Liraglutide alleviates myocardial ischemia‒reperfusion injury in diabetic mice

Fang, Binbin; Liu, Fen; Yu, Xiaolin; Luo, Jun‐Yi; Zhang, Xuehe; Zhang, Tong; Zhang, Jixin; Yang, Yining; Li, Xiaomei

doi:10.1016/j.mce.2023.111954

Cited by 5 publications

(1 citation statement)

References 30 publications

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“…The relationship between AMPK and GLP1-RA is well-known with special regard to cardiovascular benefits ( 34 ). For instance, liraglutide increased AMPK phosphorylation in the heart of diabetic mice ( 35 ), inducing effects similar to those of metformin ( 36 , 37 ). In another study, a short-term treatment with a weight-neutral dose of liraglutide could reverse the molecular pathophysiology of obesity-induced heart disease in mice through various mechanisms, among which a pivotal role is played by AMPK ( 38 ).…”

Section: The Relationship Between Ampk and Antidiabetic Drugsmentioning

confidence: 99%

GLP-1 RAs and SGLT2i: two antidiabetic agents associated with immune and inflammation modulatory properties through the common AMPK pathway

Mazzieri,

Basta,

Calafiore

et al. 2023

Front. Immunol.

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Immune cells and other cells respond to nutrient deprivation by the classic catabolic pathway of AMPK (Adenosine monophosphate kinase). This kinase is a pivotal regulator of glucose and fatty acids metabolism, although current evidence highlights its role in immune regulation. Indeed AMPK, through activation of Foxo1 (Forkhead box O1) and Foxo3 (Forkhead box O3), can regulate FOXP3, the key gene for differentiation and homeostasis of Tregs (T regulators lymphocytes). The relevance of Tregs in the onset of T1D (Type 1 diabetes) is well-known, while their role in the pathogenesis of T2D (Type 2 diabetes) is not fully understood yet. However, several studies seem to indicate that Tregs may oppose the progression of diabetic complications by mitigating insulin resistance, atherosclerosis, and damage to target organs (as in kidney disease). Hence, AMPK and AMPK-activating agents may play a role in the regulation of the immune system. The connection between metformin and AMPK is historically known; however, this link and the possible related immune effects are less studied about SGLT2i (Sodium-glucose co-transport 2 inhibitors) and GLP1-RAs (Glucagon-like peptide-1 receptor agonists). Actual evidence shows that the negative caloric balance, induced by SGLT2i, can activate AMPK. Conversely and surprisingly, an anabolizing agent like GLP-1RAs can also upregulate this kinase through cAMP (Cyclic adenosine monophosphate) accumulation. Therefore, both these drugs can likely lead to the activation of the AMPK pathway and consequential proliferation of Tregs. These observations seem to confirm not only the metabolic but also the immunoregulatory effects of these new antidiabetic agents.

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