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University of Cincinnati, Department of Psychiatry, ML # 0506, Reading, OH 45237, United States.
Physiology & Behavior (Impact Factor: 2.98). 01/2008; 92(5):924-30. DOI: 10.1016/j.physbeh.2007.06.024
Source: PubMed


Previous studies have suggested that intermittent exposure to hydrogenated vegetable shortening yields a binge/compensate pattern of feeding in rats. The present study was designed to assess whether rats would exhibit similar patterns of intake when given intermittent access to a nutritionally complete high-fat diet. Four groups of rats received varying exposure to either hydrogenated vegetable shortening or high-fat diet for 8 consecutive weeks. Animals were given daily and intermittent access to determine if the binge/compensate pattern of feeding was frequency dependent. At the conclusion of the study, body composition and plasma leptin levels were assessed to determine effects of diet and binge/compensate intake on endocrine alterations. As predicted, animals receiving intermittent access to high-fat diet displayed the binge/compensate pattern of feeding and appeared to compensate as a result of the caloric overload accompanying a particular binge episode. In addition, exposure to either shortening or high-fat diet led to alterations in body composition, while only exposure to shortening altered plasma leptin levels. These results suggest that binge-intake behavior occurs on a nutritionally complete high-fat diet and that this regimen is capable of altering both body composition and endocrine profile.

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    • "Highly palatable food activates dopaminergic neurons in the ventral tegmental area (VTA) projecting to the nucleus accumbens (NAc), amygdala and prefrontal cortex, areas involved in different aspects of reward behavior. For example when repeatedly exposed to sucrose for a short period of time after food restriction, rats show addictive behavior with food binges related to dopamine release in the NAc shell [30] and repetitive restricted exposure to fat induces similar changes [31] [32]. Long-term access to palatable food, however, will "
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    ABSTRACT: Aberrant feeding behavior can lead to obesity and obesity-related medical consequences, such as insulin resistance and diabetes. Although alterations in glucose metabolism (i.e. insulin resistance), in the presence of excessive fat tissue are often explained by the consequences of dysfunctional adipose tissue, evidence is emerging that also altered brain functions might be an important determinant of insulin resistance. In this review, we provide an overview of how feeding behavior and obesity interact with brain circuitry and how these interactions affect glucose metabolism. Because brain circuitries involved in food intake have been shown to partly control glucose metabolism as well, targeting these circuitries in obese subjects might not only affect food intake and body weight but also glucose metabolism.
    Best Practice & Research: Clinical Endocrinology & Metabolism 10/2014; DOI:10.1016/j.beem.2014.06.001 · 4.60 Impact Factor
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    • "We have previously demonstrated that when rats have unlimited access (24 h/7 days a week) to sweetened fat, they decrease their sweetened fat intake over time [31]. This suggests that the limited scheduled access of the sweetened fat promotes binge-like eating behavior, an effect that has been demonstrated by others using fat [42], [43], sweetened fat [12], [44], [45], and highly palatable chow [46], [47]. The lack of body weight differences among animals exposed to our dietary-induced binge eating protocol is consistent with similar binge-like eating models [48], [49], [50], suggesting the observed differences in intake are caused by the distinct feeding patterns or entrainment, rather than metabolic alterations caused by weight gain. "
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    ABSTRACT: 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.
    PLoS ONE 04/2014; 9(4):e93610. DOI:10.1371/journal.pone.0093610 · 3.23 Impact Factor
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    ABSTRACT: Ingestion of different nutrients, such as fats vs. sugars, normally produces different effects on physiology, the brain and behavior. However, they do share certain neural pathways for reinforcement of behavior, including the mesolimbic dopamine (DA) system. When these nutrients are consumed in the form of binges, this can release excessive DA that causes compensatory changes that are comparable to the effects of drugs of abuse. In this paper, we review data obtained with animal models of fat and sugar bingeing. The concept of "food addiction" is described and reviewed from both clinical and laboratory animal perspectives. A theory is presented in which galanin, a fat-stimulated peptide, may have a role in preventing the emergence of opiate-like withdrawal signs, which are seen in sugar-bingeing rats, but not in fat-bingeing rats. Finally, we discuss the implications of bingeing on sugars and fats for obesity and eating disorders.
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