Effects of comfort food on food intake, anxiety-like behavior and the stress response in rats

Abstract

It has been suggested that access to high caloric food attenuates stress response. The present paper investigates whether access to commercial chow enriched with glucose and fat, here referred to as comfort food alters behavioral, metabolic, and hormonal parameters of rats submitted to three daily sessions of foot-shock stress. Food intake, anxiety-like behaviors, and serum levels of insulin, leptin, corticosterone, glucose and triglycerides were determined. The rats submitted to stress decreased the intake of commercial chow, but kept unaltered the intake of comfort food. During the elevated plus maze (EPM) test, stressed rats increased the number of head dipping, entries into the open arms, as well as the time spent there, and decreased the number of stretched-attend posture and risk assessment. These effects of stress were independent of the type of food consumed. Non-stressed rats ingesting comfort food decreased risk assessment as well. Stress and comfort food increased time spent in the center of the open field and delayed the first crossing to a new quadrant. Stress increased the plasma level of glucose and insulin, and reduced triglycerides, although consumption of comfort food increases glucose, triglyceride and leptin levels; no effect on leptin level was associated to stress. The stress induced increase in serum corticosterone was attenuated when rats had access to comfort food. It was concluded that foot-shock stress has an anorexigenic effect that is independent of leptin and prevented upon access to comfort food. Foot-shock stress also has an anxiolytic effect that is potentiated by the ingestion of comfort food and that is evidenced by both EPM and open field tests.

Associations between Western and Mediterranean-type dietary patterns and anxiety and stress

“…During anxiety or stress, the choice of food changes from normal meal-type foods to high fat, high palatable snacks, which, in the present study, were located in the Western dietary pattern. In rats, consumption of high-fat and high-sugar foods attenuated stress, which was associated with the decrease of serum corticosterone levels (ORTOLANI et al, 2011).…”

Food-intake regulation during stress by the hypothalamo-pituitary-adrenal axis

“…(Chavez et al, 1997;Warne, 2009) leptin? (Dagogo-Jack et al, 1997;Miell et al, 1996;Newcomer et al, 1998;Slieker et al, 1996;York, 1996) CRH and Ucn 3 (Bernier, 2006;Ohata and Shibasaki, 2011;Smagin et al, 1998) CART (Kask et al, 2000;Xu et al, 2010) Nesfatin-1 (Goebel et al, 2009;Stengel et al, 2011) NPW (Beck et al, 2010) Melanocortins (Liu et al, 2007;Yamano et al, 2004) central monoaminergic systems (Gibson, 2006) autonomous nervous system (Seematter et al, 2004) Stress induces hyperphagia due to reduction of: sensor specific satiety (Ahn and Phillips, 2012;Ortolani et al, 2011) stressor aversiveness (Piazza and Le Moal, 1997) CRH signaling? (Foster et al, 2009;la Fleur et al, 2005;Pecoraro et al, 2004) due to activation of central reward pathways (Piazza and Le Moal, 1997), due to alterations in gut microbiota (Tehrani et al, 2012) Glucocorticoids induce hyperphagia (Dallman, 1993;Drapeau et al, 2003;Epel et al, 2000;Tataranni et al, 1996) due to increased signaling of: NPY (Gyengesi et al, 2010;Krysiak et al, 1999;McKibbin et al, 1992;White et al, 1994;Wilding et al, 1993), AgRP (Coll et al, 2005;Savontaus et al, 2002), Nociceptin …”

“…Moreover, rats submitted to footshock stress decreased the intake of commercial chow, but kept unaltered the intake of comfort food (Ortolani et al, 2011). According to Dallman, energy stores are critically important for normal activity in the central stress-response network (Dallman, 2010).…”

“…When a chronic stressor results in high GCs levels, the steroids act in brain in a feed-forward fashion to recruit a stress-response network that biases ongoing autonomic, neuroendocrine, and behavioral outflow as well as responses to novel stressors (Dallman et al, 2006). When rats are allowed to eat fat or sucrose under acute or repeated restraint stress, CRH expression in the hypothalamus and bed nucleus of stria terminalis (BNST), as well as ACTH and GC secretion are reduced (Foster et al, 2009;la Fleur et al, 2005;Ortolani et al, 2011;Pecoraro et al, 2004).…”

“…An elevation in plasma leptin levels is also anorexigenic (Ortolani et al, 2011;Won et al, 2009;Zareian et al, 2011). GCs can interact with leptin in the long-term regulation of energy intake and body adiposity.…”