Yuyue Jin
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Yuyue Jin has a total of 13 co-authors. Here are the top co-authors by number of shared publications:
- Minqi Wang
College of Animal Science, Zhejiang University, Hangzhou 310058, China
4 shared publications - Geng Wang
Key Laboratory of Molecular Animal Nutrition, Ministry of Education, College of Animal Science, Zhejiang University, Hangzhou 310058, China
3 shared publications - Haohan Chen
Key Laboratory of Molecular Animal Nutrition, Ministry of Education, College of Animal Sciences, Zhejiang University, Hangzhou 310058, China
3 shared publications - Yueying Lin
Key Laboratory of Molecular Animal Nutrition, Ministry of Education, College of Animal Sciences, Zhejiang University, Hangzhou 310058, China
3 shared publications - Haidong Wang
The Key Laboratory of Molecular Animal Nutrition, Ministry of Education, College of Animal Sciences, Zhejiang University, Hangzhou 310058, China
2 shared publications - Wanjing Sun
Key Laboratory of Molecular Animal Nutrition, Ministry of Education, College of Animal Science, Zhejiang University, Hangzhou 310058, China
2 shared publications
Latest Publications
- Open Access
Effects of Clostridium tyrobutyricum on Lipid Metabolism, Intestinal Barrier Function, and Gut Microbiota in Obese Mice Induced by High-Fat Diet
Obesity and its complications constitute a main threat to global human health. The purpose of this investigation was to explore the influences of Clostridium tyrobutyricum (Ct) on lipid metabolism, intestinal barrier function, and intestinal microbiome in obese mice induced by a high-fat diet (HFD). After establishing the obesity model, 107 CFU/mL and 108 CFU/mL C. tyrobutyricum were used to intervene in HFD-fed mice by gavage for six weeks, and indexes related to obesity were measured. In the liver of HFD-fed mice, the results revealed that C. tyrobutyricum reduced liver weight and the levels of triglyceride (TG), total cholesterol (TC), and nonesterified fatty acid (NEFA), along with decreasing red lipid droplets and fat vacuoles. After C. tyrobutyricum intervention, the mRNA expression of peroxisome proliferator-activated receptor-γ (PPARγ) was downregulated, and AMP-activated protein kinase (AMPK), peroxisome proliferator-activated receptor-α (PPARα), adipose triglyceride lipase (ATGL), and hormone-sensitive lipase (HSL) were upregulated in the liver. Additionally, C. tyrobutyricum alleviated intestinal morphology injury caused by HFD, decreased the expression of tumor necrosis factor-α (TNF-α), interleukin 6 (IL-6), and IL-1β in the colon, and upregulated tight junction protein expression. In addition, 16S rRNA sequencing revealed that C. tyrobutyricum increases the diversity of intestinal microbiota. Overall, C. tyrobutyricum improved HFD-induced lipid metabolism disorders, preserved the intestinal barrier’s integrity, and modulated the structure of the intestinal microbiome. These findings provide a novel insight into the role of C. tyrobutyricum as a probiotic in regulating lipid metabolism.
Open AccessEffects of Clostridium tyrobutyricum on Lipid Metabolism, Intestinal Barrier Function, and Gut Microbiota in Obese Mice Induced by High-Fat Diet
Obesity and its complications constitute a main threat to global human health. The purpose of this investigation was to explore the influences of Clostridium tyrobutyricum (Ct) on lipid metabolism, intestinal barrier function, and intestinal microbiome in obese mice induced by a high-fat diet (HFD). After establishing the obesity model, 107 CFU/mL and 108 CFU/mL C. tyrobutyricum were used to intervene in HFD-fed mice by gavage for six weeks, and indexes related to obesity were measured. In the liver of HFD-fed mice, the results revealed that C. tyrobutyricum reduced liver weight and the levels of triglyceride (TG), total cholesterol (TC), and nonesterified fatty acid (NEFA), along with decreasing red lipid droplets and fat vacuoles. After C. tyrobutyricum intervention, the mRNA expression of peroxisome proliferator-activated receptor-γ (PPARγ) was downregulated, and AMP-activated protein kinase (AMPK), peroxisome proliferator-activated receptor-α (PPARα), adipose triglyceride lipase (ATGL), and hormone-sensitive lipase (HSL) were upregulated in the liver. Additionally, C. tyrobutyricum alleviated intestinal morphology injury caused by HFD, decreased the expression of tumor necrosis factor-α (TNF-α), interleukin 6 (IL-6), and IL-1β in the colon, and upregulated tight junction protein expression. In addition, 16S rRNA sequencing revealed that C. tyrobutyricum increases the diversity of intestinal microbiota. Overall, C. tyrobutyricum improved HFD-induced lipid metabolism disorders, preserved the intestinal barrier’s integrity, and modulated the structure of the intestinal microbiome. These findings provide a novel insight into the role of C. tyrobutyricum as a probiotic in regulating lipid metabolism.
