Jaccard Evrim, Seyssel Kévin, Gouveia Alexandre, Vergely Catherine, Baratali Laila, Gubelmann Cédric, Froissart Marc, Favrat Bernard, Marques-Vidal Pedro, Tappy Luc, Waeber Gérard
Department of Medicine, Lausanne University Hospital (CHUV) and University of Lausanne, rue du Bugnon 46, Lausanne 1011, Switzerland.
Department of Biomedical Sciences, Faculty of Biology and Medicine, University of Lausanne, rue du Bugnon 7a, Lausanne 1005, Switzerland.
EClinicalMedicine. 2022 May 6;48:101434. doi: 10.1016/j.eclinm.2022.101434. eCollection 2022 Jun.
Chronic exposure to high iron levels increases diabetes risk partly by inducing oxidative stress, but the consequences of acute iron administration on beta cells are unknown. We tested whether the acute administration of iron for the correction of iron deficiency influenced insulin secretion and the production of reactive oxygen species.
Single-center, double-blinded, randomized controlled trial conducted between June 2017 and March 2020. 32 women aged 18 to 47 years, displaying symptomatic iron deficiency without anaemia, were recruited from a community setting and randomly allocated (1:1) to a single infusion of 1000 mg intravenous ferric carboxymaltose (iron) or saline (placebo). The primary outcome was the between group mean difference from baseline to day 28 in first and second phase insulin secretion, assessed by a two-step hyperglycaemic clamp. All analyses were performed by intention to treat. This trial was registered in ClinicalTrials.gov NCT03191201.
Iron infusion did not affect first and second phase insulin release. For first phase, the between group mean difference from baseline to day 28 was 0 μU × 10 min/mL [95% CI, -22 to 22, = 0.99]. For second phase, it was -5 μUx10min/mL [95% CI, -161 to 151; = 0.95] at the first plateau of the clamp and -249 μUx10min/mL [95% CI, -635 to 137; = 0.20] at the second plateau. Iron infusion increased serum ascorbyl/ascorbate ratio, a marker of plasma oxidative stress, at day 14, with restoration of normal ratio at day 28 relative to placebo. Finally, high-sensitive C-reactive protein levels remained similar among groups.
In iron deficient women without anaemia, intravenous administration of 1000 mg of iron in a single sitting did not impair glucose-induced insulin secretion despite a transient increase in the levels of circulating reactive oxygen species.
The Swiss National Science Foundation, University of Lausanne and Leenaards, Raymond-Berger and Placide Nicod Foundations.
长期暴露于高铁水平会部分通过诱导氧化应激增加糖尿病风险，但急性给予铁剂对β细胞的影响尚不清楚。我们测试了急性给予铁剂以纠正缺铁是否会影响胰岛素分泌和活性氧的产生。
2017年6月至2020年3月进行的单中心、双盲、随机对照试验。从社区招募了32名年龄在18至47岁之间、有缺铁症状但无贫血的女性，并将她们随机（1:1）分配接受单次静脉输注1000毫克羧麦芽糖铁（铁剂）或生理盐水（安慰剂）。主要结局是通过两步高血糖钳夹法评估从基线到第28天第一和第二阶段胰岛素分泌的组间平均差异。所有分析均按意向性分析进行。该试验已在ClinicalTrials.gov注册，注册号为NCT03191201。
铁剂输注不影响第一和第二阶段胰岛素释放。对于第一阶段，从基线到第28天的组间平均差异为0 μU×10分钟/毫升[95%置信区间，-22至22，P = 0.99]。对于第二阶段，在钳夹的第一个平台期为-5 μU×10分钟/毫升[95%置信区间，-161至151；P = 0.95]，在第二个平台期为-249 μU×10分钟/毫升[95%置信区间，-635至137；P = 0.20]。铁剂输注在第14天时增加了血清抗坏血酸/抗坏血酸盐比率，这是血浆氧化应激的一个指标，相对于安慰剂，在第28天时恢复到正常比率。最后，各小组间高敏C反应蛋白水平保持相似。
在无贫血的缺铁女性中，单次静脉给予1000毫克铁剂不会损害葡萄糖诱导的胰岛素分泌，尽管循环活性氧水平会短暂升高。
瑞士国家科学基金会、洛桑大学以及Leenaards、Raymond-Berger和Placide Nicod基金会。
