Inhibition of immobilization stress-induced anorexia, behavioral deficits, and plasma corticosterone secretion by injected leptin in rats

Abstract

Leptin, originally identified as an anti-obesity hormone, also has an important role in the regulation of mood and emotion. The present study was designed to monitor effects of injected leptin on immobilization stress-induced anorexia, behavioral deficits, and plasma corticosterone secretion in rats. Exposure to 2 h immobilization stress decreased food intake and body weight in saline-injected animals. Animals exposed to open field, elevated plus maze, and light-dark transition tests the day following immobilization exhibited anxiety-like behavior. Leptin injected at doses of 0.1 and 0.5 mg/kg also decreased food intake and body weight in unstressed animals and elicited anxiolytic effects at dose of 0.5 mg/kg, monitored on the following day. Immobilization-induced decreases in food intake, body weight, as well as stress-induced behavioral deficits in the open field, elevated plus maze, and light-dark transition test were reversed by exogenous leptin in a dose-dependent (0.1-0.5 mg/kg) manner. Acute exposure to 2 h immobilization produced a fourfold rise in plasma levels of corticosterone. Animals injected with leptin at a dose of 0.1 mg/kg, but not at dose of 0.5 mg/kg, exhibited a marginal increase in plasma corticosterone. Immobilization-induced increases of plasma corticosterone were reversed by leptin injected at doses of 0.1 or 0.5 mg/kg. The data suggest that exogenous leptin can reduce stress perception, resulting in an inhibition of stress effects on the activity of hypothalamic-pituitary-adrenal axis and behavior. The reported pharmacological effects of leptin represent an innovative approach for the treatment of stress-related disorders.

Serum Leptin and Cortisol, Related to Acutely Perceived Academic Examination Stress and Performance in Female University Students

“…Significant differences: *p \ 0.01 from no stress group, ?p \ 0.01 from mild stress groups; following one way ANOVA Acute exposure to a stressor not only stimulates HPA axis but an increase in leptin release also occurs. Thus plasma levels of leptin were increased in rats exposed to immobilization (Haque et al 2013;Patterson-Buckendahl et al 2007), forced swimming (Zareian et al 2011) or noise (Chandralekha et al 2005) stress but chronic social stress, decreased plasma levels of leptin (Patterson-Buckendahl et al 2007). Evidence suggests that psychological stressors can increase circulating levels of leptin and subjects who perceived more psychological stress had greater increase in leptin levels (Otsuka et al 2006).…”

“…Although serum leptin in all groups were highly comparable in the beginning of academic session but on the day of examination values were highest in the group which perceived moderate stress. It would suggest that antidepressant like effects of circulating leptin reported in animal (Lu et al 2006;Liu et al 2010;Haque et al 2013) as well (Lopresti et al 2015) would be greater in moderate than high stress group.…”

“…An increase in leptin release during stress can also modulate various physiological and psychological processes to cope the stressful situation (Haleem 2011(Haleem , 2014. For example stress-induced increases of leptin can reduce stress effects on behavior to elicit antidepressant like effects (Haque et al 2013;Lopresti et al 2015).…”

“…Evidence has expanded the function of leptin from the control of energy balance to the regulation of other physiological and psychological processes including responses to stress (Haleem 2014). Thus systemic administration of leptin reduced stress perception by inhibiting the activity of HPA axis (Haque et al 2013) and elicited antidepressant like effects (Lu et al 2006;Liu et al 2010;Haque et al 2013). Moreover, patients with major depression exhibited low levels of leptin in serum and cerebrospinal fluid (Kraus et al 2001;Atmaca et al 2002;Westling et al 2004;Jow et al 2006) suggesting a role of leptin in responses to stress and in depression.…”

A Study on the Effects of Agomelatine on Food Intake and Body Weight in Restraint Stress Model in Adult Swiss Albino Mice

“…Agomelatine antagonizes serotonin 2C receptor which is an important mediator of satiety [15]. It is well established from studies conducted earlier that restraint stress model in mice induces depression such as state in addition to the reduction in body weight and food intake by altered expression of food related genes like decreased ghrelin and increased Pro-opiomelanocortin [16,17].…”