This paper develops a model for coordinate regulation of feeding, metabolism, and growth based on studies in fish. Many factors involved with the control of feeding [e.g., cholecystokinin (CCK) and ghrelin (GRLN)], energy metabolism [e.g., insulin (INS), glucagon (GLU), glucagon-like peptide (GLP), and somatostatins (SS), produced in the endocrine pancreas; and leptin (LEP) produced broadly], and growth [e.g., GRLN, growth hormone (GH), insulin-like growth factors (IGFs), GH receptors (GHR), IGF receptors (IGFR)] interact at various levels. Many such interactions serve to coordinate these systems to favor anabolic processes (i.e., lipid and protein synthesis, glycogenesis) and growth, including GH promotion of feeding and stimulation of INS production/secretion and the upregulation of GHR and IGFR by GRLN. As nutrient and stored energy status change, various feedbacks serve to curtail feeding and transition the animal from an anabolic/growth state to a catabolic state. Many factors, including LEP and IGF, promote satiety, whereas SS downregulates INS signaling as well as IGF production and GHR and IGFR abundance. As INS and IGF levels fall, GH becomes disconnected from growth as a result of altered linkage of GHR to cell signaling pathways. As a result, the catabolic actions of GH, GLU, GLP, LEP, and SS prevail, mobilizing stored energy reserves. Coordinate regulation involves relative abundances of blood-borne hormones as well as the ability to adjust responsiveness to hormones (via receptor and post-receptor events) in a cell-/tissue-specific manner that results from genetic and epigenetic programming and modulation by the local milieu of hormones, nutrients, and autocrine/paracrine interactions. The proposed model of coordinate regulation demonstrates how feeding, metabolism, and growth are integrated with each other and with other processes, such as reproduction, and how adaptive adjustments can be made to energy allocation during an animal’s life history and/or in response to changes in environmental conditions.

本文基于对鱼类的研究，开发了一个协调调节摄食、新陈代谢和生长的模型。与控制进食有关的许多因素[例如胆囊收缩素 (CCK) 和生长素释放肽 (GRLN)]、能量代谢 [例如胰岛素 (INS)、胰高血糖素 (GLU)、胰高血糖素样肽 (GLP) 和生长抑素 (SS) ，在内分泌胰腺中产生；和瘦素 (LEP) 广泛产生]，并且生长 [例如，GRLN、生长激素 (GH)、胰岛素样生长因子 (IGF)、GH 受体 (GHR)、IGF 受体 (IGFR)] 在不同水平上相互作用。许多这样的相互作用有助于协调这些系统以促进合成代谢过程（即、脂质和蛋白质合成、糖生成）和生长，包括 GH 促进摄食和刺激 INS 产生/分泌以及 GRLN 上调 GHR 和 IGFR。随着营养和储存能量状态的变化，各种反馈有助于减少喂养并将动物从合成代谢/生长状态转变为分解代谢状态。许多因素，包括 LEP 和 IGF，促进饱腹感，而 SS 下调 INS 信号以及 IGF 产生和 GHR 和 IGFR 丰度。随着 INS 和 IGF 水平下降，由于 GHR 与细胞信号通路的连接发生改变，GH 与生长脱节。结果，GH、GLU、GLP、LEP 和 SS 的分解代谢作用占了上风，调动了储存的能量储备。协调调节涉及血源性激素的相对丰度以及以细胞/组织特异性方式调节对激素的反应性（通过受体和受体后事件）的能力，这种方式由遗传和表观遗传编程和局部调节引起激素、营养素和自分泌/旁分泌相互作用的环境。所提出的协调调节模型展示了摄食、新陈代谢和生长如何相互整合，以及如何与其他过程（如繁殖）整合，以及如何在动物的生命史和/或响应变化时对能量分配进行适应性调整在环境条件下。