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首页> 外文期刊>Journal of neuroendocrinology >Ghrelin receptor deletion reduces binge‐like alcohol drinking in rats
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Ghrelin receptor deletion reduces binge‐like alcohol drinking in rats

机译：Ghrelin受体缺失减少了大鼠的狂犬病饮酒

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Ghrelin is a gastric hormone that has been implicated in the neurobiology of alcohol drinking. We have recently developed a ghrelin receptor (growth hormone secretagogue receptor; GHSR ) knockout ( KO ) rat model, which exhibits reduced food consumption and body weight. In addition, recent preliminary work suggests that the gut‐microbiome, which appears to interact with the ghrelin system, may modulate alcohol drinking. In the present study, we investigated the effects of GHSR deletion on alcohol consumption utilising GHSR KO and wild‐type ( WT ) rats in three separate alcohol consumption paradigms: (i) operant self‐administration (30‐minute sessions); (ii) drinking in the dark ( DID) ( 4‐hour sessions); and (iii) intermittent access (24‐hour sessions). These paradigms model varying degrees of alcohol consumption. Furthermore, we aimed to investigate the gut‐microbiome composition of GHSR KO and WT rats before and after alcohol exposure. We found that the GHSR KO rats self‐administered significantly less alcohol compared to WT rats in the operant paradigm, and consumed less alcohol than WT in the initial stages of the DID paradigm. No genotype differences were found in the intermittent access test. In addition, we found a significant decrease in gut‐microbial diversity after alcohol exposure in both genotypes. Thus, the present results indicate that the ghrelin system may be involved in drinking patterns that result in presumably increased alcohol exposure levels. Furthermore, GHSR may constitute a potential pharmacological target for the reduction of binge‐alcohol consumption. The potential functional role of the gut‐microbiome in alcohol drinking, as well as interaction with the ghrelin system, is an interesting topic for further investigation.
机译：Ghrelin是一种胃激素，它涉及酒精饮用的神经生物学。我们最近开发了一种Ghrelin受体（生长激素促分泌素受体; GHSR）淘汰（KO）大鼠模型，其表现出降低的食物消耗和体重。此外，最近的初步工作表明，肠道微生物组似乎与Ghrelin系统相互作用，可以调节酒精饮用。在本研究中，我们调查了GHSR缺失在三个单独的酒精消费范式中利用GHSR KO和野生型（WT）大鼠的酒精消费的影响：（i）操作人员自我管理（30分钟课程）; （ii）在黑暗中喝酒（DID）（4小时课程）; （iii）间歇性访问（24小时课程）。这些范式模型不同程度的酒精消耗。此外，我们旨在研究酒精暴露前后GHSR KO和WT大鼠的肠道微生物组成。我们发现，与操作范式中的WT大鼠相比，GHSR KO大鼠明显更少的酒精，并且在DID范式的初始阶段中消耗的酒精少于WT。在间歇访问测试中没有发现基因型差异。此外，我们发现在两种基因型中的酒精暴露后肠道微生物多样性显着降低。因此，本结果表明Ghrelin系统可以参与导致可能提高的酒精暴露水平的饮用模式。此外，GHSR可以构成降低泪液消耗的潜在药理学靶标。肠道微生物组在酒精饮用中的潜在功能作用，以及与Ghrelin系统的互动，是进一步调查的有趣话题。

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