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降压治疗诱发2型糖尿病:α-内收蛋白、血管紧张素转换酶及胰岛素受体底物-1基因有何作用?

Induction of Type 2 Diabetes Mellitus with Antihypertensive Therapy: Is There Any Role of Alpha Adducin, ACE, and IRS-1 Gene?

作者信息

Gupta Sumeet, Jhawat Vikas

机构信息

Department of Pharmacology, M. M. College of Pharmacy, M. M. University, Mullana, Ambala, Haryana, India.

Department of Pharmacology, M. M. College of Pharmacy, M. M. University, Mullana, Ambala, Haryana, India.

出版信息

Value Health Reg Issues. 2017 May;12:90-98. doi: 10.1016/j.vhri.2016.10.005. Epub 2017 May 19.

DOI:10.1016/j.vhri.2016.10.005
PMID:28648322
Abstract

Hypertension and diabetes are related disorders that share common pathophysiological pathways and occur together. Although hypertension itself is a risk factor for developing diabetes, prolonged use of first-line antihypertensive therapy has also been reported to induce diabetes. Genetic polymorphism of genes affecting salt sensitivity and insulin resistance can have a role in antihypertensive therapy-induced diabetes. Polymorphism of the alpha adducin gene, angiotensin-converting enzyme gene, and insulin receptor substrate 1 gene has been found to be associated with new incident diabetes in hypertensive patients via salt sensitivity and insulin resistance. Many studies have, however, revealed a negative correlation with this hypothesis and have shown no role of antihypertensive therapy in diabetes induction. Therefore, more detailed experimental studies are needed to reach a final conclusion.

摘要

高血压和糖尿病是相关疾病,它们具有共同的病理生理途径且常同时发生。虽然高血压本身是患糖尿病的一个危险因素,但也有报道称长期使用一线抗高血压疗法会诱发糖尿病。影响盐敏感性和胰岛素抵抗的基因的遗传多态性可能在抗高血压疗法诱发的糖尿病中起作用。已发现α-加ducin基因、血管紧张素转换酶基因和胰岛素受体底物1基因的多态性通过盐敏感性和胰岛素抵抗与高血压患者新发糖尿病相关。然而,许多研究揭示了与这一假设的负相关关系,并表明抗高血压疗法在糖尿病诱发中不起作用。因此,需要更详细的实验研究才能得出最终结论。

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引用本文的文献

1
Angiotensin Converting Enzyme Gene Insertion/Deletion Polymorphism Is Not Responsible for Antihypertensive Therapy Induced New Onset of Type 2 Diabetes in Essential Hypertension.血管紧张素转换酶基因插入/缺失多态性与原发性高血压患者抗高血压治疗诱发的2型糖尿病新发无关。
Clin Med Insights Endocrinol Diabetes. 2019 Jan 23;12:1179551418825037. doi: 10.1177/1179551418825037. eCollection 2019.