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共轭亚油酸对脂肪细胞成熟调控机理研究 总被引：1，自引：0，他引：1
共轭亚油酸(CLA．Conjugated linoleic acid)是一类具有顺、反异构体的十八碳二烯酸的统称,当前,CLA的生物学功能已成为研究热点,尤其在脂肪代谢调控上,具有降低脂肪沉积和血液胆固醇水平的功效。通过对CLA的脂肪细胞成熟(包括对脂肪细胞的增殖、分化,脂肪的沉积、甘油三磷酸的沉积等过程)调控机理的综合论述,以便为CLA更深入的研究提供参考。 相似文献
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本试验旨在研究乙酸浓度对奶牛乳腺上皮细胞甘油三酯(TAG)含量及瘦素(leptin)和过氧化物酶增殖物激活受体γ(PPARγ)基因表达量的影响。将传至第3代的奶牛乳腺上皮细胞以适宜的密度培养48 h后,随机分为6个处理,各处理分别采用乙酸浓度为0(对照组)、4、6、8、10和12 mmol/L的培养液。置于37℃5%CO2培养箱继续培养48 h。收集细胞,观测脂滴形成状况,测定TAG含量及leptin和PPARγ基因表达量。结果表明:随乙酸浓度的增加,培养的奶牛脂肪前体细胞脂滴形成增多;随乙酸浓度的增加,TAG含量和PPARγ基因表达量均呈显著的线性或二次曲线增加(P<0.05),且以乙酸浓度为10和12 mmol/L时效果较好;一定浓度的乙酸可上调leptin基因表达量,尤以浓度为8、10 mmol/L时上调作用较好。结果提示,乙酸对奶牛乳腺上皮细胞内脂滴的形成、TAG的积累、leptin和PPARγ基因的表达有显著的促进作用。本试验条件下,乙酸浓度为10～12 mmol/L时能较好地促进PPARγ基因的表达,浓度为8～10 mmol/L时能较好地促进leptin基因的表达。 相似文献
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为阐明DNA甲基化对奶牛乳腺泌乳功能调控的机制,研究了甲基化抑制剂5氮杂2′脱氧胞苷（5 Aza dC）对奶牛乳腺上皮细胞中PPARγ基因启动子甲基化状态及其表达的影响,以体外培养的奶牛乳腺上皮细胞为模型,采用0.1、0.5、1.0、5.0μmol／L的5 Aza dC对奶牛乳腺上皮细胞进行处理,用EpiQuikTM DNA methyltransferase assay试剂盒进行甲基转移酶活性检测,采用CASY细胞分析仪检测细胞活力和增殖能力,利用亚硫酸氢盐测序（BSP ）技术检测了PPARγ启动子的甲基化特征,qRT PCR法检测PPARγmRNA表达的变化,Western blot检测PPARγ蛋白表达的变化。结果显示：与空白对照组相比,0.1μmol／L的5 Aza dC对奶牛乳腺细胞生长无毒性,处理96 h甲基转移酶活性极显著降低,奶牛乳腺细胞的PPARγ基因启动子甲基化程度降低,PPARγ表达升高。表明5 Aza dC可降低奶牛乳腺细胞中PPARγ启动子区域的甲基化程度,促进PPARγ表达。 相似文献
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利用PCR-SSCP技术,对约克夏、杜洛克、长白猪、金华猪、碧湖猪和嵊县花猪共6个品种258头猪的PPARγ2基因外显子1进行多态性分析,并采用SPSS程序中GLM模型分析该位点与胴体性状的相关性。研究结果发现编码区175 bp处存在A175G单核苷酸多态。国内外猪种的基因型频率间存在较大差异,在国外种猪中,AA基因型频率较高,国内猪种中AG基因型频率较高。相关性分析结果表明,在长白猪群中,PPARγ2基因与肩部背膘厚、腰荐结合部背膘厚均存在极显著相关性(P<0.01),与6/7th肋背膘厚和眼肌面积均存在显著相关性(P<0.05)。在金华猪群内,PPARγ2基因与肩部背膘厚显著相关(P<0.05)。因此推测PPARγ2基因可能是影响猪胴体性状的潜在分子育种标记。 相似文献
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The Alisma rhizoma is widely used in the therapy of diabetes in traditional folk medicine of China. Compositional analysis of the alcohol extract of Alismatis Rhizoma (AEA) revealed that the eight compounds gotten from AEA are all belonging to protostane-type triterpenes. The AEA and compounds were incubated with 3T3-L1 preadipocytes, glucose level in the 3T3-L1 adipocytes culture medium and lipid content in 3T3-L1 adipocytes were measured, and analysis of alpha-glucosidase inhibition of AEA and compounds. At the same time, the uptake of AEA by 3T3-L1 adipocytes and the metabolism of AEA in SD rats were analyzed by HPLC-ESI/MS. As result, AEA increased glucose uptake in 3T3-L1 adipocyte model, not increase adipogenesis; AEA inhibited alpha-glucosidase activity; alisol A-24-aceate (8) was absorbed by 3T3-L1 adipocytes; and two compounds were detected in blood and three were detected in urine in SD rats. So AEA had protostane-type triterpenes, these type compounds in AEA may have hypoglycemic activity via inhibition of alpha-glucosidase activity and promotion of glucose uptake. In contrast to the anti-diabetic drug thiazolidinediones, they did not induce adipogenesis, avoiding the displeased effects of rosiglitazone. 相似文献
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Juzuo Zhang Liqun Xue Ang Nie Qing Yang Xuan Peng Zhilong Chen Lisha Yang Yang Xie Anwen Yuan Junfei Xu 《Reproduction in domestic animals》2020,55(11):1479-1489
Non-infectious prenatal mortality severely affects the porcine industry, with pathological placentation as a likely key reason. Previous studies have demonstrated that peroxisome proliferator-activated receptor gamma (PPARγ) deficiency causes defects in the uteroplacental vasculature and induces embryonic losses in mice. However, its role in porcine placental angiogenesis remains unclear. In the present study, PPARγ expression was investigated in porcine uteroplacental tissues at gestational day (GD) 25, GD40 and GD70 via quantitative polymerase chain reaction (qPCR), Western blot and immunohistochemistry (IHC). Moreover, the roles of PPARγ in porcine placental angiogenesis were investigated using a cell model of porcine umbilical vein endothelial cells (PUVECs) to conduct proliferation, migration and tube formation assays in vitro and a mouse xenograft model to assess capillary formation in vivo. The results showed that PPARγ was mainly located in the glandular epithelium, trophoblast, amniotic chorion epithelium and vascular endothelium, as indicated by the higher