Research Topic

The role of Epicardial Fat Tissue in Diabetes Multiorgan Complications

About this Research Topic

Complications of Diabetes Mellitus (DM) affect human health beyond glucose metabolism and its impact on acute conditions such as severe hyperglycaemia or ketoacidosis. Chronic complications of type 2 DM (T2DM) cause irreparable damages to many organs and systems, being difficult to find an organ not affected by diabetes. Microvascular and macrovascular complications are responsible for morbidity and mortality associated to T2DM. Besides, metabolic derangements accompanying T2DM are associated with an increase in obesity and specifically in visceral fat deposits, which are prominent in these patients and are considered an independent risk factor for cardiovascular disease (CVD). Among the different type of visceral adipose tissues, epicardial fat (EAT) has received special attention given that it surrounds and infiltrates the myocardium and coronary arteries. Due to the close anatomical proximity to the heart and the absence of fascial boundaries, EAT may interact locally with the surrounding tissues through paracrine and vasocrine secretion of pro-inflammatory and pro-atherogenic adipokines which could impact directly on myocardium.
Multiple mechanisms have been proposed in the development of diabetic complications in coronary patients associated with increased EAT volume. It is clear that some pathways are not yet completely identified. Lipid composition in EAT and their oxidation are very frequent in DM, promoting mitochondrial dysfunction, enhanced inflammation, fibrogenesis and apoptosis. So far, the identification of lipid species more prone to be oxidized, as well as the impact of these products on insulin signalling pathway are relevant. In this regard, several mechanisms remain to be elucidated for the understanding of T2DM multiple organ damage.
To this point, the scope of this subject is wide, focusing not only on the impact of glucose and insulin-resistance on EAT, heart and related organs, but also on the description of new mechanisms and pathological consequences of T2DM. This Research Topic will explore how elevated EAT can lead to further complications in patients with DM. Articles covering pathophysiologic changes at the EAT expansion and it impacts on heart health, new biomarkers proposed for EAT evaluation and the impact of life style changes and pharmacological treatment are welcome. In addition, the editors appreciate studies including omics research to clarify the role of different biological species in the organ cross-talk and the challenge of selecting the appropriate methods to resolve the remaining queries.


Keywords: Diabetes, Macrovascular complications, microvascular complications, insulin-resistance, obesity, systemic low-level inflammation, glucose metabolism, chronic disease, oxidative stress, omics, EAT, epicardial fat tissue, cardiovascular disease, cardiovascular complications


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

Complications of Diabetes Mellitus (DM) affect human health beyond glucose metabolism and its impact on acute conditions such as severe hyperglycaemia or ketoacidosis. Chronic complications of type 2 DM (T2DM) cause irreparable damages to many organs and systems, being difficult to find an organ not affected by diabetes. Microvascular and macrovascular complications are responsible for morbidity and mortality associated to T2DM. Besides, metabolic derangements accompanying T2DM are associated with an increase in obesity and specifically in visceral fat deposits, which are prominent in these patients and are considered an independent risk factor for cardiovascular disease (CVD). Among the different type of visceral adipose tissues, epicardial fat (EAT) has received special attention given that it surrounds and infiltrates the myocardium and coronary arteries. Due to the close anatomical proximity to the heart and the absence of fascial boundaries, EAT may interact locally with the surrounding tissues through paracrine and vasocrine secretion of pro-inflammatory and pro-atherogenic adipokines which could impact directly on myocardium.
Multiple mechanisms have been proposed in the development of diabetic complications in coronary patients associated with increased EAT volume. It is clear that some pathways are not yet completely identified. Lipid composition in EAT and their oxidation are very frequent in DM, promoting mitochondrial dysfunction, enhanced inflammation, fibrogenesis and apoptosis. So far, the identification of lipid species more prone to be oxidized, as well as the impact of these products on insulin signalling pathway are relevant. In this regard, several mechanisms remain to be elucidated for the understanding of T2DM multiple organ damage.
To this point, the scope of this subject is wide, focusing not only on the impact of glucose and insulin-resistance on EAT, heart and related organs, but also on the description of new mechanisms and pathological consequences of T2DM. This Research Topic will explore how elevated EAT can lead to further complications in patients with DM. Articles covering pathophysiologic changes at the EAT expansion and it impacts on heart health, new biomarkers proposed for EAT evaluation and the impact of life style changes and pharmacological treatment are welcome. In addition, the editors appreciate studies including omics research to clarify the role of different biological species in the organ cross-talk and the challenge of selecting the appropriate methods to resolve the remaining queries.


Keywords: Diabetes, Macrovascular complications, microvascular complications, insulin-resistance, obesity, systemic low-level inflammation, glucose metabolism, chronic disease, oxidative stress, omics, EAT, epicardial fat tissue, cardiovascular disease, cardiovascular complications


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

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Submission Deadlines

31 December 2020 Abstract
30 April 2021 Manuscript

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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Topic Editors

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Submission Deadlines

31 December 2020 Abstract
30 April 2021 Manuscript

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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