Breast cancer is one of the most commonly diagnosed cancers and one of the most significant sources of cancer mortality. Triple negative breast cancer (TNBC) is a particularly aggressive subtype that has proven diffic...Breast cancer is one of the most commonly diagnosed cancers and one of the most significant sources of cancer mortality. Triple negative breast cancer (TNBC) is a particularly aggressive subtype that has proven difficult to treat with standard chemotherapies. Obesity has also been shown to exacerbate breast cancer, and diagnoses of these two diseases frequently overlap. Both conditions are regulated in part by the fat mass and obesity-associated (FTO) demethylase, an RNA demethylase which may drive breast cancers through epigenetic alterations to gene expression. Methods of inhibiting FTO have been researched in vitro and in vivo as an alternative or adjunct to chemotherapies in multiple cancers, including breast cancer. Translating knowledge of the role of FTO in breast cancer and the development of novel agents may allow for improvements in the treatment of this refractory cancer. This review therefore aims to provide an overview of existing and developing chemical inhibitors of FTO that could be innovatively studied for the treatment of TNBC and associated comorbidity.展开更多
Background:Osteosarcoma(OS),recognized as the predominant malignant tumor originating from bones,necessitates an in-depth comprehension of its intrinsic mechanisms to pinpoint novel therapeutic targets and enhance tre...Background:Osteosarcoma(OS),recognized as the predominant malignant tumor originating from bones,necessitates an in-depth comprehension of its intrinsic mechanisms to pinpoint novel therapeutic targets and enhance treatment methodologies.The role of fat mass and obesity-associated(FTO)in OS,particularly its correlation with malignant traits,and the fundamental mechanism,remains to be elucidated.Materials and Methods:1.The FTO expression and survival rate in tumors were analyzed.2.FTO in OS cell lines was quantified utilizing western blot and PCR.3.FTO was upregulated and downregulated separately in MG63.4.The impact of FTO on the proliferation and migration of OS cells was evaluated using CCK-8,colony formation,wound healing,and Transwell assays.5.The expression of miR-150-5p in OS cells-derived exosomes was identified.6.The binding of miR-150-5p to FTO was predicted by TargetScan and confirmed by luciferase reporter assay.7.The impact of exosome miR-150-5p on the proliferation and migration of OS cells was investigated.Results:The expression of FTO was higher in OS tissues compared to normal tissues