Disruption of beta3 adrenergic receptor increases susceptibility to DIO in mouse
Carregando...
Citações na Scopus
24
Tipo de produção
article
Data de publicação
2016
Título da Revista
ISSN da Revista
Título do Volume
Editora
BIOSCIENTIFICA LTD
Autores
PREITE, Nailliw Z.
NASCIMENTO, Bruna P. P. do
HIGA, Talita S.
EVANGELISTA, Fabiana S.
HENRIQUES, Felipe dos Santos
BATISTA JR., Miguel Luiz
BIANCO, Antonio C.
Citação
JOURNAL OF ENDOCRINOLOGY, v.231, n.3, p.259-269, 2016
Resumo
The brown adipose tissue (BAT) mediates adaptive changes in metabolic rate by responding to the sympathetic nervous system through beta-adrenergic receptors (AR). Here, we wished to define the role played by the AR beta(3) isoform in this process. This study focused on the AR beta(3) knockout mice (AR beta 3KO), including responsiveness to cold exposure, diet-induced obesity, intolerance to glucose, dyslipidaemia and lipolysis in white adipose tissue (WAT). AR beta 3KO mice defend core temperature during cold exposure (4 degrees C for 5h), with faster BAT thermal response to norepinephrine (NE) infusion when compared with wild-type (WT) mice. Despite normal BAT thermogenesis, AR beta 3KO mice kept on a high-fat diet (HFD; 40% fat) for 8 weeks exhibited greater susceptibility to diet-induced obesity, markedly increased epididymal adipocyte area with clear signs of inflammation. The HFD-induced glucose intolerance was similar in both groups but serum hypertriglyceridemia and hypercholesterolemia were less intense in AR beta 3KO animals when compared with WT controls. Isoproterenol-induced lipolysis in isolated white adipocytes as assessed by glycerol release was significantly impaired in AR beta 3KO animals despite normal expression of key proteins involved in lipid metabolism. In conclusion, AR beta(3) inactivation does not affect BAT thermogenesis but increases susceptibility to diet-induced obesity by dampening WAT lipolytic response to adrenergic stimulation.
Palavras-chave
obesity, lipolysis, adaptive thermogenesis, brown adipose tissue, beta(3) adrenergic receptor
Referências
- Arch JRS, 1996, INT J OBESITY, V20, P191
- Asensio C, 2005, DIABETES, V54, P3490, DOI 10.2337/diabetes.54.12.3490
- Atgie C, 1997, AM J PHYSIOL-CELL PH, V273, pC1136
- Bachman ES, 2002, SCIENCE, V297, P843, DOI 10.1126/science.1073160
- Batista ML, 2016, J CACHEXIA SARCOPENI, V7, P37, DOI 10.1002/jcsm.12037
- Bianco AC, 2014, THYROID, V24, P88, DOI 10.1089/thy.2013.0109
- Cannon B, 2004, PHYSIOL REV, V84, P277, DOI 10.1152/physrev.00015.2003
- CARPENE C, 1993, J PHARMACOL EXP THER, V265, P237
- Chruscinski AJ, 1999, J BIOL CHEM, V274, P16694, DOI 10.1074/jbc.274.24.16694
- Cinti S, 2006, NUTR METAB CARDIOVAS, V16, P569, DOI 10.1016/j.numecd.2006.07.009
- COLLINS S, 1994, MOL ENDOCRINOL, V8, P518, DOI 10.1210/me.8.4.518
- Cypess AM, 2009, NEW ENGL J MED, V360, P1509, DOI 10.1056/NEJMoa0810780
- Enerback S, 1997, NATURE, V387, P90, DOI 10.1038/387090a0
- Fernandes GW, 2014, J ENDOCRINOL, V221, P381, DOI 10.1530/JOE-13-0526
- Fisher MH, 1998, J CLIN INVEST, V101, P2387, DOI 10.1172/JCI2496
- Hibi M, 2016, INT J OBESITY, V40, P1655, DOI 10.1038/ijo.2016.124
- Inokuma K, 2006, AM J PHYSIOL-ENDOC M, V290, pE1014, DOI 10.1152/ajpendo.00105.2005
- Jimenez M, 2002, FEBS LETT, V530, P37, DOI 10.1016/S0014-5793(02)03387-2
- Kajimura S, 2014, ANNU REV PHYSIOL, V76, P225, DOI 10.1146/annurev-physiol-021113-170252
- Lafontan M., 1997, Human Reproduction (Oxford), V12, P6
- Lee YH, 2014, BBA-MOL BASIS DIS, V1842, P358, DOI 10.1016/j.bbadis.2013.05.011
- Lidell ME, 2010, NAT REV ENDOCRINOL, V6, P319, DOI 10.1038/nrendo.2010.64
- Lowell BB, 2000, NATURE, V404, P652
- Lowell BB, 1998, ENDOCR J, V45, pS9, DOI 10.1507/endocrj.45.Suppl_S9
- Mattsson CL, 2011, AM J PHYSIOL-ENDOC M, V301, pE1108, DOI 10.1152/ajpendo.00085.2011
- NAGASE I, 1994, JPN J VET RES, V42, P137
- Revelli JP, 1997, J CLIN INVEST, V100, P1098, DOI 10.1172/JCI119620
- Ribeiro MO, 2001, J CLIN INVEST, V108, P97, DOI 10.1172/JCI12584
- RODBELL M, 1964, J BIOL CHEM, V239, P375
- Rohrer DK, 1998, J MOL MED-JMM, V76, P764, DOI 10.1007/s001090050278
- RUDERMAN NB, 1981, AM J CLIN NUTR, V34, P1617
- Rutkowski JM, 2015, J CELL BIOL, V208, P501, DOI 10.1083/jcb.201409063
- Santulli G, 2012, DIABETES, V61, P692, DOI 10.2337/db11-1027
- Silva J Enrique, 2011, Front Biosci (Schol Ed), V3, P352, DOI 10.2741/s156
- Soloveva V, 1997, MOL ENDOCRINOL, V11, P27, DOI 10.1210/me.11.1.27
- Sun K, 2013, CELL METAB, V18, P470, DOI 10.1016/j.cmet.2013.06.016
- Sun K, 2011, J CLIN INVEST, V121, P2094, DOI 10.1172/JCI45887
- SUSULIC VS, 1995, J BIOL CHEM, V270, P29483
- Ueta CB, 2012, J ENDOCRINOL, V214, P359, DOI 10.1530/JOE-12-0155
- van der Lans AAJJ, 2014, AM J PHYSIOL-REG I, V307, pR103, DOI 10.1152/ajpregu.00021.2014
- Marken L Van, 2009, NEW ENGL J MED, V360, P1500, DOI 10.1056/NEJM0A0808718
- WEIGLE DS, 1994, FASEB J, V8, P302
- WIDEN E, 1995, NEW ENGL J MED, V333, P348, DOI 10.1056/NEJM199508103330604
- Xiao CY, 2015, OBESITY, V23, P1450, DOI 10.1002/oby.21124
- Yoneshiro T, 2011, OBESITY, V19, P13, DOI 10.1038/oby.2010.105