expression levels at GD25 and GD40 than at GD70 in endometrium and by higher expression levels at GD40 and GD70 than at GD25 in placenta. Moreover, PPARγ expression was significantly downregulated in placenta with dead foetus. In PUVECs, knocking out PPARγ significantly inhibited proliferation, migration and tube formation in vitro and inhibited capillary formation in mouse xenografts in vivo by blocking S-phase, promoting apoptosis and downregulating the angiogenic factors of VEGF and its receptors. Overall, the spatiotemporal heterogeneity of PPARγ expression in porcine uteroplacental tissue suggests its vital role in endometrial remodelling and placental angiogenesis, and PPARγ regulates placental angiogenesis through VEGF-mediated signalling. 相似文献
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T. E. Weber B. J. Kerr M. E. Spurlock 《Journal of animal physiology and animal nutrition》2008,92(5):569-577
Soy protein regulates adiponectin and peroxisome proliferator‐activated receptor α (PPARα) in some species, but the effect of dietary soy protein on adiponectin and PPARα in the pig has not been studied. Therefore, the objective of this study was to determine whether soya bean meal reduction or replacement influences serum adiponectin, adiponectin mRNA, serum metabolites and the expression of PPARα and other genes involved in lipid deposition. Thirty‐three pigs (11 pigs per treatment) were subjected to one of three dietary treatments: (i) reduced crude protein (CP) diet containing soya bean meal (RCP‐Soy), (ii) high CP diet containing soya bean meal (HCP‐Soy) or (iii) high CP diet with corn gluten meal replacing soya bean meal (HCP‐CGM) for 35 days. Dietary treatment had no effect on overall growth performance, feed intake or measures of body composition. There was no effect of dietary treatment on serum adiponectin or leptin. Dietary treatment did not affect the abundance of the mRNAs for adiponectin, PPARα, PPARγ2, lipoprotein lipase or fatty acid synthase in adipose tissue. The mRNA expression of PPARα, PPARγ2, lipoprotein lipase or fatty acid synthetase in loin muscle was not affected by dietary treatment. In liver tissue, the relative abundance of PPARα mRNA was greater (p < 0.05) in pigs fed the HCP‐Soy diets when compared to pigs fed RCP‐Soy or HCP‐CGM diets. Hepatic mRNA expression of acyl‐CoA oxidase or fatty acid synthase was not affected by dietary treatment. Western blot analysis indicated that hepatic PPARα protein levels were decreased (p < 0.05) in pigs fed the RCP‐Soy diets when compared to pigs fed the HCP‐Soy diets. These data suggest that increasing the soy protein content of swine diets increases hepatic expression of PPARα without associated changes in body composition. 相似文献
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Rheum palmatum Linn has been widely applied in the clinical treatment of diabetes mellitus. It has been found that emodin as the major bioactive component of R. palmatum L exhibits the competency to activate peroxisomal proliferator-activated receptor-γ (PPARγ) in vitro. So the aim of this study was to evaluate the anti-diabetic effects of emodin through the activation of PPARγ on high-fat diet-fed and low dose of streptozotocin (STZ)-induced diabetic mice. The diabetic mice were intraperitoneally injected with emodin for three weeks. No changes of food consumption and the body weight in emodin-treated mice were monitored daily during the entire experiment. At the end of experiment, the levels of blood glucose, triglyceride and total cholesterol in serum were significantly decreased after emodin treatment. However, serum high-density lipoprotein cholesterol (HDLc) concentration was significantly elevated. The glucose tolerance and insulin sensitivity in emodin-treated group were significantly improved. Furthermore, the results of quantitative RT-PCR analysis showed that emodin significantly elevated the mRNA expression level of PPARγ and regulated the mRNA expressions of LPL, FAT/CD36, resistin and FABPs (ap2) in liver and adipocyte tissues. No effects on the mRNA expressions of PPARα and PPARα-target genes were observed. Taken together, the results suggested that the activation of PPARγ and the modulation of metabolism-related genes were likely involved in the anti-diabetic effects of emodin. 相似文献