correlating with a worse survival rate.Furthermore,the downregulation of FTO significantly impeded the growth and metastasis of OS cells.Additionally,miR-150-5p,which was downregulated in both OS cells and their derived exosomes,was found to bind to the 3′-UTR of FTO through dual luciferase experiments.Exosomal miR-150-5p was found to decrease the expression of FTO and inhibit cell viability.Conclusions:We identified elevated levels of FTO in OS,which may be attributed to insufficient miR-150-5p levels in both the cells and exosomes.It suggests that the dysregulation of miR-150-5p and its interaction with FTO could potentially promote the development of OS.展开更多
Background Non-alcoholic fatty liver disease （NAFLD） is a complex disorder and has been closely linked to obesity.The fat mass and obesity-associated （FTO） gene is a newly discovered gene related to obesity,which ...Background Non-alcoholic fatty liver disease （NAFLD） is a complex disorder and has been closely linked to obesity.The fat mass and obesity-associated （FTO） gene is a newly discovered gene related to obesity,which enhances oxidative stress and tipogenesis in NAFLD.The forkhead transcription factor O1 （FoxO1） is another important gene involved in NAFLD,which causes lipid disorders when insulin resistance appears in the liver.However,the interactions between FTO and FoxO1 during the pathogenesis of NAFLD have not been fully elucidated.This study was designed to identify the relationship between these two factors that are involved in the development of NAFLD.Methods This study includes two parts referred to as animal and cell experiments.Twelve female SPF C57BL/6 mice were fed a high-fat diet to serve as an NAFLD animal model.Aspartate aminotransferase （AST）,alanine aminotransferase （ALT）,total triglyceride （TG）,total cholesterol （TC）,alkaline phosphatase （ALP）,high-density lipoprotein （HDL）,and low-density lipoprotein （LDL） were measured.Immunohistochemical analysis was used to detect the expression and histological localization of FTO,FoxO1,and adenosine monophosphate （AMP）-activated protein kinase （AMPK）.The L02 cells were exposed to high fat for 24,48,or 72 hours.Oil red O staining was used to detect intracellular lipid droplets.Reverse transcription-polymerase chain reaction was used for analyzing the levels of FTO and FoxO1 mRNA.Results At the end of 10 weeks,ALP,ALT,AST,and LDL were significantly increased （P ＜0.01）,while TC and TG were also significantly higher （P ＜0.05）.In addition,HDL was significantly decreased （P ＜0.05）.The FTO and FoxO1 proteins were weakly expressed in the control group,but both FTO and FoxO1 were expressed significantly