Metformin monotherapy significantly decreases epicardial adipose tissue thickness in newly diagnosed type 2 diabetes patients

Zıyrek, Murat; Kahraman, Serkan; Ozdemir, Emrah; Doğan, Ali

doi:10.1016/j.repc.2018.08.010

Cited by 45 publications

(29 citation statements)

References 28 publications

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“…The effect of metformin use on epicardial adipose tissue was investigated, and it decreases the epicardial adipose tissue. 13 Similarly, metformin use in obese children with insulin resistance decreased epicardial adipose tissues in our study.…”

Section: Discussionsupporting

confidence: 72%

“…Epicardial adipose tissue correlates with visceral adipose tissue and causes a local inflammatory response and increased insulin resistance with similar pathophysiology which ultimately results in cardiovascular risk increase. 13 Although findings are indicating a decreasing effect of metformin on epicardial adipose tissue in adults, there has been no information related to this issue in the paediatric population.…”

mentioning

confidence: 99%

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Effects of metformin on epicardial adipose tissue and atrial electromechanical delay of obese children with insulin resistance

Güneş

Özmen

et al. 2020

Cardiol Young

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Introduction: Obesity is usually related to insulin resistance and glucose metabolism disorders. The relationship between insulin resistance and epicardial adipose tissue and atrial electromechanical delay has been described in previous studies. Aim: This study aims to demonstrate the effects of metformin on epicardial adipose tissue and electromechanical delay in patients using metformin for insulin resistance. Materials and methods: A total of 30 patients using metformin for insulin resistance were included in the study. Pre-treatment and post-treatment epicardial adipose tissue and electromechanical delay were evaluated. Results: There was a statistically significant decrease in epicardial adipose tissue thickness after 3 months of metformin therapy (6.4 ± 2.1 versus 4.7 ± 2.0; p = 0.008). Furthermore, the inter-atrial and intra-atrial electromechanical delay also significantly decreased after 3 months of metformin monotherapy (23.6 ± 8.2 versus 18.1 ± 5.8; p < 0.001, 9.1 ± 2.9 versus 6.3 ± 3.6; p = 0.003, respectively). Conclusion: In this study, we show that metformin monotherapy significantly decreases epicardial adipose tissue thickness and electromechanical delay in obese children.

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Section: Discussionsupporting

confidence: 72%

mentioning

confidence: 99%

Effects of metformin on epicardial adipose tissue and atrial electromechanical delay of obese children with insulin resistance

Güneş

Özmen

et al. 2020

Cardiol Young

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“…Studies reported in abstract form have associated metformin treatment with redistribution of fat from central to subcutaneous depots 106 and with a reduction in the thickness of epicardial adipose tissue in people with type 2 diabetes. 107 Metformin treatment also modestly improves the lipid profile where, typically, small reductions in LDL cholesterol and triglycerides are seen, with little effect on HDL cholesterol. [108][109][110] A meta-analysis concluded that blood pressure was essentially unaffected by metformin in people with diabetes, 110 although a second meta-analysis demonstrated an average reduction in systolic blood pressure of about 2 mmHg, with larger effects seen in subjects with impaired glucose tolerance or obesity.…”

Section: Body Weight Fat Distribution and Other Classical Cardiovmentioning

confidence: 99%

Mechanisms of action of metformin with special reference to cardiovascular protection

Zilov

Abdelaziz

Alshammary

et al. 2019

Diabetes Metabolism Res

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Summary Management guidelines continue to identify metformin as initial pharmacologic antidiabetic therapy of choice for people with type 2 diabetes without contraindications, despite recent randomized trials that have demonstrated significant improvements in cardiovascular outcomes with newer classes of antidiabetic therapies. The purpose of this review is to summarize the current state of knowledge of metformin's therapeutic actions on blood glucose and cardiovascular clinical evidence and to consider the mechanisms that underlie them. The effects of metformin on glycaemia occur mainly in the liver, but metformin‐stimulated glucose disposal by the gut has emerged as an increasingly import site of action of metformin. Additionally, metformin induces increased secretion of GLP‐1 from intestinal L‐cells. Clinical cardiovascular protection with metformin is supported by three randomized outcomes trials (in newly diagnosed and late stage insulin‐treated type 2 diabetes patients) and a wealth of observational data. Initial evidence suggests that cotreatment with metformin may enhance the impact of newer incretin‐based therapies on cardiovascular outcomes, an important observation as metformin can be combined with any other antidiabetic agent. Multiple potential mechanisms support the concept of cardiovascular protection with metformin beyond those provided by reduced blood glucose, including weight loss, improvements in haemostatic function, reduced inflammation, and oxidative stress, and inhibition of key steps in the process of atherosclerosis. Accordingly, metformin remains well placed to support improvements in cardiovascular outcomes, from diagnosis and throughout the course of type 2 diabetes, even in this new age of improved outcomes in type 2 diabetes.

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“…AMPK is also activated in stressful conditions and glucose deprivation [202] for increase in glucose metabolism and mitochondrial biogenesis. An observational trial in diabetic patients under metformin treatment reduced the epicardial adipose tissue thickness [203]. These process in combination with the anti-inflammatory and antioxidant effects might explain the protective benefits on diabetic with cardiovascular disease [204].…”

Section: Metforminmentioning

confidence: 99%

“…Table 1 and Figure 1 show the energy substrates in pathological conditions. [203]. These process in combination with the antiinflammatory and antioxidant effects might explain the protective benefits on diabetic with cardiovascular disease [204].…”

Section: Hypertrophic Cardiomyocytes and Metabolismmentioning

confidence: 99%

Myocardium Metabolism in Physiological and Pathophysiological States: Implications of Epicardial Adipose Tissue and Potential Therapeutic Targets

Gandoy-Fieiras¹,

González-Juanàtey

Eiras

2020

IJMS

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The main energy substrate of adult cardiomyocytes for their contractility are the fatty acids. Its metabolism generates high ATP levels at the expense of high oxygen consumption in the mitochondria. Under low oxygen supply, they can get energy from other substrates, mainly glucose, lactate, ketone bodies, etc., but the mitochondrial dysfunction, in pathological conditions, reduces the oxidative metabolism. In consequence, fatty acids are stored into epicardial fat and its accumulation provokes inflammation, insulin resistance, and oxidative stress, which enhance the myocardium dysfunction. Some therapies focused on improvement the fatty acids entry into mitochondria have failed to demonstrate benefits on cardiovascular disorders. Oppositely, those therapies with effects on epicardial fat volume and inflammation might improve the oxidative metabolism of myocardium and might reduce the cardiovascular disease progression. This review aims at explain (a) the energy substrate adaptation of myocardium in physiological conditions, (b) the reduction of oxidative metabolism in pathological conditions and consequences on epicardial fat accumulation and insulin resistance, and (c) the reduction of cardiovascular outcomes after regulation by some therapies.

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Metformin monotherapy significantly decreases epicardial adipose tissue thickness in newly diagnosed type 2 diabetes patients

Cited by 45 publications

References 28 publications

Effects of metformin on epicardial adipose tissue and atrial electromechanical delay of obese children with insulin resistance

Effects of metformin on epicardial adipose tissue and atrial electromechanical delay of obese children with insulin resistance

Mechanisms of action of metformin with special reference to cardiovascular protection

Myocardium Metabolism in Physiological and Pathophysiological States: Implications of Epicardial Adipose Tissue and Potential Therapeutic Targets

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