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Neuroendocrine Interactions in the Control of Glucose- and Energy Homeostasis
Published in André Kleinridders, Physiological Consequences of Brain Insulin Action, 2023
The insulin receptor is expressed throughout the brain with particular abundance in neuropeptide Y/agouti-related peptide (NPY/AgRP)- as well as proopiomelanocortin/cocaine and amphetamine-regulated transcript (POMC/CART)-expressing neurons of the hypothalamic ARC (2, 8, 9). Intracerebroventricular injections of NPY and AgRP lead to increased food intake, decreased energy expenditure and weight gain (10–13), identifying both neuropeptides as anabolic signals. In contrast, catabolic effects were demonstrated for both CART and α-melanocyte-stimulating hormone, which is cleaved from its precursor POMC (14, 15).
Central and Peripheral Modulators of Appetite and Satiety
Published in Emmanuel C. Opara, Sam Dagogo-Jack, Nutrition and Diabetes, 2019
Gabrielle Page-Wilson, Sam Dagogo-Jack
As a central integrator of energy homeostasis, the hypothalamus also is a source of neuropeptides that inhibit food intake or induce satiety. The hypothalamic anorexigenic agents include the melanocortins, cocaine- and amphetamine-regulated transcript (CART), and serotonin.
Regulation of Food Intake
Published in Nathalie Bergeron, Patty W. Siri-Tarino, George A. Bray, Ronald M. Krauss, Nutrition and Cardiometabolic Health, 2017
Surya Panicker Rajeev, Ian W. Seetho, John P.H. Wilding, Nathalie Bergeron, Patty W. Siri-Tarino, George A. Bray, Ronald M. Krauss
Within the hypothalamus, the arcuate nucleus (ARC) at the base of the median eminence in the floor of the third ventricle integrates neural and hormonal signals regulating peripheral satiety and adiposity through neuropeptide orexigenic and anorexigenic transmission to other brain regions. These include orexigenic neuropeptides such as neuropeptide Y (NPY) and Agouti-related peptide (AgRP) and anorexigenic neuropeptides such as proopiomelanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART). Peripheral signals influence the activity of these neuronal populations to change feeding behavior and energy homeostasis [6].
Mechanistically acting anti-obesity compositions/formulations of natural origin: a patent review (2010–2021)
Published in Expert Opinion on Therapeutic Patents, 2022
Pracheta Sengupta, Niyati Tiwari, Tanya Bhatt, Atish T. Paul
The nucleus of the hypothalamus can also be directly influenced by circulating factors as it is partially outside the blood–brain barrier. There are two well-characterized neuronal populations involved in this pathway, namely, appetite inhibiting and appetite-stimulating neurons. The appetite inhibiting neurons further includes proopiomelanocortin (POMC) & cocaine and amphetamine-regulated transcript (CART) co-expressing neurons. Appetite-stimulating neurons includes neuropeptide Y (NPY) and agouti-related peptide co-expressing neurons [24–26]. One of the major genes associated with anorexigenic signaling is the melanocortin receptor genes (MC2R, MC3R, and MC4R) that stimulates melanocortin stimulating hormone (MSH) and melanin-concentrating hormone (MCH) [27]. In the hypothalamus, the neurotransmitter α-melanocyte stimulating hormone (α-MSH) is produced that act on the melanocortin receptor in another part of the hypothalamus to reduce food intake. Lack of leptin on the leptin receptor, in both animals and humans, leads to obesity (Figure 1(C)).
Efficacy and safety of lorcaserin in obesity: a systematic review and meta-analysis of randomized controlled trials
Published in Expert Review of Clinical Pharmacology, 2020
Awadhesh Kumar Singh, Ritu Singh
Lorcaserin (10 mg twice daily), a selective agonist of the 5-hydroxytryptamine 2C serotonin receptor (5-HT2C) has been approved for long-term use as an adjunct to LM by FDA since 2012, after an initial rejection in 2010. An extended release, once daily version (20 mg) of lorcaserin was approved in 2016, based on one pivotal bioequivalence and a food-effect study. The mechanism by which lorcaserin reduces body weight is akin to decrease in energy intake though the promotion of satiety. This is mediated through the 5-HTC receptor on POMC/CART (pro-opiomelanocortin/cocaine and amphetamine-regulated transcript) neuron in the arcuate nucleus of hypothalamus. Stimulation of POMC/CART causes release in α-MSH (melanocyte-stimulating hormone) which acts on MC4R (melaocortin-4 receptors) on the neurons of PVN (paraventricular nucleus) which promotes satiety [7]. An additional action of lorcaserin, on mesolimbic reward circuit has been also suggested through 5-HT2C that might be helpful in obesity treatment [8]. Majority of weight loss with lorcaserin is ascribed to decrease in energy intake and leading to decrease in fat mass and only a little due to decrease in lean mass, as measured by DEXA (dual x-ray absorptiometry) [9,10].
Trypsin inhibitors: promising candidate satietogenic proteins as complementary treatment for obesity and metabolic disorders?
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2019
Vanessa Cristina Oliveira de Lima, Grasiela Piuvezam, Bruna Leal Lima Maciel, Ana Heloneida de Araújo Morais
The elucidation of the mechanisms underlying the central nervous system responses to circulating CCK has also been a subject of intense interest. Studies over many years have contributed to the idea that CCK released from the small intestine acts directly on vagal afferent neurons that terminate in the nucleus of the solitary tract and activate upward pathways that control food behaviour53,54. However, CCK acts on CCK1 receptors to stimulate expression of the CART (Cocaine and Amphetamine-Regulated Transcript) and Y2 receptor gene, both linked to inhibition of food intake, while suppressing the expression of MCH (Melanin-Concentrating Hormone) and MCH-1 and cannabinoid (CB-1) receptors, which are linked to stimulation of food intake55.