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THE ROLE OF INSULIN RESISTANCE AND SIRT‐1 IN CARDIAC REMODELING INDUCED BY CIGARETTE SMOKE
Author(s) -
Azevedo Paula Schmidt,
Pires Vanessa,
Santos Priscila,
Gonçalves Andrea,
Okoshi Marina,
Fernandes Ana Angelica,
Roscani Meliza,
Polegato Bertha,
Paiva Sergio,
Zornoff Leonardo,
Minicucci Marcos
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.lb388
Subject(s) - insulin resistance , medicine , endocrinology , ampk , chemistry , protein kinase b , cotinine , insulin , carbohydrate metabolism , kinase , apoptosis , protein kinase a , nicotine , biochemistry
The aim of this study is to investigate if insulin resistance and SIRT‐1 participate of cardiac remodeling induced by TS. Methods 20 animals were allocated into 2 groups: group exposed to cigarette smoke (CS) and group not exposed to cigarette smoke (C). After 2 months the animals were subjected to: a) echocardiographic study; b) energy metabolism enzymes evaluation; c) Western blot for Akt, AMPK, SIRT‐1 and GLUT‐4. Cotinine and insulin was measured by ELISA kit. The HOMA‐index was calculated. The CS group showed larger left atrium size and lower ejection fraction than those of group. Serum cotinine was positive in CS exposed group (P<0,001). HOMA‐index showed insulin resistance in CS group (P<0,05). As regards the analysis of energy metabolism enzymes, phosphofructokinase (PFK); P = 0.003), lactate dehydrogenases (LDH) (P = 0.017) were greater in the TS group and citrate synthase P <0.001), complex I ( P <0.001), complex II (P <0.001), ATP synthase (P <0.001) were lower in the TS group. Akt/Aktp was similar between the groups. AMPK was reduced in CS group (p<0,001), SIRT‐1 increased in CS group (P<0,001) and GLUT‐4 (P=0,47) was similar. Conclusion Cigarette smoke induced insulin resistance, that may have reduced AMPK and probably compromised glucose metabolism and energy transformation. SIRT‐1 increases in oxidative stress set and may promote hypertrophy and apoptosis. Therefore, SIRT‐1 is also a possible metabolic pathway involved in CS induced remodeling. Support or Funding Information Supported by FAPESP