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Sisi Yan; Xiangyan Liu; Xin Li; Xiaowen Li; Ji Wang; Lixin Wen. Critique of the Chinese dietary guidelines on the consumption of cooking oils. Food Science & Nutrition 2020, 9, 583 -585.
AMA StyleSisi Yan, Xiangyan Liu, Xin Li, Xiaowen Li, Ji Wang, Lixin Wen. Critique of the Chinese dietary guidelines on the consumption of cooking oils. Food Science & Nutrition. 2020; 9 (1):583-585.
Chicago/Turabian StyleSisi Yan; Xiangyan Liu; Xin Li; Xiaowen Li; Ji Wang; Lixin Wen. 2020. "Critique of the Chinese dietary guidelines on the consumption of cooking oils." Food Science & Nutrition 9, no. 1: 583-585.
Lard, a fat rich in saturated fatty acids (SFAs), is regarded as a risk factor for metabolic diseases. Our previous study found that lard blended with soybean oil has an anti-obesity effect in adult mice. In the present study, effect of different lard blended with sunflower oil diet on lipid accumulation in adipose tissue, liver, and serum by mouse model was researched. Body weight, body fat percentage, cross-sectional area of adipocytes, liver triglycerides (TGs), and oil red stained area in mice liver of lard blend sunflower oil (L-SFO) group were significantly lower than those of sunflower oil (SFO) group, whereas no significant differences were observed between mice of lard and L-SFO groups. Serum TG and free fatty acid (FFA) levels were significantly lower in L-SFO group than in other two groups. Furthermore, data showed that sunflower oil decreased contents of hormone-sensitive lipase and carnitine palmitoyl transferase 1 (CPT-1) and increased fatty acid synthase activity in liver tissue. A mixture of lard and sunflower oil rather than only sunflower oil or lard might promote body fat loss and reduce lipid accumulation in adipose tissue, serum, and liver by promoting hydrolysis of TG, increasing β-oxidation of fatty acids. These data suggested that the use of a mixture of lard and vegetable oil (e.g. sunflower oil) for cooking, or the alternate use of lard and vegetable, may be beneficial for reducing body fat.
Sisi Yan; Xin Li; Linyu Zhang; Yu Zeng; Shuiping Liu; Xiangyan Liu; Huijuan Zhou; Lixin Wen; Ji Wang. Moderate quantity of lard mixed with sunflower oil attenuate lipid accumulation in mice. Oil Crop Science 2020, 5, 205 -212.
AMA StyleSisi Yan, Xin Li, Linyu Zhang, Yu Zeng, Shuiping Liu, Xiangyan Liu, Huijuan Zhou, Lixin Wen, Ji Wang. Moderate quantity of lard mixed with sunflower oil attenuate lipid accumulation in mice. Oil Crop Science. 2020; 5 (4):205-212.
Chicago/Turabian StyleSisi Yan; Xin Li; Linyu Zhang; Yu Zeng; Shuiping Liu; Xiangyan Liu; Huijuan Zhou; Lixin Wen; Ji Wang. 2020. "Moderate quantity of lard mixed with sunflower oil attenuate lipid accumulation in mice." Oil Crop Science 5, no. 4: 205-212.
The presence of tannic acid (TA), which is widely distributed in plants, limits the utilization of non-grain feed. Illustrating the toxicity mechanism of TA in animals is important for preventing poisoning and for clinical development of TA. The aim of the present study was to evaluate the toxic effects and possible action mechanism of TA in porcine intestinal IPEC-J2 cells, as well as cell proliferation, apoptosis, and cell cycle. We investigated the toxic effects of TA in IPEC-J2 cells combining the analysis of TA-induced apoptotic responses and effect on the cell cycle. The results revealed that TA is highly toxic to IPEC-J2 cells. The stress-inducible factors reactive oxygen species, malondialdehyde, and 8-hydroxy-2'-deoxyguanosine were increased in response to TA. Furthermore, TA suppressed mitochondrial membrane potential, reduced adenosine triphosphate production, and adversely affected B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein, caspase-9, caspase-3, cytochrome c, cyclin A, cyclin-dependent kinases, ataxia-telangiectasia mutated, and P53 expression in a dose-dependent manner. We suggest that TA induces the mitochondrial pathway of apoptosis and S phase arrest in IPEC-J2 cells.
