Evidence map›Paper›PMID 40970225›Full record

ArticleDiabetes, metabolic syndrome and obesity : targets and therapy2025

α-ALA Attenuates Cardiac Injury in Diabetic Heart Disease Mice by Modulating Inflammation and AMPKα1.

Xuan Liu, Landi Wang, Weiwei Dong, Yuchao Wang, Dayong Li

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Article in Diabetes, metabolic syndrome and obesity : targets and therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

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5 authors.

Xuan Liu *Office of Good Clinical Practice, Tianjin Fourth Center Hospital, Tianjin, People's Republic of China.
Landi Wang *Graduate School, Tianjin University, Tianjin, People's Republic of China.
Weiwei Dong *Department of Nuclear Medicine, Tianjin Fourth Center Hospital, Tianjin, People's Republic of China.
Yuchao WangGraduate School, Tianjin Medical University, Tianjin, People's Republic of China.
Dayong LiNHC 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.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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. AMPKα1, 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 AMPKα1is 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 AMPKα1. Conclusion: The results of this study provide evidence that α-ALA protects against HFD/STZ (T2DM)-induced cardiac injury by alleviating inflammation and upregulating AMPKα1.

Indexed as

AMPKα1diabetic heart diseaseinflammationα-ALA

Identifiers

PMID40970225
PMCPMC12442922

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