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Pharmacological Treatment of Obesity
Published in Emmanuel C. Opara, Sam Dagogo-Jack, Nutrition and Diabetes, 2019
Amie A. Ogunsakin, Ayotunde O. Dokun
This is a fixed-dose combination of naltrexone and bupropion. It was FDA approved in September of 2014 for management of obesity. Naltrexone is an opioid antagonist, and bupropion is an aminoketone antidepressant that inhibits dopamine and norepinephrine re-uptake inhibitors, which stimulates pro-opiomelanocortin (POMC) neurons. The exact mechanism of the naltrexone/bupropion combination leading to weight loss is not fully understood [35]. The combination is theorized to work synergistically in the hypothalamus and the mesolimbic dopamine circuit to promote satiety, reduce food intake, and enhance energy expenditure. POMC cells located in the arcuate nucleus of the hypothalamus produce melanocyte-stimulating hormone (alpha-MSH) and beta-endorphin, an endogenous opioid [36,37]. The alpha-MSH activates the melanocortin-4 receptor (MC4R), leading to decreased food intake, increased energy expenditure, and weight loss [38,39]. Beta-endorphin reduces activity of POMC cells by binding to the inhibitory mu-opioid receptor (MOP-R) [40]. Bupropion, a weak dopamine and norepinephrine reuptake inhibitor, enhances POMC cell production and release of alpha-MSH and beta-endorphin [41]. Naltrexone, an opioid antagonist, blocks the MOP-R; therefore, it disrupts beta-endorphin inhibitory feedback on POMC cells [41] (Figure 7.1).
Radiolabeled Agents for Molecular Imaging and/or Therapy
Published in George C. Kagadis, Nancy L. Ford, Dimitrios N. Karnabatidis, George K. Loudos, Handbook of Small Animal Imaging, 2018
Dimitrios Psimadas, Eirini A. Fragogeorgi
The α-melanocyte-stimulating hormones (α-MSH) are produced in the pituitary gland and regulate skin pigmentation (Miao and Quinn 2007). The G-coupled receptors for α-MSH have been found in 80% of metastases from melanomas. Many α-MSH analogs have been developed for melanoma imaging, but unfortunately their in vivo tumor targeting properties are not satisfactory. New modified derivatives are currently under development and evaluation in melanoma-bearing mice, including 18F-, 64Cu-, and 177Lu-labeled α-MSH analogs (Yang et al. 2009; Gao et al. 2011; Lim et al. 2012).
Obesity and diet
Published in Clive Handler, Gerry Coghlan, Marie-Anne Essam, Preventing Cardiovascular Disease in Primary Care, 2018
Clive Handler, Gerry Coghlan, Marie-Anne Essam
The reasons that some people like to eat more in one meal than others remain unclear. Appetite is dependent on hormonal signals from adipose tissue providing feedback to the hypothalamus. A genetic link to childhood obesity has been reported. Melanocyte-stimulating hormone produced in the hypothalamus stimulates the melanocortin 4 receptor (MC4R), which may account for 6% of cases of obesity by influencing the appetite and eating behaviour in affected people.
Migraine and obesity: what is the real direction of their association?
Published in Expert Review of Neurotherapeutics, 2023
Soodeh Razeghi Jahromi, Fahimeh Martami, Kasra Morad Soltani, Mansoureh Togha
Evidence has shown that both ictal and interictal NO levels were higher among migraineurs compared to controls [45]. It has also been shown that peptides that increase food intake also increase NO, whereas peptides that decrease food intake decrease NO [50]. Orexigenic and anorexigenic peptide signals from the gastrointestinal tract represent the feeding state for the central nervous system, while leptin and insulin convey information about the nutritional state which, together, regulate body mass/composition [51]. Orexigenic peptides increase NO [50]. Orexigenic neurons stimulate food intake and are neuropeptide hormones (neuropeptide Y (NPY)) represented by orexin and ghrelin. Anorexigenic neurons suppress the appetite, producing α-melanocyte-stimulating hormone (α-MSH) as represented by leptin and insulin and also by peptide-tyrosine-tyrosine [52]. In neuronal NOS knock-out mice (NOS KO), NPY and ghrelin did not increase feeding compared to the wild-type controls [53]. This suggests that a higher level of NO in migraineurs could result in increased food consumption.
Cosmetic skin lightening use and side effects
Published in Journal of Dermatological Treatment, 2022
Natasha Masub, Amor Khachemoune
Topical corticosteroids are among the most popular topical skin lightening agents used and may be responsible for much of the severe side effects of skin bleaching, particularly clobetasol propionate (25,29,32,51). Corticosteroids inhibit skin pigmentation by inhibiting precursor hormone propiocortin and thus inhibiting melanocyte stimulating hormone production. Systemic side effects of topical corticosteroids include Cushing syndrome, hyperglycemia, and menstrual irregularities, while dermatologic side effects include skin atrophy, striae, and acne (52). The use of topical steroids may also have an impact on fetal health during pregnancy. A Senegalese study found the use of highly potent corticosteroids for skin lightening during pregnancy was associated with smaller placentas and a higher rate of low-birth-weight infants (27).
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)).