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已发表论文
α-ALA 通过调节炎症和 AMPKα1 减轻糖尿病心肌病小鼠的心脏损伤
Authors Liu X, Wang L, Dong W, Wang Y, Li D
Received 26 May 2025
Accepted for publication 5 September 2025
Published 13 September 2025 Volume 2025:18 Pages 3491—3503
DOI https://doi.org/10.2147/DMSO.S537517
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Rebecca Conway
Xuan Liu,1,* Landi Wang,2,* Weiwei Dong,3,* Yuchao Wang,4 Dayong Li5
1Office of Good Clinical Practice, Tianjin Fourth Center Hospital, Tianjin, People’s Republic of China; 2Graduate School, Tianjin University, Tianjin, People’s Republic of China; 3Department of Nuclear Medicine, Tianjin Fourth Center Hospital, Tianjin, People’s Republic of China; 4Graduate School, Tianjin Medical University, Tianjin, People’s Republic of China; 5NHC Key Laboratory of Hormones and Development, Tianjin Key Laboratory of Metabolic Diseases, Chu Hsien-I Memorial Hospital & Tianjin Institute of Endocrinology, Tianjin Medical University, Tianjin, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Dayong Li, Email tjsdszxyywz2222@163.com
Introduction: Diabetic heart disease (DHD) is systolic and/or diastolic dysfunction of the heart muscle that occurs in patients with the presence of Type 2 diabetes mellitus. AMPKα 1, a key regulator of glucose metabolism, has been shown to promote glucose uptake and catabolism. Alpha-linolenic acid (α-ALA) is an essential fatty acid that helps to prevent cardiovascular disease and is very important for human health. However, its role as a medical agent in preventing DHD by modulating AMPKα 1is unknown.
Methods: An experimental type 2 diabetic mouse model was established by treating animals with a high-fat diet (HFD) for four weeks and intraperitoneal injection of streptozotocin (STZ) (50 mg/kg body weight). After induction of type 2 diabetes, the animals were treated orally with α-ALA (2 or 4 g/kg) for twelve weeks.
Results: The type 2 diabetic mice showed an increase in blood glucose levels, a decrease in body weight and cardiac dysfunction. Diabetic mice treated with α-ALA attenuated hyperglycaemia, dyslipidaemia, and cardiac dysfunction. In addition, α-ALA improved histological changes and fibrosis in HFD/STZ-induced mice. Type 2 diabetes in mice exacerbated the inflammatory status. α-ALA treatment significantly attenuated inflammation in diabetic hearts. The underlying mechanisms for this attenuation involved modulation of AMPKα 1.
Conclusion: The results of this study provide evidence that α-ALA protects against HFD/STZ (T2DM)-induced cardiac injury by alleviating inflammation and upregulating AMPKα 1.
Keywords: diabetic heart disease, α-ALA, AMPKα 1, inflammation
1Office of Good Clinical Practice, Tianjin Fourth Center Hospital, Tianjin, People’s Republic of China; 2Graduate School, Tianjin University, Tianjin, People’s Republic of China; 3Department of Nuclear Medicine, Tianjin Fourth Center Hospital, Tianjin, People’s Republic of China; 4Graduate School, Tianjin Medical University, Tianjin, People’s Republic of China; 5NHC Key Laboratory of Hormones and Development, Tianjin Key Laboratory of Metabolic Diseases, Chu Hsien-I Memorial Hospital & Tianjin Institute of Endocrinology, Tianjin Medical University, Tianjin, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Dayong Li, Email tjsdszxyywz2222@163.com
Introduction: Diabetic heart disease (DHD) is systolic and/or diastolic dysfunction of the heart muscle that occurs in patients with the presence of Type 2 diabetes mellitus. AMPKα 1, a key regulator of glucose metabolism, has been shown to promote glucose uptake and catabolism. Alpha-linolenic acid (α-ALA) is an essential fatty acid that helps to prevent cardiovascular disease and is very important for human health. However, its role as a medical agent in preventing DHD by modulating AMPKα 1is unknown.
Methods: An experimental type 2 diabetic mouse model was established by treating animals with a high-fat diet (HFD) for four weeks and intraperitoneal injection of streptozotocin (STZ) (50 mg/kg body weight). After induction of type 2 diabetes, the animals were treated orally with α-ALA (2 or 4 g/kg) for twelve weeks.
Results: The type 2 diabetic mice showed an increase in blood glucose levels, a decrease in body weight and cardiac dysfunction. Diabetic mice treated with α-ALA attenuated hyperglycaemia, dyslipidaemia, and cardiac dysfunction. In addition, α-ALA improved histological changes and fibrosis in HFD/STZ-induced mice. Type 2 diabetes in mice exacerbated the inflammatory status. α-ALA treatment significantly attenuated inflammation in diabetic hearts. The underlying mechanisms for this attenuation involved modulation of AMPKα 1.
Conclusion: The results of this study provide evidence that α-ALA protects against HFD/STZ (T2DM)-induced cardiac injury by alleviating inflammation and upregulating AMPKα 1.
Keywords: diabetic heart disease, α-ALA, AMPKα 1, inflammation