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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
However, there is some controversy in the insulin action on the POMC neurons as some studies report that insulin can both stimulate (38) or inhibit (36) POMC neurons. There is a publication showing that insulin in POMC neurons can display either excitation (11%), inhibition (51%) or no-responsivity (38%) and that in POMC neurons of diet-induced obese mice the neuronal response is quite different (3% excitation, 65% inhibition, 32% no-response) (39). Interestingly, disruption of insulin signalling from POMC neurons did not affect energy or glucose homeostasis (36), but it is known that POMC has a critical role in the regulation of metabolism as some human studies show that some POMC gene mutations display early-onset obesity (40, 41).
Disorders of Pigmentation
Published in Ayşe Serap Karadağ, Lawrence Charles Parish, Jordan V. Wang, Roxburgh's Common Skin Diseases, 2022
Michael Joseph Lavery, Charles Cathcart, Hasan Aksoy
Melanin synthesis is controlled by the melanocyte-stimulating hormone (MSH), which is derived from propiomelanocortin (POMC). POMC is also the precursor for adrenocorticotropic hormone (ACTH), which is raised in Addison’s disease. This accounts for the cutaneous hyperpigmentation seen in this condition. Once synthesized, melanin is then packaged into melanosomes and transported to neighboring keratinocytes.
Neuropeptide Regulation of Ion Channels and Food Intake
Published in Tian-Le Xu, Long-Jun Wu, Nonclassical Ion Channels in the Nervous System, 2021
POMC is the precursor of melanocyte-stimulating hormone (MSH), adrenocorticotrophin (ACTH), and beta-endorphin. Activation of POMC neurons mainly excites postsynaptic MC4R-expressing neurons in the PVN to produce inhibitory regulation on food intake. Due to the high-density MC4R expression, PVN becomes a major target for both AgRP and POMC neurons to maintain energy homeostasis. In addition to PVN, POMC neurons in the arcuate nucleus also innervate other brain areas such as the lateral hypothalamus and ventromedial hypothalamus for the functional regulation of food intake (Sohn 2015).
Leptin’s Immune Action: A Review Beyond Satiety
Published in Immunological Investigations, 2023
Alice Abend Bardagi, Clarissa dos Santos Paschoal, Giovanna Ganem Favero, Luisa Riccetto, Maria Luisa Alexandrino Dias, Gil Guerra Junior, Giovanna Degasperi
The arcuate nucleus, located at the base of the hypothalamus (Bouret et al. 2004), expresses a higher density of LepRb in its neurons, suggesting that leptin has a big role in hunger-satiety regulation in this region (Flak and Myers 2016). This nucleus sustains connections with the ventromedial, dorsomedial, and paraventricular nuclei, which also express leptin receptors, implying that they are also involved in modulating the hunger cycle (Perello and Raingo 2013). In the arcuate nucleus, leptin activates POMC-producing neurons. Consequently, POMC is cleaved into alpha-melanocyte-stimulating hormone (α-MSH), which inhibits food intake via melanocortin receptors 3 and 4 (MC3R and MC4R). Leptin also inhibits AgRP, NPY, and GABAergic neurons, thus inhibiting the hunger feeling (Coppari et al. 2005). During fasting periods, the activation of AgRP, NPY, and GABAergic neurons motivate and enable food seeking behaviors; on the other hand, anorexigenic neurons are activated by the increase in leptin blood levels after food intake (Davis et al. 2011).
Possible roles of brain derived neurotrophic factor and corticotropin releasing hormone neurons in the nucleus of hippocampal commissure functioning within the avian neuroendocrine regulation of stress
Published in Stress, 2021
Hakeem J. Kadhim, Seong W. Kang, Wayne J. Kuenzel
Activation of parvocellular neurons within the avian hypothalamic paraventricular nucleus (PVN) resulted in an increase of corticotropin releasing hormone (CRH) and arginine vasotocin (AVT) (Kuenzel & Jurkevich, 2010). When CRH and AVT reach the anterior pituitary (APit), CRH binds to two G-protein coupled receptors, CRHR1 and CRHR2; AVT or AVP binds to the V1aR and V1bR. They, in turn, stimulate proopiomelanocortin (POMC) synthesis that is further processed to adrenocorticotropic hormone (ACTH) (Bonfiglio et al., 2011). In adrenal glands, ACTH activates the avian interrenal tissue to produce the stress hormone, corticosterone (CORT) (Herman et al., 2016; Romero, 2004). Stress hormone binds to glucocorticoid receptors (GRs) located on different tissues to provide energy for immediate use (McEwen, 2007) as well as to induce a negative feedback that regulates hypothalamic-pituitary-adrenocortical (HPA) axis activity (Keller-Wood, 2015; Chrousos, 2009; Vandenborne et al., 2005). Additionally, CRH neurons were identified in the nucleus of the hippocampal commissure (NHpC), an extra-hypothalamic structure, suggesting that the NHpC may be involved in the regulation of the stress response (Nagarajan et al., 2017a, 2014; Xie et al., 2010).
From leptin to lasers: the past and present of mouse models of obesity
Published in Expert Opinion on Drug Discovery, 2021
Joshua R. Barton, Adam E. Snook, Scott A. Waldman
Stimulation and inhibition of appetitive circuits by light-sensitive channels (optogenetics), is in the forefront in the study of obesity over the last decade. Many studies use stereotactic injection of Adeno-Associated viruses (AAV) to infect neurons with channelrhodopsin. To further dissect the functionality of AGRP and POMC neurons in the ARC, AGRP-Cre and POMC-Cre mice were again used to discriminate between the two neuronal populations [130]. These mice were stereotactically injected with AAV-FLEX-rev-ChR2:tdtomato, a virus encoding a fluorescently-labeled ChR2 that would only be expressed in neurons that also expressed Cre. Stimulation of AGRP+ ARC neurons resulted in an 8-fold increase in food consumption over 1 hr in mice with high levels of ChR2 expression. POMC stimulation decreased food consumption over a longer time course, resulting in a cumulative decrease in food intake and body weight after 24hrs.