Ji Wang; Haisi Xiao; Yuanyuan Zhu; Shuiping Liu; Zhihang Yuan; Jing Wu; Lixin Wen. Tannic Acid Induces the Mitochondrial Pathway of Apoptosis and S Phase Arrest in Porcine Intestinal IPEC-J2 Cells. Toxins 2019, 11, 397 .
AMA StyleJi Wang, Haisi Xiao, Yuanyuan Zhu, Shuiping Liu, Zhihang Yuan, Jing Wu, Lixin Wen. Tannic Acid Induces the Mitochondrial Pathway of Apoptosis and S Phase Arrest in Porcine Intestinal IPEC-J2 Cells. Toxins. 2019; 11 (7):397.
Chicago/Turabian StyleJi Wang; Haisi Xiao; Yuanyuan Zhu; Shuiping Liu; Zhihang Yuan; Jing Wu; Lixin Wen. 2019. "Tannic Acid Induces the Mitochondrial Pathway of Apoptosis and S Phase Arrest in Porcine Intestinal IPEC-J2 Cells." Toxins 11, no. 7: 397.
Although mTOR (the mammalian target of rapamycin) can regulate intracellular free Ca2+concentration in normal cultured podocytes, it remains elusive as to how mTORC2/AKT-mediated Ca2+participates in the process of T-2 toxin-induced apoptosis. The potential signaling responsible for intracellular Ca2+ concentration changes was investigated using immunoblot assays in an in vitro model of TM3 cell injury induced by T-2 toxin. Changes in Ca2+ were assessed using the Ca2+-sensitive fluorescent indictor dye Fura 2-AM. The cytotoxicity of TM3 cells was assessed with an MTT bioassay, and apoptosis was measured using Annexin V-FITC staining. Following T-2 toxin treatment, the growth of cells, phospho-mTORSer2481, phospho-mTORSer2448, and phospho-AktSer473 were significantly decreased in a time-dependent manner, whereas Ca2+ and apoptosis were increased. T-2 toxin-induced apoptosis was prevented by BAPTA-AM (a Ca2+chelator) and MHY1485 (an mTOR activator), and the application of mTOR activator MHY1485 also prevented the increase of intracellular free Ca2+concentration in TM3 cells. Our results strongly suggest that T-2 toxin exposure induces apoptosis in TM3 cells by inhibiting mTORC2/AKT to promote Ca2+ production.
Ji Wang; Chenglin Yang; Zhihang Yuan; Jine Yi; Jing Wu. T-2 Toxin Exposure Induces Apoptosis in TM3 Cells by Inhibiting Mammalian Target of Rapamycin/Serine/Threonine Protein Kinase(mTORC2/AKT) to Promote Ca2+Production. International Journal of Molecular Sciences 2018, 19, 3360 .
AMA StyleJi Wang, Chenglin Yang, Zhihang Yuan, Jine Yi, Jing Wu. T-2 Toxin Exposure Induces Apoptosis in TM3 Cells by Inhibiting Mammalian Target of Rapamycin/Serine/Threonine Protein Kinase(mTORC2/AKT) to Promote Ca2+Production. International Journal of Molecular Sciences. 2018; 19 (11):3360.
Chicago/Turabian StyleJi Wang; Chenglin Yang; Zhihang Yuan; Jine Yi; Jing Wu. 2018. "T-2 Toxin Exposure Induces Apoptosis in TM3 Cells by Inhibiting Mammalian Target of Rapamycin/Serine/Threonine Protein Kinase(mTORC2/AKT) to Promote Ca2+Production." International Journal of Molecular Sciences 19, no. 11: 3360.