Department of Physiology, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, P.O. Box 9101, 6500 HB, Nijmegen, the Netherlands.
Department of Internal Medicine, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Nijmegen, 6500 HB, the Netherlands.
Sci Rep. 2022 Apr 19;12(1):6433. doi: 10.1038/s41598-022-10436-0.
In a cohort of adults with type 1 diabetes, we examined the prevalence of hypomagnesemia and the correlation of serum magnesium levels with metabolic determinants, such as glycaemic control (as HbA), inflammatory markers and circulating cytokines. Furthermore, we assessed if a surrogate for insulin resistance is essential for the possible association of serum magnesium with metabolic determinants. Individuals with type 1 diabetes, aged above 18 years, were included and clinical characteristics were obtained from questionnaires and clinical records. In venous blood samples we measured cytokines and adipose-tissue specific secretion proteins. Serum magnesium concentrations were measured and correlated with clinical data and laboratory measurements using univariate and multivariate regression models. Hierarchical multiple regression of serum magnesium with insulin resistance was adjusted for diabetes and potential magnesium confounders. The prevalence of hypomagnesemia (serum magnesium levels < 0.7 mmol/L) was 2.9% in a cohort consisting of 241 individuals with type 1 diabetes. The magnesium concentration in the cohort was not associated with HbA (r = - 0.12, P-value = 0.068) nor with any inflammatory marker or adipokine. However, insulin dose (IU/kg), a surrogate measure of resistance in type 1 diabetes, moderated the association of serum magnesium (mmol/L) with HbA (mmol/mol) with a B coefficient of - 71.91 (95% CI: - 119.11; -24.71), P-value = 0.003) and Log high-sensitivity C-reactive protein (Log mg/L) - 2.09 (95% CI: - 3.70; - 0.48), P-value = 0.011). The association of low serum magnesium levels with glycaemic control (HbA) and high-sensitivity C-reactive protein in individuals with type 1 diabetes is limited to subjects using a high insulin dose and suggests that insulin resistance, a type 2 diabetes feature, is a prerequisite for hypomagnesemia.
在一组 1 型糖尿病成年人中，我们研究了低镁血症的患病率，以及血清镁水平与代谢决定因素（如糖化血红蛋白（HbA））、炎症标志物和循环细胞因子的相关性。此外，我们评估了胰岛素抵抗的替代指标是否对血清镁与代谢决定因素的可能相关性至关重要。纳入年龄大于 18 岁的 1 型糖尿病患者，通过问卷调查和临床记录获取临床特征。在静脉血样本中，我们测量了细胞因子和脂肪组织特异性分泌蛋白。使用单变量和多变量回归模型测量血清镁浓度，并与临床数据和实验室测量值相关联。使用多元逐步回归模型，将血清镁与胰岛素抵抗进行分层调整，以调整糖尿病和潜在的镁混杂因素。在由 241 名 1 型糖尿病患者组成的队列中，低镁血症（血清镁水平<0.7mmol/L）的患病率为 2.9%。该队列的镁浓度与 HbA（r=−0.12，P 值=0.068）或任何炎症标志物或脂肪因子均无相关性。然而，胰岛素剂量（IU/kg），1 型糖尿病的抵抗替代指标，调节了血清镁（mmol/L）与 HbA（mmol/mol）的相关性，B 系数为−71.91（95%可信区间：−119.11；−24.71），P 值=0.003）和 Log 高敏 C 反应蛋白（Log mg/L）-2.09（95%可信区间：-3.70；-0.48），P 值=0.011）。在使用高胰岛素剂量的 1 型糖尿病患者中，低血清镁水平与血糖控制（HbA）和高敏 C 反应蛋白之间的相关性仅限于患者，这表明胰岛素抵抗，2 型糖尿病的特征，是低镁血症的先决条件。
