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首页> 外文期刊>Endocrinology, Diabetes & Metabolism >Brain substrate metabolism and ?‐cell function in humans: A positron emission tomography study
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Brain substrate metabolism and ?‐cell function in humans: A positron emission tomography study

机译：脑底物质代谢和α-CELL在人类中的功能：正电子发射断层扫描研究

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Aims Recent clinical studies have shown enhanced brain glucose uptake during clamp and brain fatty acid uptake in insulin‐resistant individuals. Preclinical studies suggest that the brain may be involved in the control of insulin secretion. The aim of this study was to investigate whether brain metabolism assessed as brain glucose and fatty acid uptake is associated with the parameters of β‐cell function in humans. Materials and methods We analysed cross‐sectional data of 120 subjects across a wide range of BMI and insulin sensitivity. Brain glucose uptake (BGU) was measured during euglycaemic‐hyperinsulinaemic clamp (n?=?67) and/or during fasting (n?=?45) using [sup18/supF]‐fluorodeoxyglucose (FDG) positron emission tomography (PET). In another group of subjects (n?=?34), brain fatty acid uptake was measured using [sup18/supF]‐fluoro‐6‐thia‐heptadecanoic acid (FTHA) PET during fasting. The parameters of β‐ cell function were derived from OGTT modelling. Statistical analysis was performed with whole‐brain voxel‐based statistical parametric mapping. Results In non‐diabetics, BGU during euglycaemic hyperinsulinaemic?clamp correlated positively with basal insulin secretion rate ( r =?0.51, P =?.0008) and total insulin output ( r =?0.51, P =?.0008), whereas no correlation was found in type 2 diabetics. BGU during clamp correlated positively with potentiation in non‐diabetics ( r =?0.33, P =?.02) and negatively in type 2 diabetics ( r =??0.61, P =?.02). The associations in non‐diabetics were not explained with whole‐body insulin sensitivity or BMI. No correlations were found between baseline (fasting) BGU and basal insulin secretion rate, whereas baseline brain fatty acid uptake correlated directly with basal insulin secretion rate ( r =?0.39, P =?.02) and inversely with potentiation ( r =??0.36, P =?.04). Conclusions Our study provides coherent, though correlative, evidence that, in humans, the brain may be involved in the control of insulin secretion independently of insulin sensitivity.
机译：目的近期的临床研究显示出在夹层和脑脂肪酸摄取期间增强的脑葡萄糖摄取，耐胰岛素抗性个体。临床前研究表明大脑可能参与胰岛素分泌的控制。本研究的目的是探讨评估为脑葡萄糖和脂肪酸摄取的脑代谢是否与人类β细胞功能的参数有关。材料和方法我们分析了各种BMI和胰岛素敏感性的120个受试者的横截面数据。在使用[ 18-sup> f] -fluorodox鎓（FDG）正电子（FDG）正电子期间，在休息期 - 超细含液夹（N =α67）和/或在禁食时测量脑葡萄糖摄取（BGU）和/或在禁食时（n？= 45）排放断层扫描（宠物）。在另一组受试者中（n？=β34）中，使用[ 18/poIs-庚二甲酸（Ftha）PET在禁食期间测量脑脂肪酸摄取。 β-细胞功能的参数来自OGTT建模。基于全脑体素的统计参数映射进行统计分析。导致非糖尿病患者，BGU期间的EGLYCAIN血液血液血液瘤夹夹均带有基础胰岛素分泌率正相关（R = 0.51，P =β.0008）和总胰岛素输出（R = 0.51，P = 3 0008），而没有在2型糖尿病患者中发现了相关性。在夹持过程中BGU与非糖尿病患者（R = 0.33，p =β.0）的增强性相关，在2型糖尿病患者中呈负增强（R =Δ0.61，p = 02）。非糖尿病患者的关联未用全身胰岛素敏感性或BMI解释。基线（禁食）BGU和基底胰岛素分泌率之间没有相关性，而基线脑脂肪酸摄取直接与基础胰岛素分泌率（R = 0.39，P = 02）和逆转（R = ?? 0.36，p = 04）。结论我们的研究提供了连贯的，虽然具有相关性，证据表明，在人类中，大脑可能涉及独立于胰岛素敏感性的胰岛素分泌控制。

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