Binge-like eating attenuates nisoxetine feeding suppression, stress activation, and brain norepinephrine activity.
Stress is often associated with binge eating. A critical component of the control of stress is the central norepinephrine system. We investigated how dietary-induced binge eating alters central norepinephrine and related behaviors. Young male Sprague Dawley rats received calorie deprivation (24 h) and /or intermittent sweetened fat (vegetable shortening with sucrose; 30 min) twice a week for 10 weeks. The groups were Restrict Binge (calorie deprivation/sweetened fat), Binge (sweetened fat), Restrict (calorie deprivation), and Naive (no calorie deprivation/no sweetened fat). Dietary-induced binge eating was demonstrated by Restrict Binge and Binge, which showed an escalation in 30-min intake over time. Feeding suppression following nisoxetine (3 mg/kg; IP), a selective norepinephrine reuptake inhibitor, was not evident in Restrict Binge (Restrict Binge: 107±13, Binge: 52±9, Restrict: 80±8, Naive: 59±13% of saline injection at 1 h). In subsequent experiments with Restrict Binge and Naive, Restrict Binge had reduced corticosterone (Restrict Binge: 266±25; Naive: 494±36 ng/ml) and less feeding suppression (Restrict Binge: 81±12, Naive: 50±11% of non-restraint intake at 30 min) following restraint stress (1 h). Dietary-induced binge eating in Restrict Binge was not altered by a dorsal noradrenergic bundle lesion caused by N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP4), but frontal cortex norepinephrine was positively correlated with the average 30-min intake post-lesion (0.69; p<0.01). In a separate set of animals, single-unit in vivo electrophysiological recording of locus coeruleus-norepinephrine neural activity demonstrated reduced sensory-evoked response as a consequence of the Restrict Binge schedule (Restrict Binge: 8.1±0.67, Naive: 11.9±1.09 Hz). These results, which suggest that a consequence of dietary-induced binge eating is to attenuate the responsiveness of the brain norepinephrine system, will further our understanding of how highly palatable foods dampen the stress neuraxis.
Department of Animal Sciences, Rutgers, The State University of New Jersey, New Brunswick, New Jersey, United States of America; Graduate Program in Endocrinology and Animal Biosciences, Rutgers, The State University of New Jersey, New Brunswick, New Jersey, United States of America; New Jersey Institute for Food, Nutrition, and Health, Rutgers, The State University of New Jersey, New Brunswick, New Jersey, United States of America.
Nicholas T
NT
Bello
Department of Animal Sciences, Rutgers, The State University of New Jersey, New Brunswick, New Jersey, United States of America.
Chung-Yang
CY
Yeh
Department of Animal Sciences, Rutgers, The State University of New Jersey, New Brunswick, New Jersey, United States of America; Graduate Program in Endocrinology and Animal Biosciences, Rutgers, The State University of New Jersey, New Brunswick, New Jersey, United States of America.
Jessica L
JL
Verpeut
Department of Animal Sciences, Rutgers, The State University of New Jersey, New Brunswick, New Jersey, United States of America.
Amy L
AL
Walters
D000818:Animals; D001835:Body Weight; D001921:Brain / Q000378:metabolism*; D002032:Bulimia; D002149:Energy Intake; D005247:Feeding Behavior / Q000187:drug effects*; D005473:Fluoxetine / Q000031:analogs & derivatives* / Q000494:pharmacology; D008297:Male; D009638:Norepinephrine / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley
D005473:Fluoxetine; C011386:nisoxetine; D009638:Norepinephrine