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Hypothalamic Neuronal Circuits Are Modulated by Insulin and Impact Metabolism 1
Published in André Kleinridders, Physiological Consequences of Brain Insulin Action, 2023
Tadeu de Oliveira Diz, Sabela Casado, Rubén Nogueiras, Sulay Tovar
Insulin action over POMC neurons in the ARC stimulates the release of POMC peptide that is processed to generate α-melanocyte-stimulating hormone (α-MSH). This α-MSH activates second-order neurons through direct interaction with the melanocortin receptors (MCRs) which are part of the central melanocortin system, essential for the regulation of long-term energy homeostasis. The two main MCRs in the hypothalamus are melanocortin 3 receptor (MC3R) and melanocortin 4 receptor (MC4R), they are G protein-coupled receptors with a high level of constitutive activity and play a critical role in mediating the anorexigenic signal through α-MSH and the orexigenic signal through AgRP, respectively (28, 47). The activation of MC4R by α-MSH signals decreases energy intake. Moreover, POMC neurons’ action over distinct MC4R expressing neuronal populations causes a decrease in insulin secretion or increases insulin sensitivity independently of their effect on food intake and energy expenditure (48).
Current advancements in pharmacotherapy for cancer cachexia
Published in Expert Opinion on Pharmacotherapy, 2023
Guilherme Wesley Peixoto da Fonseca, Ryosuke Sato, Maria Janieire de Nazaré Nunes Alves, Stephan von Haehling
Anorexia and weight loss are cardinal features of cancer cachexia. The central melanocortin system, a key regulator in promoting energy homeostasis balance, controls body weight through an interconnected and complex neural network located in the hypothalamus [37]. In the arcuate nucleus, there are two classes of neurons responsible for stimulating (1) orexigenic pathways via agouti-related peptides (AgRP) and neuropeptide Y (NPY) and (2) anorexigenic pathways working through pro-opiomelanocortin (POMC) [38]. The counterbalance action between AgRP/NPY and POMC relies on a neuroendocrine circuit mediated mainly by ghrelin increased in a hunger state and leptin elevated in a fed state.