higher （P ＜0.01） in the experimental group,and the expression of the two factors was significantly correlated.AMPK in the high-fat group showed a low level of correlation with FTO,but not with FoxO1.Oil Red O staining results showed that the cells cultured in 50％ fetal bovine serum for 24,48,or 72 hours exhibited steatosis.FTO and FoxO1 mRNA were increased in the high-fat group compared with the normal group （P ＜0.01）.The expression levels of FTO and FoxO1 mRNA were the highest at 48 hours （P ＜0.05）.Conclusions A high-fat diet leads to higher expression of FTO,phosphorylation of FoxO1,and decreased phosphorylation of AMPK.These results suggest that the interactions between FTO and FoxO1 are closely related to the pathogenesis of NAFLD.展开更多
目的探究脂肪含量和肥胖相关蛋白(fat mass and obesity-associated protein,FTO)和丝氨酸-苏氨酸激酶蛋白激酶D2(serine-threonine kinase protein kinase D2,PRKD2)在糖尿病肾病(diabetic kidney disease,DKD)进展中的调控作用和调节...目的探究脂肪含量和肥胖相关蛋白(fat mass and obesity-associated protein,FTO)和丝氨酸-苏氨酸激酶蛋白激酶D2(serine-threonine kinase protein kinase D2,PRKD2)在糖尿病肾病(diabetic kidney disease,DKD)进展中的调控作用和调节机制。方法采用35 mmol/L葡萄糖对足细胞(MPC5细胞)进行高糖刺激24h构建DKD体外模型。采用FTO过表达载体(pcDNA-FTO)和PRKD2过表达载体(pcDNA-PRKD2),或空载体(vector)转染高糖诱导的MPC5细胞。通过RT-qPCR检测FTO和PRKD2过表达效率;MeRIP检测PRKD2 mRNA的N6-甲基腺苷(N6-methyladenosine,m6A)修饰水平;ELISA检测Caspase-3活性、IL-6,TNF-α和单核细胞趋化蛋白-1(monocyte chemotactic protein-1,MCP-1)分泌量;流式细胞术分析细胞凋亡率;Western blot评估FTO和PRKD2蛋白水平,以及SIRT1/HIF-1α通路关键蛋白表达水平;Pearson分析FTO和PRKD2水平的相关性。结果与无高糖诱导对照组比较,高糖诱导的足细胞中FTO蛋白(0.51±0.04 vs 1.00±0.03)和PRKD2蛋白(0.45±0.03 vs 1.01±0.04)水平显著下调,差异具有统计学意义(t=13.17,16.76,均P<0.001)。高糖诱导的足细胞中FTO蛋白水平和PRKD2蛋白水平呈正相关(r2=0.7051,P<0.001)。与vector组相比,pcDNA-FTO组PRKD2 mRNA的m6A水平(0.56±0.09 vs1.01±0.13)降低,PRKD2 mRNA水平(3.16±0.14 vs 1.03±0.02)显著升高,差异具有统计学意义(t=51.37,11.82,均P<0.001)。与control组(IL-6:512.76±61.85 pg/ml,TNF-α:28.17±2.83 pg/ml,MCP-1:157.31±17.69 pg/ml)和vector组(IL-6:498.41±87.51 pg/ml,TNF-α:26.35±5.47 pg/ml,MCP-1:165.52±16.87 pg/ml)比较,pcDNA-PRKD2组IL-6(301.86±21.85 pg/ml),TNF-α(11.06±4.12 pg/ml),MCP-1分泌量(81.45±9.03pg/ml)显著减少,差异具有统计学意义(F=7.51,10.47,61.97,均P<0.01)。与control组(Caspase-3:689.65±79.5U/L,细胞凋亡率:22.31%±2.69%)和vector组(Caspase-3:715.91±113.58 U/L,细胞凋亡率:21.07%±3.28%)比较,pcDNA-PRKD2组Caspase-3活性(437.64±104.76 U/L)和细胞凋亡率(8.41%±3.15%)下降,差异具有统计学意义(F=2.35,79.13,均P<0.01)。与control组(SIRT1:1.01±0.05,HIF-1α:1.03±0.07)和vector组(SIRT1:0.97±0.05,HIF-1α:1.02±0.03)相比,pcDNA-PRKD2组SIRT1蛋白(3.51±0.15)水平升高,HIF-1α蛋白(0.37±0.07)水平降低,差异具有统计学意义(F=31.54,8.31,均P<0.01)。结论FTO介导m6A修饰的PRKD2通过SIRT1/HIF-1α通路抑制高糖诱导的足细胞炎症反应和细胞凋亡。展开更多
