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Recent studies from our lab have demonstrated that intermittent high-fat diet access reduces alcohol drinking in rats. However, it was unclear if caloric overload, palatability, or diet itself triggered reduced alcohol drinking. It is also unknown if a similar paradigm could reduce relapse-like alcohol drinking. The presented study tested the hypothesis that acute intermittent palatable diet (PD) access would rescue relapse-like drinking and palatability, but not diet itself contributes to reduced drinking. Male Long Evans rats received six-weeks intermittent or chronic chow (controls) or PDs (high-fat diet, high-sugar diet) exposure, and alcohol testing occurred following PDs suspension. Alcohol intake was not significantly different among groups in either condition, suggesting that diet itself did not impact alcohol drinking. A subset of these rats received two-weeks intermittent PDs (Int-PDs) exposure and alcohol testing reinitiated while Int-PDs access continued. Alcohol intake significantly escalated (~137% compared to baseline; alcohol deprivation effect) in the chow controls, whereas it remained unchanged in PD groups. These data demonstrate the critical importance of acute intermittent PDs availability and its protective effect in relapse-like drinking. To assess the contribution of palatability in reduced alcohol drinking, a separate group of rats received two-weeks intermittent high-sugar diet (Int-HSD) or saccharin (Int-SAC) access and tested for alcohol drinking while Int-HSD/SAC continued. Alcohol drinking significantly decreased (~30%) in both HSD and SAC groups compared to the controls. These data identify the critical parameters by which acute intermittent PD access reduces alcohol drinking and could have important therapeutic implications in the management of alcoholism., Competing Interests: Declaration of Competing Interest None., (Copyright © 2020 Elsevier Inc. All rights reserved.)

We have previously shown that 6 weeks of intermittent high-fat diet (Int-HFD) pre-exposure significantly reduced alcohol drinking in rats, providing preliminary evidence of the effectiveness of a dietary intervention in reducing alcohol intake. However, the functional framework and underlying neurobiological mechanisms of such dietary intervention are unknown. Here, we examined the impact of Int-HFD pre-exposure duration on alcohol drinking, plasma feeding peptides, and central neurotransmitter receptors gene expression. Male Long Evans rats ( n = 6-7/group) received no pre-exposure, 1 or 2 weeks pre-exposure to Int-HFD and alcohol drinking (two-bottle choice) was evaluated. We observed HFD pre-exposure-dependent decrease in alcohol drinking, with a significant decrease observed following 2 weeks of Int-HFD pre-exposure. No significant between-group differences in plasma feeding peptides (i.e., ghrelin, leptin, insulin) were detected. A PCR array revealed that the expression of several neurotransmitter receptors was significantly ( p < 0.05 and ≥2-fold) altered in the striatum and ventral tegmental area compared to controls. These data suggest that pre-exposure to a palatable diet is critical to reduce alcohol drinking in rats, possibly through genetic alterations in the brain reward circuitry. Importantly, the present study is a step forward in identifying the critical framework needed to evaluate the therapeutic potential of nutritional contingency in the management of alcoholism.

While a bidirectional positive link between palatable food intake and alcohol drinking has been suggested, several rodents studies report reduced alcohol drinking following palatable diets exposure. These studies utilized purified rodents' diets high in sugar/fat; however, the effects of hyper-palatable food (HPF) rich in fat and sugar on alcohol drinking remain unclear. Furthermore, neural substrates involved in HPF-mediated changes in alcohol consumption are poorly understood. Therefore, the present study evaluated the effects of patterned feeding of a hyper-palatable food (Oreo cookies) on alcohol drinking as well as dopamine (DA) and serotonin (5-HT) content in rat's mesocorticolimbic (medial-prefrontal cortex, orbitofrontal cortex, amygdala, and nucleus accumbens) circuitry. Male Long Evans rats received 8-weeks of intermittent (Mon, Tue, Wed) Oreo cookies access, which induced a patterned feeding, in which rats in the Oreo group overconsumed calories on HPF days whereas underconsumption was observed on chow only (Thu, Fri) days. Following HPF exposure, alcohol consumption was evaluated while patterned feeding continued. Alcohol intake in the Oreo group was significantly lower as compared to the chow controls. However, alcohol intake in the Oreo group increased to the levels seen in the group receiving chow following the suspension of patterned HPF feeding. Finally, DA levels in the nucleus accumbens were significantly greater, whereas its metabolite (DOPAC) levels were lower in the Oreo group compared to the chow controls. Surprisingly, 5-HT levels remained unaltered in all tested brain areas. Together, these data suggest that HPF-associated increased DA availability and reduced DA turnover within mesocorticolimbic circuitry may regulate alcohol drinking following patterned HPF feeding. [ABSTRACT FROM AUTHOR]