Key result
Liraglutide ameliorated cardiac dysfunction in diabetic rats, significantly increasing left ventricular systolic pressure from 91.39 mmHg to 110.76 mmHg.
Why the study?
Liraglutide shows potent cardioprotective effects through incompletely understood mechanisms, and this study investigated whether it improves cardiac function in type 2 diabetic rats by enhancing caveolin-3 expression.
Does liraglutide improve cardiac function and ameliorate diabetic cardiomyopathy in a rat model of type 2 diabetes mellitus?
Does liraglutide improve cardiac function and ameliorate diabetic cardiomyopathy in a rat model of type 2 diabetes mellitus?
Liraglutide ameliorates diabetic cardiomyopathy in a rat model by reducing oxidative stress and improving Cav3/eNOS/NO signaling and Cav3-RyR2 interaction.
Answers are grounded in this paper and cite their sources.
Should not yet change practice; leaves open Cav3 as a mediator of liraglutide cardioprotection in T2DM.
Background Liraglutide (LIRA), a Glucagon-like peptide-1 receptor agonist (GLP-1RA), showed potent cardioprotective effects with the mechanism remained incompletely understood. Caveolin-3 (Cav3) is the cardiomyocytes specific caveolae structural protein, decreased in the diabetic heart. Therefore, this study aimed to investigate whether LIRA exerts its effect on cardiac function in rats with type 2 diabetes mellitus (T2DM) via enhance Cav3 expression. Methods T2DM rats were used as study subjects and randomly divided into four groups: 1) CON group, 2) CON+L group, 3) DM group and 4) DM+L group. All rats received either saline or LIRA 0.2 mg/kg (by i.p injection) per day for 4 weeks. After the model was successfully established, cardiac function was determined by invasive hemodynamic evaluation methods. Immunohistochemistry and western blot were performed to understand the molecular mechanism between cardiac function and LIRA. Results Based on our results, DM group displayed higher blood glucose than Con group (20.57±2.75 mol/L vs. 4.34±0.21 mol/L), while blood glucose level in DM+L group was lower than DM group after received LIRA (10.36±1.84 mol/L). LVSP (91.39±4.98 mmHg), LV +dp/dtmax (4040.74±197.72 mmHg/s) were significantly reduced in DM group, and diabetic rats also exhibited reduced -dp/dtmax (2926.5±142.3 mmHg/s) and elevated LVEDP (10.87±0.83 mmHg). LIRA treatment showed a trend to enhance LVSP (110.76±5.61 mmHg) and ± dp/dtmax (5860.41±200.32 mmHg and 3996.8±179.3 mmHg), decreased LVEDP (7.23±0.58 mmHg). The expression of Cav3, eNOS and RyR2 was significantly decreased in the myocardium in DM group, which increased in DM+L group after LIRA administrated. Hemodynamic data showed DM rats exhibited impairment of myocardial function, while LIRA improved cardiac systolic and diastolic function, attenuate diabetic cardiomyopathy injury by improving Cav3/eNOS/NO signaling, reducing ROS level in cardiac tissues, and increasing interaction of Cav3 and ryanodine receptor 2 (RyR2). Conclusions Liraglutide ameliorates cardiac dysfunction in rats with type 2 diabetes mellitus via reducing ROS level in cardiac tissues, improving Cav3/eNOS/NO signaling and increasing interaction of Cav3 and RyR2. Keywords Type-2 diabetes Mellitus, liraglutide, caveolin-3, ryanodine receptor2, myocardial dysfunction
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Li et al. (2021) studied Type 2 diabetes mellitus and diabetic cardiomyopathy (n=66). Liraglutide vs. Saline was evaluated on Left ventricular systolic pressure (LVSP) (p=<0.05). Liraglutide ameliorated cardiac dysfunction in diabetic rats, significantly increasing left ventricular systolic pressure from 91.39 mmHg to 110.76 mmHg.