-3ß. Meanwhile, TAS increased the mRNA expression of liver PDK1, PI3K, and GS and decreased the mRNA expression of GSK-3ß. Conclusion: TAS can ameliorate T2DM-related abnormal glucose and blood lipid metabolism, intestinal dysbiosis, and IR.


Assuntos
Diabetes Mellitus Experimental , Diabetes Mellitus Tipo 2 , Resistência à Insulina , Saponinas , Ratos , Masculino , Animais , Diabetes Mellitus Tipo 2/complicações , Diabetes Mellitus Tipo 2/tratamento farmacológico , Glicemia/metabolismo , Glicogênio Sintase Quinase 3 beta/metabolismo , Glicogênio Sintase Quinase 3 beta/farmacologia , Saponinas/farmacologia , Saponinas/metabolismo , Disbiose/tratamento farmacológico , Ratos Sprague-Dawley , Diabetes Mellitus Experimental/complicações , Diabetes Mellitus Experimental/tratamento farmacológico , Fígado/metabolismo , Fosfatidilinositol 3-Quinases/metabolismo , RNA Mensageiro/metabolismo , Colesterol/metabolismo
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