Diabetic Med:妊娠期糖尿病暴露与儿童肥胖之间的关联基本上不能由后代肥胖的遗传风险所解释

2018-01-01 MedSci MedSci原创

近日,国际杂志 《Diabetic Med》上在线发表一项关于妊娠期糖尿病暴露与儿童肥胖之间的关联基本上不被后代肥胖的遗传风险所解释的研究。 研究人员研究了282名7-12岁儿童,他们参加了“探索儿童围产期结局研究”。BMI的遗传风险评分计算为91个BMI升高风险等位基因的计数。校正临床和人口统计学协变量,使用多变量线性和逻辑回归模型来估计后代遗传风险评分与暴露于妊娠糖尿病和儿童肥胖(BMI

近日,国际杂志 《Diabetic Med》上在线发表一项关于妊娠期糖尿病暴露与儿童肥胖之间的关联基本上不被后代肥胖的遗传风险所解释的研究。

研究人员研究了2827-12儿童,他们参加了“探索儿童围产期结局研究”。BMI的遗传风险评分计算为91BMI升高风险等位基因的计数。校正临床和人口统计学协变量,使用多变量线性和逻辑回归模型来估计后代遗传风险评分与暴露于妊娠糖尿病和儿童肥胖(BMI和腰围)之间的相关性。后代遗传风险对孕产妇妊娠期糖尿病与儿童期结局之间的关联的贡献通过比较具有和没有遗传风险评分的模型中的妊娠糖尿病变量的回归系数来估计。

研究发现,后代BMI遗传风险评分与儿童BMIP=0.006)和腰围(P=0.02)相关,与妊娠糖尿病(P=0.05)相关。后代BMI遗传风险对妊娠糖尿病与儿童BMI [7.7%(95CI -3.3,18.8]或腰围[5.8%(95CI -3.1,14.8; 两者的P=0.2]关联不大。

研究表明,子代肥胖的遗传风险并不能解释妊娠期糖尿病暴露与儿童肥胖之间的显著比例。妊娠期糖尿病与儿童肥胖之间的关联可能是通过替代途径解释的,包括直接宫内效应或产后共享环境。

原始出处:

S. Raghavan, W. Zhang, I. V. Yang, L. A. Langeet al. Association between gestational diabetes mellitus exposure and childhood adiposity is not substantially explained by offspring genetic risk of obesity.Diabetic Med,15 November 2017.

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  5. 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time=2018-01-02, status=1, ipAttribution=), GetPortalCommentsPageByObjectIdResponse(id=274748, encodeId=c5bf2e474828, content=很好, beContent=null, objectType=article, channel=null, level=null, likeNumber=61, replyNumber=0, topicName=null, topicId=null, topicList=[], attachment=null, authenticateStatus=null, createdAvatar=https://wx.qlogo.cn/mmopen/oLAjfB7s1ib2emBzjO0FtqTJ05AqrEEdRmp6tmlsLXqpzfxWdtgbbgPGWRHagoK9fLTd3IayRPgkJVIVBWtdlmnkBhOIR4cFM/0, createdBy=e8d51649330, createdName=飘飘爱, createdTime=Tue Jan 02 15:24:18 CST 2018, time=2018-01-02, status=1, ipAttribution=)]
  8. 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time=2018-01-02, status=1, ipAttribution=), GetPortalCommentsPageByObjectIdResponse(id=274748, encodeId=c5bf2e474828, content=很好, beContent=null, objectType=article, channel=null, level=null, likeNumber=61, replyNumber=0, topicName=null, topicId=null, topicList=[], attachment=null, authenticateStatus=null, createdAvatar=https://wx.qlogo.cn/mmopen/oLAjfB7s1ib2emBzjO0FtqTJ05AqrEEdRmp6tmlsLXqpzfxWdtgbbgPGWRHagoK9fLTd3IayRPgkJVIVBWtdlmnkBhOIR4cFM/0, createdBy=e8d51649330, createdName=飘飘爱, createdTime=Tue Jan 02 15:24:18 CST 2018, time=2018-01-02, status=1, ipAttribution=)]
  9. 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time=2018-01-02, status=1, ipAttribution=), GetPortalCommentsPageByObjectIdResponse(id=274748, encodeId=c5bf2e474828, content=很好, beContent=null, objectType=article, channel=null, level=null, likeNumber=61, replyNumber=0, topicName=null, topicId=null, topicList=[], attachment=null, authenticateStatus=null, createdAvatar=https://wx.qlogo.cn/mmopen/oLAjfB7s1ib2emBzjO0FtqTJ05AqrEEdRmp6tmlsLXqpzfxWdtgbbgPGWRHagoK9fLTd3IayRPgkJVIVBWtdlmnkBhOIR4cFM/0, createdBy=e8d51649330, createdName=飘飘爱, createdTime=Tue Jan 02 15:24:18 CST 2018, time=2018-01-02, status=1, ipAttribution=)]
    2018-01-02 wxl882001

