Endocrine and metabolic function in male Carioca High-conditioned Freezing rats F. Mousovich-Neto a , A.L. Lourenço a , J. Landeira-Fernandez b , V.M. Corrêa da Costa a, ⁎ a Laboratório de Fisiologia Endócrina Doris Rosenthal, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, CCS, Bloco G, Cidade Universitária, Ilha do Fundão, Rio de Janeiro, RJ 21949-902, Brazil b Laboratório de Neurociência Comportamental, Departamento de Psicologia, Pontifícia Universidade Católica do Rio de Janeiro, Rua Marquês de São Vicente, 225, Rio de Janeiro, RJ 22453-900, Brazil HIGHLIGHTS • Endocrine and metabolic functions are affected in a rat model of anxiety disorder. • Anxiety may contribute to the development of metabolic diseases. • A rat model of anxiety disorder induces an increase in corticosterone serum levels. abstract article info Article history: Received 24 March 2014 Received in revised form 21 January 2015 Accepted 22 January 2015 Available online 23 January 2015 Keywords: Anxiety Corticosterone Thyroid function Metabolism Fat depots The aim of this study was to characterize Carioca High-conditioned Freezing rats (CHF) regarding their en- docrine and metabolic backgrounds. We found an increase in serum corticosterone (CTRL: 96.7 ± 21.65 vs CHF: 292.0 ± 40.71 ng/ml) and leptin (CTRL: 9.5 ± 1.51 vs CHF: 19.2 ± 4.32 ng/ml). Serum testosterone (CTRL: 3.3 ± 0.29 vs CHF: 2.0 ± 0.28 ng/ml) and T3 (CTRL: 52.4 ± 2.74 vs CHF: 42.7 ± 2.94 ng/dl) were de- creased in the CHF group, but serum TSH and T4 were unaffected. Body weight and food intake were un- changed, nevertheless retroperitoneal fat (CTRL: 2.2 ± 0.24 vs CHF: 4.8 ± 0.64 g) and epididymal fat (CTRL: 2.6 ± 0.20 vs CHF: 4.8 ± 0.37 g) depot weights were around 2-fold higher in CHF animals. BAT weight was similar in both groups. Serum triglycerides (CTRL: 41.4 ± 6.03 vs CHF: 83.2 ± 17.09 mg/dl) and total cholesterol (CTRL: 181.6 ± 5.61 vs CHF: 226.4 ± 13.04 mg/dl) were higher in the CHF group. Fasting glycemia (CTRL: 68.7 ± 3.04 vs CHF: 82.3 ± 2.99 mg/dl) was also higher in the CHF group, however glu- cose tolerance test response and serum insulin levels were similar between the groups. Oxygen consumption (CTRL: 10.5 ± 0.40 vs CHF: 7.9 ± 0.58 VO 2 ml/min/kg 0.75 ) and BAT D2 activity (CTRL: 0.7 ± 0.17 vs CHF: 0.3 ± 0.04 fmol T4/min/mg ptn) were lower in the CHF group. Our data show that anxiety could impair endo- crine and metabolic functions and may contribute to the development of metabolic diseases. © 2015 Elsevier Inc. All rights reserved. 1. Introduction Anxiety can be defined as a response to a potentially dangerous sit- uation and is accompanied by a characteristic set of behavioral and physiological responses, including avoidance, vigilance, arousal, and ac- tivation of the hypothalamic–pituitary–adrenal (HPA) and sympatho- adrenal axes. This set of responses has adaptive value and is evoked to protect the individual from danger [39,40]. However, for some individ- uals, anxiety responses can become persistent, uncontrolled, excessive, and inappropriate, without any adaptive meaning; thus, it can become a disorder that requires clinical intervention [35]. Anxiety disorders rep- resent one of the most prevalent mental disorders worldwide [2,22]. A common characteristic of anxiety disorders is deregulation of the HPA axis, resulting in increased serum glucocorticoid levels [30,44]. Glucocorticoids (cortisol in humans and corticosterone in rodents) are metabolically active hormones that play an important role in the stress response and act on different biological systems. However, sustained elevations for long periods of time may have deleterious effects on different systems and thus lead to metabolic dysfunction, such as an in- crease in fat depots, insulin resistance, and dyslipidemia [42]. Some ev- idence indicates that anxiety disorders in rats are related to metabolic disturbances [6]. Human data also show a correlation between anxiety disorders and obesity [1,25]. Anxiety has been studied from neuroanatomical, neurochemical, and behavioral perspectives, but metabolic studies are scarce. Our Physiology & Behavior 142 (2015) 90–96 ⁎ Corresponding author at: Instituto de Biofísica Carlos Chagas Filho, CCS Bloco G, Cidade Universitária, Ilha do Fundão, Rio de Janeiro, RJ 21949-900, Brazil. E-mail address: vmccosta@biof.ufrj.br (V.M. Corrêa da Costa). http://dx.doi.org/10.1016/j.physbeh.2015.01.028 0031-9384/© 2015 Elsevier Inc. All rights reserved. Contents lists available at ScienceDirect Physiology & Behavior journal homepage: www.elsevier.com/locate/phb