Key result
Imeglimin administered for 9 or 90 days in a rat model of metabolic syndrome decreased LV end-diastolic pressure and ROS production, and increased LV tissue perfusion compared to untreated animals.
Why the study?
It was unknown whether imeglimin-induced decreases in ROS overproduction and improved glucose homeostasis confer protective effects on metabolic syndrome-related LV and vascular dysfunctions.
Does imeglimin improve cardiorenal and vascular dysfunction in a rat model of metabolic syndrome?
Does imeglimin improve cardiorenal and vascular dysfunction in a rat model of metabolic syndrome?
In a rat model of metabolic syndrome, imeglimin improved cardiac diastolic and vascular function independently of glucose control.
Imeglimin shows cardiorenal effects in rats; hypothesis-generating for human metabolic syndrome trials and should not yet change practice.
INTRODUCTION: Imeglimin, a glucose-lowering agent targeting mitochondrial bioenergetics, decreases reactive oxygen species (ROS) overproduction and improves glucose homeostasis. We investigated whether this is associated with protective effects on metabolic syndrome-related left ventricular (LV) and vascular dysfunctions. METHODS: rats to assess the effects on LV function, LV tissue perfusion, LV oxidative stress and vascular function induced by imeglimin administered orally for 9 or 90 days at a dose of 150 mg/kg twice daily. RESULTS: Compared to untreated animals, 9- and 90-day imeglimin treatment decreased LV end-diastolic pressure and LV end-diastolic pressure-volume relation, increased LV tissue perfusion and decreased LV ROS production. Simultaneously, imeglimin restored acetylcholine-mediated coronary relaxation and mesenteric flow-mediated dilation. One hour after imeglimin administration, when glucose plasma levels were not yet modified, imeglimin reduced LV mitochondrial ROS production and improved LV function. Ninety-day imeglimin treatment reduced related LV and kidney fibrosis and improved kidney function. CONCLUSION: In a rat model, mimicking Human metabolic syndrome, imeglimin immediately countered metabolic syndrome-related cardiac diastolic and vascular dysfunction by reducing oxidative stress/increased NO bioavailability and improving myocardial perfusion and after 90-day treatment myocardial and kidney structure, effects that are, at least in part, independent from glucose control.
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Lachaux et al. (2020) studied metabolic syndrome. imeglimin vs. untreated animals was evaluated on LV function, LV tissue perfusion, LV oxidative stress and vascular function. Imeglimin administered for 9 or 90 days in a rat model of metabolic syndrome decreased LV end-diastolic pressure and ROS production, and increased LV tissue perfusion compared to untreated animals.
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