Intermittent access to a nutritionally complete high-fat diet attenuates alcohol drinking in rats.

Binge eating disorder and alcohol use disorder (AUD) frequently co-occur in the presence of other psychiatric conditions. Data suggest that binge eating engages similar behavioral and neurochemical processes common to AUD, which might contribute to the etiology or maintenance of alcoholism. However, it is unclear how binge feeding behavior and alcohol intake interact to promote initiation or maintenance of AUD. We investigated the impact of binge-like feeding on alcohol intake and anxiety-like behavior in male Long Evans rats. Rats received chow (controls) or extended intermittent access (24h twice a week; Int-HFD) to a nutritionally complete high-fat diet for six weeks. Standard rodent chow was available ad-libitum to all groups and food intake was measured. Following HFD exposure, 20.0% ethanol, 2.0% sucrose intake and endocrine peptide levels were evaluated. Anxiety-like behavior was measured using a light-dark (LD) box apparatus. Rats in the Int-HFD group displayed a binge-like pattern of feeding (alternations between caloric overconsumption and voluntary caloric restriction). Surprisingly, alcohol intake was significantly attenuated in the Int-HFD group whereas sugar consumption was unaffected. Plasma acyl-ghrelin levels were significantly elevated in the Int-HFD group, whereas glucagon-like peptide-1 levels did not change. Moreover, rats in the Int-HFD group spent more time in the light side of the LD box compared to controls, indicating that binge-like feeding induced anxiolytic effects. Collectively, these data suggest that intermittent access to HFD attenuates alcohol intake through reducing anxiety-like behavior, a process potentially controlled by elevated plasma ghrelin levels.

Binge-like intake of HFD attenuates alcohol intake in rats.

Binge eating and binge alcohol intake are behavioral manifestations of pathological feeding and alcohol use disorder (AUD), respectively. Binge-feeding and AUD have high comorbidity with other psychiatric disorders such as depression, which could have important implications for the management of these conditions. Importantly, these behaviors share many common features suggesting a singular etiology. However, the nature by which binge-feeding affects the development or maintenance of AUD is unclear. The present study examined the impact of a binge-feeding from a nutritionally complete high-fat diet (HFD) on initiation and maintenance of alcohol intake, anxiolytic behavior and central genetic changes in brain regions that control alcohol-reinforced behaviors. To do this, male Long-Evans rats received chow (controls) or HFD every three days (HFD-3D) or every day (HFD-ED) for 5weeks. Rodent chow and water were available ad-libitum to all groups throughout the experiment. Following 5weeks of HFD cycling, 20.0% ethanol or 2.0% sucrose intake was evaluated. In addition, anxiety-like behavior was measured using a light-dark box apparatus. Both HFD-3D and -ED groups of rats consumed significantly large amount of food during 2h HFD access sessions and reduced their chow intake in the next 22h. Surprisingly, binge-fed rats displayed attenuated acquisition of alcohol intake whereas sucrose consumption was unaffected. Rats exposed to HFD spent more time in the light side compared to chow controls, indicating that binge-feeding induced anxiolytic effects. In addition, alterations in the brain neurotensin system were observed following HFD exposure. These data indicate that binge-feeding behavior induces behavioral and genetic changes that help explain how alcohol intake is influenced by co-morbid eating disorders.