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首页> 外文期刊>Endocrinology >Assessing Interactions Between Ghsr and Mc3r Reveals a Role for AgRP in the Expression of Food Anticipatory Activity in Male Mice
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Assessing Interactions Between Ghsr and Mc3r Reveals a Role for AgRP in the Expression of Food Anticipatory Activity in Male Mice

机译：评估Ghsr和Mc3r之间的相互作用揭示了AgRP在雄性小鼠食物预期活性表达中的作用

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摘要

The stomach hormone ghrelin and hypothalamic melanocortin neurons belong to a gut-brain circuit controlling appetite and metabolic homeostasis. Mice lacking melanocortin-3 receptor (Mc3rKO) or growth hormone secretagogue receptor (GhsrKO) genes exhibit attenuated food anticipatory activity (FAA), a rise in locomotor activity anticipating mealtime, suggesting common circuitry regulating anticipatory responses to nutrient loading. To investigate the interaction between Ghsrs and Mc3rs, we compared food anticipatory responses in GhsrKO, Mc3rKO, and double Ghsr;Mc3r knockout (DKO) mice subjected to a hypocaloric restricted feeding (RF) protocol in constant dark or 12-hour light, 12-hour dark settings. DKO are viable, exhibiting no overt behavioral or metabolic phenotypes in ad libitum or fasting conditions. FAA was initially attenuated in all mutant strains in constant darkness. However, GhsrKO eventually exhibited a robust food anticipatory response, suggesting compensation. Mc3rKO and DKO did not compensate, indicating a continued requirement for Mc3rs in maintaining the expression of FAA in situations of RF. Abnormal regulation of hypothalamic agouti-related peptideeuropeptide Y (AgRP/Npy) neurons previously observed during fasting may contribute to attenuated FAA in Mc3rKO. AgRP and Npy expression measured 1 hour before food presentation correlated positively with FAA. Absence of Mc3rs (but not Ghsrs) was associated with lower AgRP/Npy expression, suggesting attenuated responses to signals of negative energy balance. These observations support the importance of Mc3rs as modulators of anticipatory responses to feeding, with mice able to compensate for loss of Ghsrs. The behavioral deficits of Mc3rKO displayed during RF may be partially explained by reduced hunger sensations owing to abnormal regulation of orexigenic AgRP/Npy neurons.
机译：胃激素ghrelin和下丘脑黑皮质素神经元属于控制食欲和代谢稳态的肠脑回路。缺乏黑皮质素3受体（Mc3rKO）或生长激素促分泌素受体（GhsrKO）基因的小鼠表现出减弱的食物预期活性（FAA），预期进食时间的运动活动增加，表明调节营养物预期反应的常见电路。为了研究Ghsrs与​​Mc3rs之间的相互作用，我们比较了GhsrKO，Mc3rKO和双重Ghsr; Mc3r基因敲除（DKO）小鼠在恒定黑暗或12小时光照，12小时光照下的食物预期反应一小时的黑暗设置。 DKO是可行的，在随意或禁食条件下不表现出明显的行为或代谢表型。在所有变种菌株中，FAA最初在恒定的黑暗中被减弱。然而，GhsrKO最终表现出强烈的食品预期反应，提示其补偿。 Mc3rKO和DKO没有补偿，这表明在RF情况下继续要求Mc3rs维持FAA的表达。先前在禁食期间观察到的下丘脑刺突相关肽/神经肽Y（AgRP / Npy）神经元的异常调节可能导致Mc3rKO中的FAA减弱。食物呈现前1小时测得的AgRP和Npy表达与FAA呈正相关。缺少Mc3rs（而不是Ghsrs）与较低的AgRP / Npy表达相关，表明对负能量平衡信号的响应减弱。这些观察结果支持了Mc3rs作为预期的进食反应调节剂的重要性，其中小鼠能够补偿Ghsrs的损失。在RF期间显示的Mc3rKO的行为缺陷可以部分归因于由于致食性AgRP / Npy神经元的异常调节而导致的饥饿感降低。

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