Vitoria Academic Center, Federal University of Pernambuco, Rua do Alto do Reservatório, S/N, Bela Vista, CEP 55608-680 Vitória de Santo Antão, PE, Brazil.
Federal University of Bahia, School of Nutrition, Rua Basilio da Gama, s/n, Campus Canela, CEP: 40.110-907 Salvador, BA, Brazil.
Life Sci. 2022 Nov 15;309:120947. doi: 10.1016/j.lfs.2022.120947. Epub 2022 Sep 9.
Eating behavior is regulated by central and peripheral signals, which interact to modulate the response to nutrient intake. Central control is mediated by the hypothalamus through neuropeptides that activate the orexigenic and anorexigenic pathways. Energy homeostasis depends on the efficiency of these regulatory mechanisms. This neuroendocrine regulation of hunger and appetite can be modulated by nutritional sensors such as adenosine monophosphate-activated protein kinase (AMPK). Thus, this systematic review discusses the literature on correlations between AMPK and hypothalamic neuropeptides regarding control of eating behavior. Lilacs, PubMed/Medline, ScienceDirect, and Web of Science were searched for articles published from 2009 to 2021 containing combinations of the following descriptors: "eating behavior," "hypothalamus," "neuropeptide," and "AMPK." Of the 1330 articles found initially, 27 were selected after application of the inclusion and exclusion criteria. Of the selected articles, 15 reported decreased AMPK activity, due to interventions using angiotensin II infusion, fructose, glucose, cholecystokinin, leptin, or lipopolysaccharide (LPS) injection; dietary control through a low-protein diet or a high-fat diet (60 % fat); induction of hyperthyroidism; or injection of AMPK inhibitors. Seven studies showed a decrease in neuropeptide Y (NPY) through CV4 AICAR administration; fructose, glucose, leptin, or angiotensin II injections; or infusion of LPS from Escherichia coli and liver kinase B1 (LKB1) overexpression. Eleven studies reported a decrease in food consumption due to a decrease in AMPK activity and/or hypothalamic neuropeptides such as NPY. The results indicate that there is a relationship between AMPK and the control of eating behavior: a decrease in AMPK activity due to a dietary or non-dietary stimulus is associated with a consequent decrease in food intake. Furthermore, AMPK activity can be modulated by glucose, thyroid hormones, estradiol, leptin, and ghrelin.
进食行为受中枢和外周信号的调节，这些信号相互作用以调节对营养摄入的反应。中枢控制是通过下丘脑内的神经肽介导的，这些神经肽激活食欲肽和厌食肽途径。能量平衡取决于这些调节机制的效率。这种饥饿和食欲的神经内分泌调节可以通过营养传感器如单磷酸腺苷激活蛋白激酶 (AMPK) 来调节。因此，本系统综述讨论了关于 AMPK 与下丘脑神经肽在控制进食行为方面相关性的文献。通过 Lilacs、PubMed/Medline、ScienceDirect 和 Web of Science 检索了 2009 年至 2021 年发表的包含以下描述符组合的文章：“进食行为”、“下丘脑”、“神经肽”和“AMPK”。在最初发现的 1330 篇文章中，经过纳入和排除标准的应用，选择了 27 篇文章。在所选择的文章中，有 15 篇报道 AMPK 活性降低，原因是使用血管紧张素 II 输注、果糖、葡萄糖、胆囊收缩素、瘦素或脂多糖 (LPS) 注射；通过低蛋白饮食或高脂肪饮食 (60%脂肪) 进行饮食控制；诱导甲状腺功能亢进；或注射 AMPK 抑制剂。有 7 项研究表明，通过 CV4 AICAR 给药、果糖、葡萄糖、瘦素或血管紧张素 II 注射或大肠杆菌脂多糖 (LPS) 输注，神经肽 Y (NPY) 减少。11 项研究报告称，由于 AMPK 活性和/或下丘脑神经肽如 NPY 的降低，食物摄入量减少。结果表明，AMPK 与进食行为的控制之间存在关系：由于饮食或非饮食刺激导致 AMPK 活性降低与随后的食物摄入量减少有关。此外，AMPK 活性可以通过葡萄糖、甲状腺激素、雌二醇、瘦素和胃饥饿素来调节。
