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Disruption of fasting and post-load glucose homeostasis are largely independent and sustained by distinct and early major beta-cell function defects: a cross-sectional and longitudinal analysis of the Relationship between Insulin Sensitivity and Cardiovascular risk (RISC) study cohort.
Metabolism ( IF 9.8 ) Pub Date : 2020-02-14 , DOI: 10.1016/j.metabol.2020.154185 Alessandro Mengozzi 1 , Domenico Tricò 2 , Lorenzo Nesti 1 , John Petrie 3 , Kurt Højlund 4 , Asimina Mitrakou 5 , Michael Krebs 6 , Andrea Mari 7 , Andrea Natali 1 ,
Metabolism ( IF 9.8 ) Pub Date : 2020-02-14 , DOI: 10.1016/j.metabol.2020.154185 Alessandro Mengozzi 1 , Domenico Tricò 2 , Lorenzo Nesti 1 , John Petrie 3 , Kurt Højlund 4 , Asimina Mitrakou 5 , Michael Krebs 6 , Andrea Mari 7 , Andrea Natali 1 ,
Affiliation
BACKGROUND/AIMS
Uncertainty still exists on the earliest beta-cell defects at the bases of the type 2 diabetes. We assume that this depends on the inaccurate distinction between fasting and post-load glucose homeostasis and aim at providing a description of major beta-cell functions across the full physiologic spectrum of each condition.
METHODS
In 1320 non-diabetic individuals we performed an OGTT with insulin secretion modeling and a euglycemic insulin clamp, coupled in subgroups to glucose tracers and IVGTT; 1038 subjects underwent another OGTT after 3.5 years. Post-load glucose homeostasis was defined as mean plasma glucose above fasting levels (δOGTT). The analysis was performed by two-way ANCOVA.
RESULTS
Fasting plasma glucose (FPG) and δOGTT were weakly related variables (stβ = 0.12) as were their changes over time (r = -0.08). Disruption of FPG control was associated with an isolated and progressive decline (approaching 60%) of the sensitivity of the beta-cell to glucose values within the normal fasting range. Disruption of post-load glucose control was characterized by a progressive decline (approaching 60%) of the slope of the full beta-cell vs glucose dose-response curve and an early minor (30%) decline of potentiation. The acute dynamic beta-cell responses, neither per se nor in relation to the degree of insulin resistance appeared to play a relevant role in disruption of fasting or post-load homeostasis. Follow-up data qualitatively and quantitatively confirmed the results of the cross-sectional analysis.
CONCLUSION
In normal subjects fasting and post-load glucose homeostasis are largely independent, and their disruption is sustained by different and specific beta-cell defects.
中文翻译：
空腹和负荷后葡萄糖稳态的破坏在很大程度上是独立的，并由明显的早期主要β细胞功能缺陷维持：胰岛素敏感性与心血管风险（RISC）研究队列之间关系的横断面和纵向分析。
背景/目的不确定性仍然存在于最早的2型糖尿病患者的β细胞缺陷上。我们认为这取决于空腹和负荷后葡萄糖稳态之间的不准确区别，目的是在每种情况的整个生理范围内提供主要β细胞功能的描述。方法在1320名非糖尿病患者中，我们进行了具有胰岛素分泌模型和正常血糖胰岛素钳夹的OGTT，并在亚组中结合了葡萄糖示踪剂和IVGTT。3.5年后，对1038名受试者进行了另一次OGTT。负荷后葡萄糖稳态被定义为高于禁食水平的平均血浆葡萄糖（δOGTT）。通过双向ANCOVA进行分析。结果空腹血糖（FPG）和δOGTT是弱相关变量（stβ= 0.12），随时间的变化也是如此（r = -0.08）。FPG控制的中断与正常禁食范围内β细胞对葡萄糖值的敏感性逐渐孤立（逐渐降低）（接近60％）有关。负荷后葡萄糖控制的破坏的特征是完整的β细胞对葡萄糖剂量-反应曲线的斜率逐渐下降（接近60％），而增强作用则早期轻微下降（30％）。急性动态β-细胞反应本身与胰岛素抵抗程度无关，似乎与空腹或负荷后体内稳态的破坏有关。后续数据定性和定量地证实了横截面分析的结果。结论在正常受试者中，禁食和负荷后葡萄糖体内稳态在很大程度上是独立的，
更新日期：2020-02-20
中文翻译：
空腹和负荷后葡萄糖稳态的破坏在很大程度上是独立的，并由明显的早期主要β细胞功能缺陷维持：胰岛素敏感性与心血管风险（RISC）研究队列之间关系的横断面和纵向分析。
背景/目的不确定性仍然存在于最早的2型糖尿病患者的β细胞缺陷上。我们认为这取决于空腹和负荷后葡萄糖稳态之间的不准确区别，目的是在每种情况的整个生理范围内提供主要β细胞功能的描述。方法在1320名非糖尿病患者中，我们进行了具有胰岛素分泌模型和正常血糖胰岛素钳夹的OGTT，并在亚组中结合了葡萄糖示踪剂和IVGTT。3.5年后，对1038名受试者进行了另一次OGTT。负荷后葡萄糖稳态被定义为高于禁食水平的平均血浆葡萄糖（δOGTT）。通过双向ANCOVA进行分析。结果空腹血糖（FPG）和δOGTT是弱相关变量（stβ= 0.12），随时间的变化也是如此（r = -0.08）。FPG控制的中断与正常禁食范围内β细胞对葡萄糖值的敏感性逐渐孤立（逐渐降低）（接近60％）有关。负荷后葡萄糖控制的破坏的特征是完整的β细胞对葡萄糖剂量-反应曲线的斜率逐渐下降（接近60％），而增强作用则早期轻微下降（30％）。急性动态β-细胞反应本身与胰岛素抵抗程度无关，似乎与空腹或负荷后体内稳态的破坏有关。后续数据定性和定量地证实了横截面分析的结果。结论在正常受试者中，禁食和负荷后葡萄糖体内稳态在很大程度上是独立的，
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