目的探讨邻苯二甲酸二(2-乙基己基)酯(di-2-ethylhexyl phthalate,DEHP)诱导睾丸间质细胞铁死亡中RNA去甲基化酶脂肪量和肥胖相关蛋白(fat mass and obesity-associated protein,FTO)的作用及机制。方法40只3周龄C57BL/6雄性小鼠通过随...目的探讨邻苯二甲酸二(2-乙基己基)酯(di-2-ethylhexyl phthalate,DEHP)诱导睾丸间质细胞铁死亡中RNA去甲基化酶脂肪量和肥胖相关蛋白(fat mass and obesity-associated protein,FTO)的作用及机制。方法40只3周龄C57BL/6雄性小鼠通过随机数字表法分为对照组(玉米油)和3组DEHP染毒组(5、250、500 mg/kg体质量),连续灌胃35 d;TM3小鼠睾丸间质细胞以0、100、200、400μmol/L邻苯二甲酸单(2-乙基己基)酯(mono-2-ethylhexyl phthalate,MEHP)处理24 h,质粒转染构建Fto过表达TM3细胞。ELISA检测血清睾酮水平,免疫组化检测睾丸组织中蛋白表达,比色法检测睾丸中Fe 2+、丙二醛和脂质过氧化物水平。甲基化RNA免疫共沉淀、RT-PCR和Western blot检测N6-甲基腺嘌呤(N6-methyladenosine,m6A)修饰水平。结果250、500 mg/kg DEHP染毒组小鼠的血清睾酮水平显著降低(P<0.01),睾丸组织Fe 2+、丙二醛、脂质过氧化物水平显著升高(P<0.01),RNA去甲基化酶FTO、铁死亡相关分子铁蛋白重链1(ferritin heavy chain 1,FTH1)和谷胱甘肽过氧化酶4(glutathione peroxidase 4,GPX4)蛋白水平显著下调(P<0.05),转铁蛋白受体(transferrin receptor,TFRC)、膜铁转运蛋白(ferroportin,FPN)、环氧合酶-2(cyclooxygenase-2,COX-2)和酰基辅酶A合成酶长链家族成员4(acyl-CoA synthetase long-chain family member 4,ACSL4)蛋白水平显著上调(P<0.05)。MEHP处理TM3细胞24 h后,细胞活力下降、胞内活性氧(ROS)含量升高,线粒体膜电位(mitochondrial membrane potential,MMP)显著降低(P<0.01),Fto的mRNA和蛋白水平均显著下调(P<0.01),其余铁死亡相关蛋白的变化也与睾丸组织中趋势一致,提示睾丸间质细胞发生了铁死亡。以铁死亡抑制剂Fer-1干预或过表达Fto均能显著抑制MEHP诱导的TM3细胞毒性和铁死亡(P<0.05),同时过表达Fto使Gpx4和Fth1 mRNA的m6A修饰水平降低(P<0.05)。结论FTO表达抑制引起Gpx4、Fth1的m6A修饰异常可能是DEHP诱导睾丸间质细胞铁死亡的机制。展开更多
Obesity has become a major public health concern worldwide. Obesity is a complex disease influenced by both genetic and environmental factors. Epidemiological studies have indicated that environmental factors, such as...Obesity has become a major public health concern worldwide. Obesity is a complex disease influenced by both genetic and environmental factors. Epidemiological studies have indicated that environmental factors, such as excessive energy intake and lack of physical activity, might contribute to the development of obesity. Genetic factors also play an important role in the pathogenesis of obesity Indeed, approximately 40%-70% of the variation in body mass index （BMI） can be attributed to genetic factors.展开更多
目的研究FTO(fat-mass and obesity associated)基因SNP rs9939609和rs1421085多态性与儿童青少年单纯性肥胖及其代谢指标的相关性。方法以2004至2006年于复旦大学附属儿科医院内分泌门诊就诊的汉族单纯性肥胖和超重儿童青少年分别作为...目的研究FTO(fat-mass and obesity associated)基因SNP rs9939609和rs1421085多态性与儿童青少年单纯性肥胖及其代谢指标的相关性。方法以2004至2006年于复旦大学附属儿科医院内分泌门诊就诊的汉族单纯性肥胖和超重儿童青少年分别作为肥胖组和超重组;选择上海市某中学正常体重汉族学生作为正常对照组。分别测量身高和体重,计算BMI。测定血清空腹葡萄糖(FPG)、空腹胰岛素(FIns)、三酰甘油(TG)和总胆固醇(TC)水平。计算胰岛素抵抗指数(HOMA-IR)和胰岛素敏感指数(QUICKI)。抽提外周血基因组DNA,采用Taqman-MGB探针技术检测FTO基因SNPrs9939609和rs1421085多态性,分析不同基因型与代谢指标和BMI的相关性。结果肥胖组纳入236例,超重组纳入239例,正常对照组纳入241名。肥胖+超重组的BMI、FPG、FIns、TG和HOMA-IR显著高于正常对照组;②肥胖、超重和正常对照组rs9939609分型成功率分别为94.9%(224/236例)、97.9(234/239例)和95.9%(231/241名),rs1421085分型成功率分别为92.8%(219/236例)、97.1%(232/239例)和95.4%(230/241名)。rs9939609AA基因型频率:肥胖组为2.7%,超重组为0.4%,正常对照组为1.7%,肥胖+超重组A等位基因频率显著高于正常对照组(OR=1.437,P=0.048);rs1421085CC基因型频率:肥胖组为2.7%,超重组为0.9%,正常对照组为1.7%,肥胖+超重组C等位基因频率高于正常对照组,但差异无统计学意义(OR=1.388,P=0.0760);③rs1421085TC+CC基因型和rs9939609TA+AA基因型儿童青少年的BMI显著高于TT基因型(rs9939609:P=0.0003;rs1421085:P=0.0005);rs1421085TC+CC基因型和rs9939609TA+AA基因型与FPG、FIns、TG、TC、HOMA-IR、QUICKI无显著相关性。结论FTO基因SNP rs9939609和rs1421085多态性与中国汉族儿童青少年肥胖和(或)超重存在相关性。A等位基因频率远低于欧洲人群,对BMI的作用效果与欧洲人群相似,但对代谢指标影响存在显著差异。展开更多
