ACE-modulated adiposity is related to higher energy expenditure and independent of lipolysis and glucose incorporation into lipids in adipocytes
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Citações na Scopus
1
Tipo de produção
article
Data de publicação
2017
Título da Revista
ISSN da Revista
Título do Volume
Editora
AMER PHYSIOLOGICAL SOC
Autores
HIGA, Talita Sayuri
FERRAZ-DE-CAMPOS, Tarcila Beatriz
TAKADA, Julie
TORRES-LEAL, Francisco Leonardo
EVANGELISTA, Fabiana Sant'Anna
LIMA, Fabio Bessa
Citação
PHYSIOLOGICAL GENOMICS, v.49, n.12, p.712-721, 2017
Resumo
Emerging evidence suggests that both systemic and white adipose tissue-renin-angiotensin system components influence body weight control. We previously demonstrated that higher angiotensin-converting enzyme (ACE) gene expression is associated with lower body adiposity in a rodent model. In this study, we tested the hypothesis that a higher ACE gene dosage reduces fat accumulation by increasing energy expenditure and modulating lipolysis and glucose incorporation into lipids in adipocytes. After a 12 wk follow-up period, transgenic mice harboring three ACE (3ACE) gene copies displayed diminished WAT mass, lipid content in their carcasses, adipocyte hypotrophy, and higher resting oxygen uptake (Vo(2) ) in comparison with animals with one ACE gene copy (1ACE) after long fasting (12 h). No differences were found in food intake and in the rates of lipolysis and glucose incorporation into lipids in adipocytes. To assess whether this response involves increased angiotensin II type I receptor (AT1R) activation. AT1R blocker (losartan) was used in a separate group of 3ACE mice with body weight and adiposity comparable to that in the other 3ACE animals. We suggest that fasting-induced lower adiposity observed in animals with 3ACE gene copies might be associated with a higher expense of energy reserves; this response did not involve AT1R activation.
Palavras-chave
ACE gene, adipose tissue, lipogenesis, lipolysis, energy expenditure
Referências
- Alves MF, 2005, BRAZ J MED BIOL RES, V38, P861, DOI 10.1590/S0100-879X2005000600007
- Bazin R, 2001, ADIPOSE TISSUE PROTO, DOI 10.1385/1-59259-231-7:121
- Bergmeyer H. U., 1974, METHODS ENZYMATIC AN
- BERNARDIS LL, 1968, J ENDOCRINOL, V40, P527, DOI 10.1677/joe.0.0400527
- BONORA E, 1989, J CLIN ENDOCR METAB, V68, P374, DOI 10.1210/jcem-68-2-374
- Brandsch C, 2010, LIPIDS HEALTH DIS, V9, DOI 10.1186/1476-511X-9-50
- Caron KMI, 2002, P NATL ACAD SCI USA, V99, P8248, DOI 10.1073/pnas.112222199
- Coelho MS, 2010, REGUL PEPTIDES, V162, P61, DOI 10.1016/j.regpep.2010.03.008
- Frantz ED, 2014, METAB SYNDR RELAT D, V12, P191, DOI 10.1089/met.2013.0129
- de Kloet AD, 2011, AM J PHYSIOL-ENDOC M, V301, pE1081, DOI 10.1152/ajpendo.00307.2011
- de Kloet AD, 2009, ENDOCRINOLOGY, V150, P4114, DOI 10.1210/en.2009-0065
