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DIABETOLOGIA:胰岛素停用和随后的胰岛素治疗后1型糖尿病患者的基质代谢,激素和细胞因子水平以及脂肪组织信号传导,以模拟酮症酸中毒的起始步骤

2019-04-03 不详 网络

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缺乏胰岛素和感染/炎症是糖尿病酮症酸中毒(DKA)最常见的两个原因。我们以胰岛素戒断后再给予胰岛素作为临床模型,确定对底物代谢的影响,并检测抗调节激素和细胞因子水平的升高和脂肪组织信号的改变是否参与了DKA的早期阶段。

9名无并发症1糖尿病患者,两次交叉设计随机研究,每次5小时,然后2.5小时高剂量胰岛素钳:(1)胰岛素控制的血糖正常(对照)和(214小时后大学医院环境中的胰岛素停用。

结果显示,胰岛素停用增加了葡萄糖水平(6.1±0.5 vs 18.6±0.5 mmol / l),NEFA3-OHB127±18 vs 1837±298μmol/ l),胰高血糖素,皮质醇和生长激素,降低HCO 3 -pH值,不影响儿茶酚胺或细胞因子水平。全身能量消耗,内源性葡萄糖产生(1.55±0.13 vs 2.70±0.31 mg kg -1  min -1),葡萄糖周转,非氧化性葡萄糖处理,脂质氧化,棕榈酸通量(73 [范围39-104] vs 239 [151-474]μmol/ min),蛋白质氧化和苯丙氨酸通量均增加,而葡萄糖氧化减少。在脂肪组织中,AktSer473磷酸化和G0S2 mRNA水平降低,而CGI-58(也称为ABHD5mRNA增加。脂肪甘油三酯脂肪酶(ATGL)和激素敏感性脂肪酶磷酸化的蛋白质水平未改变。胰岛素治疗在胰岛素撤除后显著降低血浆葡萄糖浓度,对前臂净葡萄糖摄取没有任何可检测的影响。

释放反调节激素和总体增加的分解代谢,包括脂解作用,是由胰岛素停用诱导的前酸中毒酮症的突出特征,并且涉及Akt胰岛素信号传导的抑制和ATGL活性的转录调节。胰岛素停用后胰岛素治疗期间前臂净葡萄糖摄取量没有任何增加表明肌肉胰岛素抵抗的存在。

原始出处:

Thomas S. VossMikkel H. Vendelbo,Substrate metabolism, hormone and cytokine levels and adipose tissue signalling in individuals with type 1 diabetes after insulin withdrawal and subsequent insulin therapy to model the initiating steps of ketoacidosis

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    2019-12-25 baoya
  3. 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  5. 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  6. 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  7. 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  8. 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authenticateStatus=null, createdAvatar=null, createdBy=281337296540, createdName=ms7899726347904398, createdTime=Wed Dec 18 11:46:00 CST 2019, time=2019-12-18, status=1, ipAttribution=), GetPortalCommentsPageByObjectIdResponse(id=1676161, encodeId=0a3a16e61610b, content=<a href='/topic/show?id=6bac955861e' target=_blank style='color:#2F92EE;'>#酸中毒#</a>, beContent=null, objectType=article, channel=null, level=null, likeNumber=84, replyNumber=0, topicName=null, topicId=null, topicList=[TopicDto(id=95586, encryptionId=6bac955861e, topicName=酸中毒)], attachment=null, authenticateStatus=null, createdAvatar=null, createdBy=c5dd27335710, createdName=hywen7335, createdTime=Wed Mar 04 16:46:00 CST 2020, time=2020-03-04, status=1, ipAttribution=)]
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