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Adiponectin and p53 mRNA in epicardial and subcutaneous fat from heart failure patients
Author(s) -
Agra Rosa M.,
TeijeiraFernández Elvis,
PascualFigal Domingo,
SánchezMás Jesús,
FernándezTrasancos Ángel,
GonzálezJuanatey José R.,
Eiras Sonia
Publication year - 2014
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/eci.12186
Subject(s) - adiponectin , adipose tissue , isoprenaline , medicine , heart failure , endocrinology , epicardial fat , stimulation , messenger rna , real time polymerase chain reaction , chemistry , obesity , insulin resistance , gene , biochemistry
Abstract Objective Heart failure ( HF ) is associated with a pro‐inflammatory state in epicardial fat, but the involved mechanisms are not entirely clear. The aim of our study was to assess the relationship between p53 and adiponectin mRNA in epicardial adipose tissue ( EAT ) and subcutaneous adipose tissue ( SAT ) in patients with heart failure and its sympathetic regulation. Methods Epicardial adipose tissue and SAT samples were obtained from 63 patients undergoing elective cardiac surgery. EAT and SAT explants culture from seven patients were stimulated with isoprenaline 0·1 or 1 uM for 6 h. p53 and adiponectin mRNA expression was measured in frozen biopsies or explants culture from both fat pads by real‐time polymerase chain reaction ( PCR ). Results We observed that EAT expressed more p53 mRNA than SAT (1·73 ± 0·07 vs. 1·69 ± 0·04, P < 0·001) and its levels were higher in HF patients (1·75 ± 0·07 vs. 1·70 ± 0·04, P < 0·01 in EAT and 1·70 ± 0·04 vs. 1·67 ± 0·04, P < 0·05 in SAT ). Moreover, p53 mRNA expression was negatively correlated with adiponectin in EAT . After analysing the p53 mRNA regulation by isoprenaline, we observed that only EAT p53 expression increased after adrenergic stimulation (1·63 ± 0·01 vs. 1·66 ± 0·02; P = 0·024). Conclusions p53 mRNA expression levels, inversely correlated with adiponectin, increase in EAT of HF patients and can be regulated by sympathetic activation pathway. Our findings can help to explain the deleterious effect of sympathetic activation in HF .