摘要
背景:糖尿病患者因心血管并发症而死亡的风险增加。补充特定的含硫氨基酸正在迅速成为糖尿病及相关心血管并发症的一种可能的治疗佐剂。 观察:众所周知,氧化应激在糖尿病性心血管疾病的发病机制中起着重要的作用,氧化应激与血脂异常、胰岛素抵抗等代谢综合征症状有关。半胱氨酸和牛磺酸是最常见的含硫氨基酸,其细胞水平在糖尿病期间下降,这可能导致心肌病的发展。虽然含硫药物对心脏细胞和亚细胞的功能有多种作用,但它们也具有抗氧化作用,因此在不同的病理生理条件下可能发挥有益的作用。 结论:半胱氨酸和牛磺酸可降低心肌氧化应激,可能是减轻糖尿病所致心脏亚细胞和功能异常的重要机制。
关键词: 含硫氨基酸,牛磺酸,半胱氨酸,糖尿病,糖尿病心肌病,预防性营养。
Current Medicinal Chemistry
Title:Attenuation of Diabetes-induced Cardiac and Subcellular Defects by Sulphur-containing Amino Acids
Volume: 25 Issue: 3
关键词: 含硫氨基酸,牛磺酸,半胱氨酸,糖尿病,糖尿病心肌病,预防性营养。
摘要: Background: Patients with diabetes mellitus have an increased risk of mortality due to cardiovascular complications. Supplementation with specific sulphur-containing amino acids is rapidly emerging as a possible therapeutic adjuvant for diabetes and associated cardiovascular complications.
Observations: It is well-known that oxidative stress plays an important role in the pathogenesis of diabetes-induced cardiovascular disease, which is invariably associated with abnormal blood lipid profile, insulin resistance and other symptoms of metabolic syndrome. Cysteine and taurine are among the most common sulphur-containing amino acids and their cellular levels decline during diabetes that may contribute to the development of the cardiomyopathy. Although sulphur-containing agents exert multiple actions on cellular and subcellular functions in the heart, they also exhibit antioxidant properties and thus may exert beneficial effects in different pathophysiological conditions.
Conclusion: It is concluded that reduction of oxidative stress by cysteine and taurine may serve as an important mechanism for the attenuation of diabetes-induced subcellular and functional abnormalities in the heart.
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Cite this article as:
Attenuation of Diabetes-induced Cardiac and Subcellular Defects by Sulphur-containing Amino Acids, Current Medicinal Chemistry 2018; 25 (3) . https://dx.doi.org/10.2174/0929867324666170705115207
DOI https://dx.doi.org/10.2174/0929867324666170705115207 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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