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Modulation of Inflammatory Effects of Cytokines by the Neuropeptide α-MSH
Published in Sami I. Said, Proinflammatory and Antiinflammatory Peptides, 2020
J. M. Lipton, Nilum Rajora, R. A. Star, S. Taherzadeh, Anna Catania, Giuliana Ceriani, G. Boccoli
The evidence that certain cytokines are crucial to inflammatory reactions in peripheral tissue is clear, and new details of the complexity of the influence of these soluble mediators in peripheral inflammation come with successive issues of scientific journals. There is likewise increasing evidence of the importance of proinflammatory cytokines in CNS disease such as multiple sclerosis (2–5) and Alzheimer’s disease or CNS infection with HIV (6). In the case of CNS inflammation, proinflammatory cytokines may be produced by glia or neurons or by peripheral monocyte/macrophages that migrate into the tissue. Whatever the origin of inflammatory cytokines within the brain, there is movement in the scientific community toward evaluation of anticytokine agents for the treatment of neurodegenerative disease and CNS reperfusion injury. It may be that the endogenous anticytokine neuropeptide α-MSH will be useful in such treatments.
Endocrinology
Published in Kristen Davies, Shadaba Ahmed, Core Conditions for Medical and Surgical Finals, 2020
Addison's disease is the primary insufficiency of the adrenal gland, meaning that the lack of production caused by a problem within the adrenal gland is resulting in the insufficiency (see box). Because the rest of the hypothalamic–pituitary–adrenal (HPA) axis is working correctly, an excess of ACTH is produced by negative feedback, which forms the basis behind the short Synacthen test (see box). ACTH is itself a product of a larger precursor protein, POMC, which also produces melanocyte-stimulating hormone (MSH). The increase in ACTH production causes an increase in MSH, leading to pigmentation, a hallmark of Addison's disease.
Hypothalamic Control Centers
Published in Nate F. Cardarelli, The Thymus in Health and Senescence, 2019
In 1932 Krieg observed that the SCN has axons projecting to the paraventricular nucleus.46 Also neuronal links between the pineal and the PVN have been noted,195 as well as connections with other hypothalamic nuclei.196 The PVN has been implicated in melanocyte-stimulating hormone (MSH) secretion, in that the releasing factor concentrates therein.197 MSH content in the PVN is regulated by photic input, probably from the SCN.198,199 Severance of the neural connection between SCN and PVN stops certain photoperiod-mediated events.83 MSH regulates skin color, attention, arousal, and vigilance.198
Relationship Between Appetite-Related Peptides and Frailty in Older Adults
Published in Endocrine Research, 2023
Burcu Candemir, İbrahim İleri, Mehmet Muhittin Yalçın, Aydın Tuncer Sel, Berna Göker, Özlem Gülbahar, İlhan Yetkin
Peptide YY is a peptide that is secreted from the ileum and colon in response to nutrition and reduces appetite and hence called “ileal brake.” It inhibits the secretion of ghrelin, delays gastric emptying, and suppresses the secretory function of the pancreas and stomach.30 It also works centrally by inhibiting mRNA expression of NPY and AgRP in the arcuate nucleus.30 Alpha MSH, which is the product of the POMC gene, has a significant impact on food intake and energy balance. The effects of α-MSH on food intake and body weight are mediated in the brain via two melanocortin receptors (MCR), MC3-R and MC4-R. Melanocortin receptor-4 is localized primarily in the central nervous system and is responsible for the appetite-reducing effects of α -MSH. Functional mutations of MC4-R have been associated with hyperphagia and obesity in mice.31 CART is an anorexigenic hormone that shows its anorexigenic effect through the inhibition of NPY neurons and central release of glucagon-like peptide-1.32 Some authors reported increased CART mRNA expression with aging, while others found no changes.33–35 In the present study, our results suggested that α-MSH and CART levels were independent predictors of frailty. However, small predictive values raise the question of whether our findings are of any possible clinical significance. Nevertheless, the results of this study, which have a novel premise, will shed light on future studies.
Is there a therapeutic potential in combining bupropion and naltrexone in schizophrenia?
Published in Expert Review of Neurotherapeutics, 2022
Samer A. El Hayek, Malek A. Shatila, Jana A. Adnan, Luna E. Geagea, Firas Kobeissy, Farid R. Talih
BUPNAT is an oral extended-release tablet composed of a combination of the dopamine (DA) and norepinephrine (NE) reuptake inhibitor bupropion (BUP) and the µ-opioid receptor antagonist naltrexone (NAT) [18]. The BUP 90 mg/NAT 8 mg formulation (marketed under the brand name Contrave by Orexigen Therapeutics), is typically titrated to 4 tablets per day (BUP 360 mg/NAT 32 mg) by the fourth week of treatment [19]. The development of the drug started in the late 2000s. It gained FDA approval for the treatment of obesity in 2014 [20]. It is hypothesized to work via the stimulation of the hypothalamic pro-opiomelanocortin (POMC) neurons that release alpha-melanocyte-stimulating hormone (α-MSH). α-MSH, in turn, targets specific receptors that serve to reduce caloric intake and increase energy expenditure. When α-MSH is released, POMC neurons also simultaneously secrete µ-opioid receptor agonists. This activates a negative feedback loop on the system. BUPNAT works on both pathways by stimulating POMC neurons (via its BUP component) and inhibiting the negative feedback loop (through the NAT component) [21] (Figure 1).
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)).