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

Abstract

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 (24 hr 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.

Access schedules mediate the impact of high fat diet on ethanol intake and insulin and glucose function in mice

“…Our finding that ad libitum HFD access decreases ad libitum EtOH intake (UAE+HFD group) is a common finding in the literature in both male and female rodents (Feng et al, 2012;Gelineau et al, 2017;Sirohi et al, 2017aSirohi et al, , 2017b. This may be due to a number of factors.…”

“…A similar positive relationship for EtOH-induced increases in HFD intake has been shown in some animal models (Barson et al, 2009). While the inverse relationship of HFD exposure stimulating EtOH intake has also been suggested in some animal models (Carrillo et al, 2004), the majority of findings indicate that HFD exposure decreases EtOH consumption (Feng et al, 2012;Gelineau et al, 2017;Sirohi et al, 2017aSirohi et al, , 2017b. The majority of these previous studies, however, have examined EtOH intake in the face of HFD access without specific focus on metabolic function, or examined metabolic effects of EtOH and HFD without taking intake behaviors into account.…”

“…Importantly, findings from the LAE model suggest that HFD does not greatly alter EtOH intake when EtOH access is limited, regardless of EtOH reward value. This is an important consideration given the previous preclinical literature indicating a reduction in EtOH intake by HFD, but numerous clinical findings indicate that EtOH stimulates HFD intake and vice versa (Breslow et al, 2013;Caton et al, 2004;Feng et al, 2012;Gelineau et al, 2017;Piazza-Gardner and Barry, 2014;Sirohi et al, 2017aSirohi et al, , 2017b. Intriguingly, mice that had HFD on a limited, intermittent schedule (iHFD-E mice) developed binge eating patterns that appeared to trigger increased EtOH consumption in a limited access schedule.…”

Growth hormone secretagogue receptor signalling affects high‐fat intake independently of plasma levels of ghrelin andLEAP2, in a 4‐day binge eating model

“…For example, a recent study found that i.c.v.‐injected ghrelin shifts diet preference, increasing RC intake and reducing HF intake, in rats exposed to a 2‐week binge eating protocol with simultaneous access to both diets . Also, it was shown that rats intermittently and time‐limited fed with different palatable diets for several weeks displayed higher plasma ghrelin levels before each binge eating event . In particular, one study found that increments of plasma ghrelin levels positively correlated with food anticipatory activity and that a GHSR antagonist decreased such behaviour, whereas another study showed that blockade of plasma ghrelin increments attenuated the magnitude of binge‐like HF intake .…”

“…58 Also, it was shown that rats intermittently and time-limited fed with different palatable diets for several weeks displayed higher plasma ghrelin levels before each binge eating event. [59][60][61][62][63] In particular, one study found that increments of plasma ghrelin levels positively correlated with food anticipatory activity and that a GHSR antagonist decreased such behaviour, 60 whereas another study showed that blockade of plasma ghrelin increments attenuated the magnitude of binge-like HF intake. 63 Moreover, two studies found that mice or rats intermittently and time-limited fed with a palatable diet over several weeks displayed a reduction of plasma ghrelin levels immediately after the last binge eating event.…”