为了研究阿勒泰大尾羊和小尾寒羊不同脂肪组织及其他组织之间基因表达的差异,探讨脂肪与肥胖相关基因(fat mass and obesity associated gene,FTO)与绵羊体脂沉积的相关性。随机各选择6只6月龄雄性阿勒泰大尾羊和小尾寒羊,禁食24h后屠宰...为了研究阿勒泰大尾羊和小尾寒羊不同脂肪组织及其他组织之间基因表达的差异,探讨脂肪与肥胖相关基因(fat mass and obesity associated gene,FTO)与绵羊体脂沉积的相关性。随机各选择6只6月龄雄性阿勒泰大尾羊和小尾寒羊,禁食24h后屠宰,分别采集下丘脑、海马、背最长肌、心肌和脂肪组织样本,应用冰冻组织切片技术,测定脂肪细胞的面积,用real-time PCR检测FTO基因在各组织中的表达水平。结果显示,阿勒泰大尾羊尾脂脂肪细胞面积极显著高于肾周脂脂肪细胞面积(P<0.01)。阿勒泰大尾羊与小尾寒羊下丘脑和海马FTO基因表达水平无显著差异,背最长肌、心肌FTO基因表达水平阿勒泰大尾羊的极显著高于小尾寒羊的(P<0.01),肾周脂中FTO基因表达水平阿勒泰大尾羊的显著高于小尾寒羊的(P<0.05)。阿勒泰大尾羊肾周脂、心周脂和尾脂中FTO基因表达水平在肾周脂、心周脂、尾脂之间无显著差异。结果表明,FTO基因表达水平在阿勒泰大尾羊和小尾寒羊之间存在品种间的差异。展开更多
目的体脂量和肥胖相关（fat mass and obesity associated,FTO）基因与体质指数增加以及过多能量摄入相关。文中探讨FTO基因多态性与环境因素的交互作用对哈萨克族学龄儿童肥胖的影响。方法从＂伊犁哈萨克自治州哈萨克族学龄儿童超重肥...目的体脂量和肥胖相关（fat mass and obesity associated,FTO）基因与体质指数增加以及过多能量摄入相关。文中探讨FTO基因多态性与环境因素的交互作用对哈萨克族学龄儿童肥胖的影响。方法从＂伊犁哈萨克自治州哈萨克族学龄儿童超重肥胖调查＂中选择279名6~13岁小学生,根据中国肥胖问题工作组提出的《中国学龄儿童青少年超重、肥胖筛查体质指数值分类标准》中不同年龄、性别的BMI判定,分为肥胖组（141名）和正常组（138名）,进行体格检查、问卷调查以及FTO基因rs9939609多态性检测。结果采用主成分方法进行探索性因子分析,共提取不良饮食习惯、食欲状况、户外活动、挑食情况、活动方式和睡眠时间6个因子。Logistic回归分析显示,FTO基因rs9939609与食欲状况、户外活动的交互作用归因百分依次为76.49%、79.95%。结论在哈萨克族学龄儿童中,食欲状况、户外活动可能修饰FTO基因与肥胖的关系,但需要进一步前瞻性的干预性研究证实该种影响作用。展开更多
文摘Breast cancer is one of the most commonly diagnosed cancers and one of the most significant sources of cancer mortality. Triple negative breast cancer (TNBC) is a particularly aggressive subtype that has proven difficult to treat with standard chemotherapies. Obesity has also been shown to exacerbate breast cancer, and diagnoses of these two diseases frequently overlap. Both conditions are regulated in part by the fat mass and obesity-associated (FTO) demethylase, an RNA demethylase which may drive breast cancers through epigenetic alterations to gene expression. Methods of inhibiting FTO have been researched in vitro and in vivo as an alternative or adjunct to chemotherapies in multiple cancers, including breast cancer. Translating knowledge of the role of FTO in breast cancer and the development of novel agents may allow for improvements in the treatment of this refractory cancer. This review therefore aims to provide an overview of existing and developing chemical inhibitors of FTO that could be innovatively studied for the treatment of TNBC and associated comorbidity.