    了解一下

    0

  10. 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time=2018-01-02, status=1, ipAttribution=), GetPortalCommentsPageByObjectIdResponse(id=274748, encodeId=c5bf2e474828, content=很好, beContent=null, objectType=article, channel=null, level=null, likeNumber=61, replyNumber=0, topicName=null, topicId=null, topicList=[], attachment=null, authenticateStatus=null, createdAvatar=https://wx.qlogo.cn/mmopen/oLAjfB7s1ib2emBzjO0FtqTJ05AqrEEdRmp6tmlsLXqpzfxWdtgbbgPGWRHagoK9fLTd3IayRPgkJVIVBWtdlmnkBhOIR4cFM/0, createdBy=e8d51649330, createdName=飘飘爱, createdTime=Tue Jan 02 15:24:18 CST 2018, time=2018-01-02, status=1, ipAttribution=)]
    2018-01-02 飘飘爱

    很好

    0

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由此可见,糖尿病与限制性肺功能损害有关,但与阻塞性肺功能损害无关。

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近日,国际杂志 《Diabetic Med》上在线发表一项关于胰腺脂肪和脂肪肝之间的代谢交联对局部炎症和胰岛素分泌的影响的研究。 肥胖相关的异位脂肪堆积与2型糖尿病的发展有关。关于胰腺和肝脏的脂肪变性是否影响胰岛素分泌仍然是有争议的。在本研究中,研究人员调查了人类胰岛脂肪细胞与胰岛的交叉作用以及致糖尿病因子,即棕榈酸酯和胎球蛋白-A(一种从脂肪肝释放的肝细胞因子)的作用。 研究人员对人

Diabetologia:VLDL和载脂蛋白CIII通过Toll样受体2在小鼠骨骼肌细胞中诱导ER应激和炎症并减弱胰岛素信号传导

近日,国际杂志 《Diabetic Med》上在线发表一项关于VLDL和载脂蛋白CIII通过Toll样受体2在小鼠骨骼肌细胞中诱导ER应激和炎症并减弱胰岛素信号传导的研究。 在这里,研究人员目的是调查VLDL和载脂蛋白(apo)CIII是否诱导骨骼肌内质网(ER)应激,炎症和胰岛素抵抗。研究人员在来自过表达apoCIII转基因小鼠的C2C12肌管,分离的骨骼肌和骨骼肌中进行研究。 研究

Diabetologia:FGF21改善肥胖糖尿病倾向性小鼠模型中的葡萄糖体内平衡,而与体脂变化无关

近日,国际杂志 《Diabetic Med》上在线发表一项关于FGF21改善肥胖糖尿病倾向性小鼠模型中的葡萄糖体内平衡,而与体脂变化无关的研究。 成纤维细胞生长因子21(FGF21)被认为是用于治疗2型糖尿病的潜在治疗候选物。然而,由于在肥胖和糖尿病条件下FGF21水平会升高,研究人员旨在测试外源性FGF21是否足以预防新西兰肥胖(NZO)小鼠(多发性肥胖和2型糖尿病的模型)中的糖尿病和β细

Diabetologia:长时间暴露于胰岛素的小鼠和人足细胞通过胰岛素受体的溶酶体和蛋白酶降解诱导胰岛素抵抗

近日,国际杂志 《Diabetic Med》上在线发表一项关于长时间暴露于胰岛素的小鼠和人足细胞通过胰岛素受体的溶酶体和蛋白酶降解诱导胰岛素抵抗的研究。 足细胞是肾小球滤过屏障的胰岛素-应答细胞,并且在在防止蛋白尿中具有重要作用,也是糖尿病性肾病的标志特征。虽然有证据表明足细胞的胰岛素信号丢失是有害的,但有关糖尿病足细胞胰岛素抵抗发展的分子机制尚不清楚。因此,研究人员的目地是在糖尿病肾病早期

Diabetologia:乳糜微粒刺激小鼠和人类细胞中肠促胰岛素的分泌

近日,国际杂志 《Diabetologia》上在线发表一项关于乳糜微粒刺激小鼠和人类细胞中肠促胰岛素的分泌的研究。 脂质是胰高血糖素样肽(GLP)-1和葡萄糖依赖性促胰岛素肽(GIP)分泌的有力刺激物。这种效应被认为涉及肠内分泌细胞的顶端表面游离脂肪酸受体1(FFA1)和G蛋白偶联受体119(GPR119)脂质消化产物。然而,最近的证据表明,脂质可能是基底外侧感知的,并且脂肪酸吸收和乳糜微粒