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首页> 外文期刊>Journal of neuroendocrinology >Ghrelin receptor in agouti‐related peptide neurones regulates metabolic adaptation to calorie restriction
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Ghrelin receptor in agouti‐related peptide neurones regulates metabolic adaptation to calorie restriction

机译：agouti相关肽神经元中的Ghrelin受体调节卡路里限制的代谢适应

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Abstract Ghrelin is a gut hormone that signals to the hypothalamus to stimulate growth hormone release, increase food intake and promote fat deposition. The ghrelin receptor, also known as growth hormone secretagogue receptor ( GHS ‐R), is highly expressed in the brain, with the highest expression in agouti‐related peptide (Ag RP ) neurones in the hypothalamus. Compelling evidence indicates that ghrelin serves as a survival hormone with respect to maintaining blood glucose and body weight during nutritional deficiencies. Recent studies have demonstrated that Ag RP neurones are involved in metabolic and behavioural adaptation to an energy deficit to improve survival. In the present study, we used a neuronal subtype‐specific GHS ‐R knockout mouse ( AgRP‐Cre;Ghsr f/f ) to investigate the role of GHS ‐R in hypothalamic Ag RP neurones in metabolic and behavioural adaptation to hypocaloric restricted feeding. We subjected the mice to a restricted feeding regimen of 40% mild calorie restriction ( CR ), with one‐quarter of food allotment given in the beginning of the light cycle and three‐quarters given at the beginning of the dark cycle, to mimic normal mouse intake pattern. The CR ‐fed AgRP‐Cre;Ghsr f/f mice exhibited reductions in body weight, fat mass and blood glucose. Metabolic profiling of these CR ‐fed AgRP‐Cre;Ghsr f/f mice showed a trend toward reduced basal metabolic rate, significantly reduced core body temperature and a decreased expression of thermogenic genes in brown adipose tissue. This suggests a metabolic reset to a lower threshold. Significantly increased physical activity, a trend toward increased food anticipatory behaviour and altered fuel preferences were also observed in these mice. In addition, these CR ‐fed AgRP‐Cre;Ghsr f/f mice exhibited a decreased counter‐regulatory response, showing impaired hepatic glucose production. Lastly, hypothalamic gene expression in AgRP‐Cre;Ghsr f/f mice revealed increased Ag RP expression and a decreased expression of genes in β‐oxidation pathways. In summary, our data suggest that GHS ‐R in Ag RP neurones is a key component of the neurocircuitry involved in metabolic adaptation to calorie restriction.
机译：摘要Ghrelin是一种肠道激素，其向下丘脑发出刺激生长激素释放，增加食物摄入并促进脂肪沉积。胰岛素受体，又称生长激素分泌蛋白受体（GHS -R），在脑中高度表达，在下丘脑中具有最高的agouti相关的肽（Ag RP）神经元的表达。令人信服的证据表明，在营养缺陷期间，Ghrelin是在维持血糖和体重的生存激素。最近的研究表明，AG RP神经元涉及代谢和行为适应，以改善存活的能量缺陷。在本研究中，我们使用了神经元亚型特异性GHS -R敲除小鼠（AGRP-CRE; GHSR F / F），以探讨GHS -R在丘脑常压AGRP神经元中的代谢和行为适应对低自由基喂养的作用。我们将小鼠与约40％轻度卡路里限制（CR）的限制饲养方案进行了40％的饲养方案，在浅循环开始时，在暗循环开始时给出的四分之三，以模仿正常的四分之三鼠标进气模式。 CR -FED AGRP-CRE; GHSR F / F小鼠表现出体重，脂肪肿块和血糖的降低。这些CR的代谢分析 - F / F小鼠的GHSR F / F小鼠表现出降低基础代谢率的趋势，核心体温显着降低，棕色脂肪组织中的热基因的表达降低。这表明代谢重置为较低的阈值。在这些小鼠中也观察到体育活动显着提高了身体活动，趋势增加了粮食预期行为和改变的燃料偏好。此外，这些CR -FED AGRP-CRE; GHSR F / F小鼠表现出降低的反调节响应，表现出肝脏葡萄糖产生受损。最后，AgrP-CRE中的下丘脑基因表达; GHSR F / F小鼠揭示了β-氧化途径中基因的增加的增加。总之，我们的数据表明，AG RP神经元中的GHS -R是涉及对卡路里限制的代谢适应的神经循环的关键组成部分。

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