Santos 2019 MiPschool Coimbra

From Bioblast
Uncoupling Protein 1 inhibition and mitochondrial respiration in epicardial adipose tissue from hear failure patients.

Link: MitoEAGLE

Santos D, Fonseca AC, Di Nunzio G, Oliveria A, Burrgeiro A, Lourenco N, Antunes M, Carvalho E (2019)

Event: MiPschool Coimbra 2019


Cardiovascular diseases are the principal cause of death and morbidity on diabetic population. Epicardial adipose tissue (EAT) is a specific fat depot that involves almost 80% of the heart. Under physiological conditions, EAT is responsible for the secretion of bioactive molecules that regulate metabolic and immune functions, with protective effect to cardiomyocytes and coronary arteries. Metabolic alterations in fat may affect metabolic pathways, such as fatty acid oxidation (FAO) and cardiac metabolism by modulating FA uptake and insulin action. Despite the important physiological role of EAT in cardiovascular metabolism, few studies have been carried out in order to evaluate its oxidative capacity. The aim of this study was to characterize mitochondrial respiration in EAT in comparison to paired subcutaneous adipose tissue (SAT) biopsies.

High resolution respirometry protocols using the OROBOROS technology were used, it was possible to measure FAO in EAT and SAT after UCP1 inhibition. EAT and SAT were collected from non-diabetic and diabetic patients undergoing cardiac surgery at Cardiothoracic Surgery Unit, University Hospital of Coimbra.

EAT from non-diabetic patients shows increased mitochondrial respiration in comparison to SAT, at the basal level (p≀0,05), as well as OXPHOS mediated by FAO and by pyruvate, malate and glutamate (p≀0,05). However, no differences were found when comparing nondiabetic with diabetic patients.

In the present study, we show increased mitochondrial respiration in EAT due to the contribution of FAO, even after UCP1 inhibition with GDP, when compared to SAT. These results emphasize that EAT lipid metabolism is important and is a primary source of substrates to the nearby cardiomyocyte. Due the anatomical relation and proximity between EAT and the heart, the metabolic characterization of EAT might contribute to the discovery of early biomarkers for potential therapeutic targets in cardiac disease.

β€’ Bioblast editor: Plangger M

Labels: MiParea: Respiration, Comparative MiP;environmental MiP  Pathology: Cardiovascular 

Organism: Human  Tissue;cell: Heart, Fat 

Regulation: Inhibitor  Coupling state: OXPHOS  Pathway: F, N  HRR: Oxygraph-2k 


Santos D(1), Fonseca AC(1), Di Nunzio G(1), Oliveria A(1), Burrgeiro A(1), Lourenço N(2), Antunes M(3), Carvalho E(1)
  1. Center Neurosciences Cell Biology (CNC)
  2. Center Informatics Systems Univ Coimbra (CISUC), Dept Informatics Engineering; Univ Coimbra
  3. Cardiothoracic Surgery Unit, Univ Hospital Coimbra; Portugal. -
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