- Open Access
- 11 October 2022
- Published by MDPI AG in Fermentation
- Vol. 8 (10) , 531
Production of Butyric Acid from Hydrolysate of Rice Husk Treated by Alkali and Enzymes in Immobilized Fermentation by Clostridium tyrobutyricum CtΔpta
Rice husk, as a cellulose-rich by-product in agriculture, has been considered as a low-cost substrate for the production of bioethanol and chemicals. In this study, rice husk was pretreated with an alkali, followed by cellulose and β-glucosidase hydrolysis optimized by an orthogonal experiment and response surface methodology (RSM), respectively. Under the optimal treatment conditions, a hydrolysate containing a high reducing sugar yield (77.85%) was obtained from the rice husk. Then, the hydrolysate was used as a carbon substrate for butyric acid production through Clostridium tyrobutyricum Δpta fermentation. Compared to free-cell fermentation, higher concentrations of butyric acid (50.01 g/L vs. 40.8 g/L and 49.03 g/L vs. 27.49 g/L) were observed in immobilized-cell fermentation for the carbon source of glucose and hydrolysate, respectively. A final butyric acid concentration of 16.91 g/L, a yield of 0.31 g/g, and an overall productivity of 0.35 g/L/h from rice husk hydrolysate were obtained in the repeated-fed-batch mode. Taken together, rice husk hydrolysate can be effectively utilized for the bioproduction of butyrate with immobilized-cell fermentation.
- 11 October 2022
- Published by MDPI AG in Fermentation
- Vol. 8 (10) , 531
Open AccessProduction of Butyric Acid from Hydrolysate of Rice Husk Treated by Alkali and Enzymes in Immobilized Fermentation by Clostridium tyrobutyricum CtΔpta
Rice husk, as a cellulose-rich by-product in agriculture, has been considered as a low-cost substrate for the production of bioethanol and chemicals. In this study, rice husk was pretreated with an alkali, followed by cellulose and β-glucosidase hydrolysis optimized by an orthogonal experiment and response surface methodology (RSM), respectively. Under the optimal treatment conditions, a hydrolysate containing a high reducing sugar yield (77.85%) was obtained from the rice husk. Then, the hydrolysate was used as a carbon substrate for butyric acid production through Clostridium tyrobutyricum Δpta fermentation. Compared to free-cell fermentation, higher concentrations of butyric acid (50.01 g/L vs. 40.8 g/L and 49.03 g/L vs. 27.49 g/L) were observed in immobilized-cell fermentation for the carbon source of glucose and hydrolysate, respectively. A final butyric acid concentration of 16.91 g/L, a yield of 0.31 g/g, and an overall productivity of 0.35 g/L/h from rice husk hydrolysate were obtained in the repeated-fed-batch mode. Taken together, rice husk hydrolysate can be effectively utilized for the bioproduction of butyrate with immobilized-cell fermentation.
- 22 February 2022
- Published by Elsevier in Food Research International
- Vol. 155, 111003
Galactooligosaccharides as a protective agent for intestinal barrier and its regulatory functions for intestinal microbiota
- 22 February 2022
- Published by Elsevier in Food Research International
- Vol. 155, 111003
Galactooligosaccharides as a protective agent for intestinal barrier and its regulatory functions for intestinal microbiota
- Open Access
Clostridium tyrobutyricum Protects against LPS-Induced Colonic Inflammation via IL-22 Signaling in Mice
This study aimed to investigate the effects of Clostridium tyrobutyricum (C. tyrobutyricum) on colonic immunity and the role of IL-22 in the protective function of C. tyrobutyricum. Mice were supplemented with 108 CFU/mL C. tyrobutyricum daily for 20 days, followed by injecting with LPS for 24 h. In vivo interference of IL-22 via injecting with an adeno-associated virus was conducted to elucidate the role of IL-22 in C. tyrobutyricum attenuating colonic inflammation. The results showed that C. tyrobutyricum decreased the mRNA expression of IL-6 and IL-1β. C. tyrobutyricum enhanced the mRNA expression of IL-22 and the expression of MUC2 in the colon. The in vivo interference results showed that C. tyrobutyricum enhanced the mRNA expression of IL-6 and IL-1β while decreased the expression of MUC2 after knocking down IL-22. The flow cytometric analysis showed that C. tyrobutyricum decreased the proportions of macrophages, DCs, and mast cells and effectively regulated the proportion of Th17 cells, indicating that C. tyrobutyricum may stimulate the expression of IL-22 via regulating Th17 cells. Our study concluded that C. tyrobutyricum protected against LPS-induced colonic barrier dysfunction and inflammation via IL-22 signaling, suggesting that C. tyrobutyricum could be a potential probiotic in regulating colonic health.
Open AccessClostridium tyrobutyricum Protects against LPS-Induced Colonic Inflammation via IL-22 Signaling in Mice
This study aimed to investigate the effects of Clostridium tyrobutyricum (C. tyrobutyricum) on colonic immunity and the role of IL-22 in the protective function of C. tyrobutyricum. Mice were supplemented with 108 CFU/mL C. tyrobutyricum daily for 20 days, followed by injecting with LPS for 24 h. In vivo interference of IL-22 via injecting with an adeno-associated virus was conducted to elucidate the role of IL-22 in C. tyrobutyricum attenuating colonic inflammation. The results showed that C. tyrobutyricum decreased the mRNA expression of IL-6 and IL-1β. C. tyrobutyricum enhanced the mRNA expression of IL-22 and the expression of MUC2 in the colon. The in vivo interference results showed that C. tyrobutyricum enhanced the mRNA expression of IL-6 and IL-1β while decreased the expression of MUC2 after knocking down IL-22. The flow cytometric analysis showed that C. tyrobutyricum decreased the proportions of macrophages, DCs, and mast cells and effectively regulated the proportion of Th17 cells, indicating that C. tyrobutyricum may stimulate the expression of IL-22 via regulating Th17 cells. Our study concluded that C. tyrobutyricum protected against LPS-induced colonic barrier dysfunction and inflammation via IL-22 signaling, suggesting that C. tyrobutyricum could be a potential probiotic in regulating colonic health.