Evidence supports the working hypothesis that a specific subset of AgRP neurons express the AT1A receptor (Agtr1a), and that these receptors simultaneously (i) identify the subset of AgRP neurons involved in RMR control, and (ii) serve a critical molecular role in the integrative control of RMR. We hypothesize that molecular dysfunctions specifically within the Agtr1a-expressing subset of AgRP neurons contributes to the development of SLR and weight loss-associated adaptations in RMR control. Pomc, proopiomelanocortin; αMSH, α-melanocyte stimulating hormone; Mc4r, melanocortin type 4 receptor; Agrp, Agouti-related peptide; ANG, angiotensin II; BAT SNA, brown adipose tissue sympathetic nerve activity; RMR, resting metabolic rate.