- DiGirolamo M., 2001, ADIPOSE TISSUE PROTO, DOI 10.1385/1-59259-231-7:181
- Engeli S, 2005, HYPERTENSION, V45, P356, DOI 10.1161/01.HYP.0000154361.47683.d3
- Esther CR, 1996, LAB INVEST, V74, P953
- Evangelista FS, 2006, PHYSIOL GENOMICS, V27, P231, DOI 10.1152/physiolgenomics.00022.2006
- Favre GA, 2014, J RENIN-ANGIO-ALDO S, V15, P396, DOI 10.1177/1470320314537695
- Feldmann HM, 2009, CELL METAB, V9, P203, DOI 10.1016/j.cmet.2008.12.014
- Ferre P, 2007, HORM RES, V68, P72, DOI 10.1159/000100426
- Fine JB, 1997, INT J OBESITY, V21, P764, DOI 10.1038/sj.ijo.0800469
- Fouque D, 2008, KIDNEY INT, V73, P391, DOI 10.1038/sj.ki.5002585
- FREDERICH RC, 1995, NAT MED, V1, P1311, DOI 10.1038/nm1295-1311
- Goossens GH, 2007, INT J OBESITY, V31, P382, DOI 10.1038/sj.ijo.0803388
- Gorzelniak K, 2002, J HYPERTENS, V20, P965, DOI 10.1097/00004872-200205000-00032
- Heimann AS, 2005, PHYSIOL GENOMICS, V20, P173, DOI 10.1152/physiolgenomics.00145.2004
- Hilgers KF, 1997, HYPERTENSION, V29, P216, DOI 10.1161/01.HYP.29.1.216
- Hiraoka J, 1997, BIOCHEM BIOPH RES CO, V231, P582, DOI 10.1006/bbrc.1997.6145
- HONNOR RC, 1985, J BIOL CHEM, V260, P5122
- Huang W, 2001, P NATL ACAD SCI USA, V98, P13330, DOI 10.1073/pnas.231476798
- Janke J, 2002, DIABETES, V51, P1699, DOI 10.2337/diabetes.51.6.1699
- Jayasooriya AP, 2008, P NATL ACAD SCI USA, V105, P6531, DOI 10.1073/pnas.0802690105
- Jones BH, 1997, ENDOCRINOLOGY, V138, P1512, DOI 10.1210/en.138.4.1512
- Karlsson C, 1998, J CLIN ENDOCR METAB, V83, P3925, DOI 10.1210/jc.83.11.3925
- KATSUYA T, 1995, ARTERIOSCL THROM VAS, V15, P779, DOI 10.1161/01.ATV.15.6.779
- Kim S, 2001, BIOCHEM J, V357, P899, DOI 10.1042/0264-6021:3570899
- Krege JH, 1997, HYPERTENSION, V29, P150, DOI 10.1161/01.HYP.29.1.150
- KREGE JH, 1995, NATURE, V375, P146, DOI 10.1038/375146a0
- Lemes VAF, 2013, GENE, V532, P197, DOI 10.1016/j.gene.2013.09.065
- Li B, 2000, NAT MED, V6, P1115
- Liao CC, 2013, J AGR FOOD CHEM, V61, P11082, DOI 10.1021/jf4026647
- Pelletier CC, 2013, KIDNEY INT, V83, P878, DOI 10.1038/ki.2013.9
- Premaratna SD, 2012, INT J OBESITY, V36, P233, DOI 10.1038/ijo.2011.95
- Rideout TC, 2010, MOL NUTR FOOD RES, V54, pS7, DOI 10.1002/mnfr.201000027
- Riera-Fortuny C, 2005, INT J OBESITY, V29, P78, DOI 10.1038/sj.ijo.0802829
- Rodbell M., 1964, J BIOL CHEM, V239, P357
- Rogero MM, 2011, NUTRIENTS, V3, P792, DOI 10.3390/nu3090792
- Santos EL, 2008, INT IMMUNOPHARMACOL, V8, P247, DOI 10.1016/j.intimp.2007.07.021
- Santos EL, 2009, BIOCHEM PHARMACOL, V78, P951, DOI 10.1016/j.bcp.2009.06.018
- Silva GJJ, 2006, PHYSIOL GENOMICS, V27, P237, DOI 10.1152/physiolgenomics.00023.2006
- Strazzullo P, 2003, ANN INTERN MED, V138, P17, DOI 10.7326/0003-4819-138-1-200301070-00007
- van Harmelen V, 2000, OBES RES, V8, P337, DOI 10.1038/oby.2000.40
- Wacker MJ, 2008, MED SCI MONITOR, V14, pCR353
- Weisinger RS, 2009, PHYSIOL BEHAV, V98, P192, DOI 10.1016/j.physbeh.2009.05.009