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首页> 外文期刊>Diabetes, obesity & metabolism >Brain glucose uptake is associated with endogenous glucose production in obese patients before and after bariatric surgery and predicts metabolic outcome at follow-up
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Brain glucose uptake is associated with endogenous glucose production in obese patients before and after bariatric surgery and predicts metabolic outcome at follow-up

机译:脑葡萄糖摄取与肥胖患者之前和之后的内源性葡萄糖产生相关,并在后续行动中预测代谢结果

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Aims To investigate further the finding that insulin enhances brain glucose uptake (BGU) in obese but not in lean people by combining BGU with measures of endogenous glucose production (EGP), and to explore the associations between insulin-stimulated BGU and peripheral markers, such as metabolites and inflammatory markers. Materials and methods A total of 20 morbidly obese individuals and 12 lean controls were recruited from the larger randomized controlled SLEEVEPASS study. All participants were studied under fasting and euglycaemic hyperinsulinaemic conditions using fluorodeoxyglucose-positron emission tomography. Obese participants were re-evaluated 6 months after bariatric surgery and were followed-up for similar to 3 years. Results In obese participants, we found a positive association between BGU and EGP during insulin stimulation. Across all participants, insulin-stimulated BGU was associated positively with systemic inflammatory markers and plasma levels of leucine and phenylalanine. Six months after bariatric surgery, the obese participants had achieved significant weight loss. Although insulin-stimulated BGU was decreased postoperatively, the association between BGU and EGP during insulin stimulation persisted. Moreover, high insulin-stimulated BGU at baseline predicted smaller improvement in fasting plasma glucose at 2 and 3 years of follow-up. Conclusions Our findings suggest the presence of a brain-liver axis in morbidly obese individuals, which persists postoperatively. This axis might contribute to further deterioration of glucose homeostasis.
机译:旨在进一步调查胰岛素在肥胖中提高脑葡萄糖摄取(BGU)的发现,但通过将BGU与内源性葡萄糖生产(EGP)的措施相结合,并探讨胰岛素刺激的BGU和外周标记之间的关联作为代谢物和炎症标志物。材料和方法总共20例病态肥胖的个体和12个精益对照,从较大的随机对照的方式研究中招募。所有参与者都使用氟脱氧葡萄糖 - 正电子发射断层扫描在禁食和劣质性超胰岛素血症条件下进行了研究。肥胖参与者在牛肝外科后6个月重新评估,随访了3年。结果在肥胖参与者中,我们在胰岛素刺激期间发现BGU和EGP之间的阳性关联。遍布所有参与者,胰岛素刺激的BGU与全身性炎症标志物和血浆和苯丙氨酸的血浆水平正相关。肥胖手术后六个月,肥胖参与者取得了重量损失。虽然术后胰岛素刺激的BGU减少,但在胰岛素刺激期间BGU和EGP之间的关联持续存在。此外,基线的高胰岛素刺激的BGU预测了在2和3年后的禁食血浆葡萄糖的更小。结论我们的研究结果表明,术后肥胖个体的脑肝轴的存在,术后持续存在。该轴可能有助于进一步恶化葡萄糖稳态。

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