文摘Background:Osteosarcoma(OS),recognized as the predominant malignant tumor originating from bones,necessitates an in-depth comprehension of its intrinsic mechanisms to pinpoint novel therapeutic targets and enhance treatment methodologies.The role of fat mass and obesity-associated(FTO)in OS,particularly its correlation with malignant traits,and the fundamental mechanism,remains to be elucidated.Materials and Methods:1.The FTO expression and survival rate in tumors were analyzed.2.FTO in OS cell lines was quantified utilizing western blot and PCR.3.FTO was upregulated and downregulated separately in MG63.4.The impact of FTO on the proliferation and migration of OS cells was evaluated using CCK-8,colony formation,wound healing,and Transwell assays.5.The expression of miR-150-5p in OS cells-derived exosomes was identified.6.The binding of miR-150-5p to FTO was predicted by TargetScan and confirmed by luciferase reporter assay.7.The impact of exosome miR-150-5p on the proliferation and migration of OS cells was investigated.Results:The expression of FTO was higher in OS tissues compared to normal tissues correlating with a worse survival rate.Furthermore,the downregulation of FTO significantly impeded the growth and metastasis of OS cells.Additionally,miR-150-5p,which was downregulated in both OS cells and their derived exosomes,was found to bind to the 3′-UTR of FTO through dual luciferase experiments.Exosomal miR-150-5p was found to decrease the expression of FTO and inhibit cell viability.Conclusions:We identified elevated levels of FTO in OS,which may be attributed to insufficient miR-150-5p levels in both the cells and exosomes.It suggests that the dysregulation of miR-150-5p and its interaction with FTO could potentially promote the development of OS.
文摘Background Non-alcoholic fatty liver disease （NAFLD） is a complex disorder and has been closely linked to obesity.The fat mass and obesity-associated （FTO） gene is a newly discovered gene related to obesity,which enhances oxidative stress and tipogenesis in NAFLD.The forkhead transcription factor O1 （FoxO1） is another important gene involved in NAFLD,which causes lipid disorders when insulin resistance appears in the liver.However,the interactions between FTO and FoxO1 during the pathogenesis of NAFLD have not been fully elucidated.This study was designed to identify the relationship between these two factors that are involved in the development of NAFLD.Methods This study includes two parts referred to as animal and cell experiments.Twelve female SPF C57BL/6 mice were fed a high-fat diet to serve as an NAFLD animal model.Aspartate aminotransferase （AST）,alanine aminotransferase （ALT）,total triglyceride （TG）,total cholesterol （TC）,alkaline phosphatase （ALP）,high-density lipoprotein （HDL）,and low-density lipoprotein （LDL） were measured.Immunohistochemical analysis was used to detect the expression and histological localization of FTO,FoxO1,and adenosine monophosphate （AMP）-activated protein kinase （AMPK）.The L02 cells were exposed to high fat for 24,48,or 72 hours.Oil red O staining was used to detect intracellular lipid droplets.Reverse transcription-polymerase chain reaction was used for analyzing the levels of FTO and FoxO1 mRNA.Results At the end of 10 weeks,ALP,ALT,AST,and LDL were significantly increased （P ＜0.01）,while TC and TG were also significantly higher （P ＜0.05）.In addition,HDL was significantly decreased （P ＜0.05）.The FTO and FoxO1 proteins were weakly expressed in the control group,but both FTO and FoxO1 were expressed significantly higher （P ＜0.01） in the experimental group,and the expression of the two factors was significantly correlated.AMPK in the high-fat group showed a low level of correlation with FTO,but not with FoxO1.Oil Red O staining results showed that the cells cultured in 50％ fetal bovine serum for 24,48,or 72 hours exhibited steatosis.FTO and FoxO1 mRNA were increased in the high-fat group compared with the normal group （P ＜0.01）.The expression levels of FTO and FoxO1 mRNA were the highest at 48 hours （P ＜0.05）.Conclusions A high-fat diet leads to higher expression of FTO,phosphorylation of FoxO1,and decreased phosphorylation of AMPK.These results suggest that the interactions between FTO and FoxO1 are closely related to the pathogenesis of NAFLD.
