Suppression of Resting Metabolism by the Angiotensin AT2 Receptor. Cell Rep 2016 Aug 09;16(6):1548-1560
Date
08/02/2016Pubmed ID
27477281Pubmed Central ID
PMC4981564DOI
10.1016/j.celrep.2016.07.003Scopus ID
2-s2.0-84979752805 (requires institutional sign-in at Scopus site) 39 CitationsAbstract
Activation of the brain renin-angiotensin system (RAS) stimulates energy expenditure through increasing of the resting metabolic rate (RMR), and this effect requires simultaneous suppression of the circulating and/or adipose RAS. To identify the mechanism by which the peripheral RAS opposes RMR control by the brain RAS, we examined mice with transgenic activation of the brain RAS (sRA mice). sRA mice exhibit increased RMR through increased energy flux in the inguinal adipose tissue, and this effect is attenuated by angiotensin II type 2 receptor (AT2) activation. AT2 activation in inguinal adipocytes opposes norepinephrine-induced uncoupling protein-1 (UCP1) production and aspects of cellular respiration, but not lipolysis. AT2 activation also opposes inguinal adipocyte function and differentiation responses to epidermal growth factor (EGF). These results highlight a major, multifaceted role for AT2 within inguinal adipocytes in the control of RMR. The AT2 receptor may therefore contribute to body fat distribution and adipose depot-specific effects upon cardio-metabolic health.
Author List
Littlejohn NK, Keen HL, Weidemann BJ, Claflin KE, Tobin KV, Markan KR, Park S, Naber MC, Gourronc FA, Pearson NA, Liu X, Morgan DA, Klingelhutz AJ, Potthoff MJ, Rahmouni K, Sigmund CD, Grobe JLAuthors
Justin L. Grobe PhD Professor in the Physiology department at Medical College of WisconsinCurt Sigmund PhD Chair, Professor in the Physiology department at Medical College of Wisconsin
MESH terms used to index this publication - Major topics in bold
AdipocytesAdipose Tissue, White
Angiotensin II
Animals
Brain
Energy Metabolism
Mice, Inbred C57BL
Obesity
Receptor, Angiotensin, Type 2
Renin-Angiotensin System
