Cardiac fibrosis and vascular remodeling are attenuated by metformin in obese rats

Burla, A; Lobato, Núbia de Souza; Fortes, Zuleica Bruno; Oigman, Wille; Neves, Mário Fritsch

doi:10.1016/j.ijcard.2011.09.012

Cited by 31 publications

(18 citation statements)

References 52 publications

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“…Based on animal work, it appears that metformin exerts its cardioprotective effect at the cellular level by affecting cardiac remodeling and preventing further oxidative injury to the cells [14,30]. Rena et al [17] reviewed the molecular mechanism of actions of metformin and suggested that metformininduced activation of AMP-activated protein kinase may be important in enhanced expression of eNOS and PPARγ-coactivator-1α which are important regulators of mitochondrial biogenesis and function and play important role in the development of heart failure.…”

Section: Discussionmentioning

confidence: 99%

The Effect of Metformin Use on Left Ventricular Ejection Fraction and Mortality Post-Myocardial Infarction

Abualsuod

Rutland

Watts

et al. 2015

Cardiovasc Drugs Ther

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Section: Discussionmentioning

confidence: 99%

The Effect of Metformin Use on Left Ventricular Ejection Fraction and Mortality Post-Myocardial Infarction

Abualsuod

Rutland

Watts

et al. 2015

Cardiovasc Drugs Ther

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“…Metformin has also been reported to improve endothelial function in normoinsulinemic, normalweight polycystic ovary syndrome patients (35), suggesting a possible direct effect of the drug on arterial cells beside putative secondary effects due to the glucose-lowering properties. Furthermore, several animal studies show that metformin improves endothelial function and reduces remodeling; for example, in a rat model of induced obesity and insulin resistance, metformin has been shown to attenuate hypertrophic vascular remodeling (36). Likewise, in a rat model of nonobese T2D, metformin improved the levels of glycation, vascular oxidative stress, and nitric oxide availability and normalized endothelial function on aorta (37).…”

Section: Discussionmentioning

confidence: 99%

Metformin, but Not Rosiglitazone, Attenuates the Increasing Plasma Levels of a New Cardiovascular Marker, Fibulin-1, in Patients With Type 2 Diabetes

et al. 2014

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OBJECTIVEThe extracellular matrix protein fibulin-1 is upregulated in the arterial wall in type 2 diabetes (T2D) and circulates in increased concentrations in diabetes. Metformin is an antidiabetic drug with beneficial cardiovascular disease effects in diabetes. We hypothesized that metformin would influence the increased level of plasma fibulin-1 in diabetes. RESEARCH DESIGN AND METHODSAfter a 4-week run-in period, 371 eligible patients with T2D were randomized to treatment groups in a factorial design including insulin alone (control), +metfor-min, +rosiglitazone, or +both metformin and rosiglitazone. Plasma fibulin-1 was analyzed at the beginning of the study and after 18 and 24 months. RESULTSPlasma fibulin-1 increased in all groups throughout the 2-year period; however, the increase was strongly attenuated among patients treated with metformin. A highly significant difference was observed when the mean change in plasma fibulin-1 was compared between metformin-and non-metformin-treated individuals both at 18 and 24 months of treatment, but rosiglitazone had no effect. Metformin and rosiglitazone alone reduced the HbA 1c levels to comparable levels and in combination even further. CONCLUSIONSMetformin attenuates the increase in plasma fibulin-1 concentrations in T2D, independently of glycemic effects. Changes in fibulin-1 may reflect an important element in diabetic arteriopathy that can be influenced by metformin. Increased mortality and morbidity owing to a higher incidence of cardiovascular diseases (CVDs) is a major clinical challenge in type 2 diabetes (T2D) (1,2). Several studies have demonstrated that management of hypertension, LDL cholesterol, and other major CVD risk factors have reduced micro-and macrovascular complications in patients with T2D; however, optimal risk reduction is still not achieved when these important risk factors are controlled, indicating that further attempts are needed to control the CVD risk burden (3-5). One assumption is that improvement

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“…13 Furthermore, metformin treatment attenuated vascular remodeling in monosodium glutamate-induced obese rats. 14 Numerous experimental studies indicate that activation of adenosine monophosphate-activated protein kinase (AMPK) partly mediates the pleiotropic effects of metformin. [15][16][17] As a stress-activated protein kinase, AMPK plays a role in the regulation of energy and metabolic homeostasis.…”

mentioning

confidence: 99%

Metformin stimulates ischemia-induced revascularization through an eNOS dependent pathway in the ischemic hindlimb mice model

Takahashi

Shibata

Ouchi

et al. 2015

Journal of Vascular Surgery

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Cardiac fibrosis and vascular remodeling are attenuated by metformin in obese rats

Abstract: Hypertrophic vascular remodeling and cardiac collagen deposition were significantly evident in MSG-induced obese rats. Metformin treatment was able to reduce insulin resistance and attenuated this adverse cardiac and vascular remodeling.

Cited by 31 publications

References 52 publications

The Effect of Metformin Use on Left Ventricular Ejection Fraction and Mortality Post-Myocardial Infarction

The Effect of Metformin Use on Left Ventricular Ejection Fraction and Mortality Post-Myocardial Infarction

Metformin, but Not Rosiglitazone, Attenuates the Increasing Plasma Levels of a New Cardiovascular Marker, Fibulin-1, in Patients With Type 2 Diabetes

Metformin stimulates ischemia-induced revascularization through an eNOS dependent pathway in the ischemic hindlimb mice model

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