基金supported by National Basic Research Program of China (973 Program,2013CB530605)Beijing Health System LeadingTalent Grant (2009-1-08)the Research Fund forthe Doctoral Program of Higher Education of China (20120131120004)
文摘Obesity has become a major public health concern worldwide. Obesity is a complex disease influenced by both genetic and environmental factors. Epidemiological studies have indicated that environmental factors, such as excessive energy intake and lack of physical activity, might contribute to the development of obesity. Genetic factors also play an important role in the pathogenesis of obesity Indeed, approximately 40%-70% of the variation in body mass index （BMI） can be attributed to genetic factors.
文摘为了研究阿勒泰大尾羊和小尾寒羊不同脂肪组织及其他组织之间基因表达的差异,探讨脂肪与肥胖相关基因(fat mass and obesity associated gene,FTO)与绵羊体脂沉积的相关性。随机各选择6只6月龄雄性阿勒泰大尾羊和小尾寒羊,禁食24h后屠宰,分别采集下丘脑、海马、背最长肌、心肌和脂肪组织样本,应用冰冻组织切片技术,测定脂肪细胞的面积,用real-time PCR检测FTO基因在各组织中的表达水平。结果显示,阿勒泰大尾羊尾脂脂肪细胞面积极显著高于肾周脂脂肪细胞面积(P<0.01)。阿勒泰大尾羊与小尾寒羊下丘脑和海马FTO基因表达水平无显著差异,背最长肌、心肌FTO基因表达水平阿勒泰大尾羊的极显著高于小尾寒羊的(P<0.01),肾周脂中FTO基因表达水平阿勒泰大尾羊的显著高于小尾寒羊的(P<0.05)。阿勒泰大尾羊肾周脂、心周脂和尾脂中FTO基因表达水平在肾周脂、心周脂、尾脂之间无显著差异。结果表明,FTO基因表达水平在阿勒泰大尾羊和小尾寒羊之间存在品种间的差异。
文摘目的体脂量和肥胖相关（fat mass and obesity associated,FTO）基因与体质指数增加以及过多能量摄入相关。文中探讨FTO基因多态性与环境因素的交互作用对哈萨克族学龄儿童肥胖的影响。方法从＂伊犁哈萨克自治州哈萨克族学龄儿童超重肥胖调查＂中选择279名6~13岁小学生,根据中国肥胖问题工作组提出的《中国学龄儿童青少年超重、肥胖筛查体质指数值分类标准》中不同年龄、性别的BMI判定,分为肥胖组（141名）和正常组（138名）,进行体格检查、问卷调查以及FTO基因rs9939609多态性检测。结果采用主成分方法进行探索性因子分析,共提取不良饮食习惯、食欲状况、户外活动、挑食情况、活动方式和睡眠时间6个因子。Logistic回归分析显示,FTO基因rs9939609与食欲状况、户外活动的交互作用归因百分依次为76.49%、79.95%。结论在哈萨克族学龄儿童中,食欲状况、户外活动可能修饰FTO基因与肥胖的关系,但需要进一步前瞻性的干预性研究证实该种影响作用。
