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Current Trends in Performance- and Image-Enhancing Substance Use Among Gym Goers, Exercisers, and Athletes
Published in Ornella Corazza, Andres Roman-Urrestarazu, Handbook of Novel Psychoactive Substances, 2018
Neha P. Ainsworth, Jake Shelley, Andrea Petróczi
Melanotan-1 (MT1) and melanotan-2 (MT2) are synthetic analogues of the peptide α-melanocyte-stimulating hormone (Habbema, Halk, Neumann, & Bergman, 2017). Initially developed as a candidate for treating female sexual dysfunction and erectile dysfunction, its current off-label use within certain communities (including the gym-going community) is for the purposes of tanning (Habbema et al., 2017). MT1 and MT2 are both available at hair salons and tanning salons and can be purchased online (Habbema et al., 2017). To facilitate melanogenesis, exposure to UV-B radiation through tanning beds or direct sunlight is necessary (Dorr et al., 2004). Administration is subcutaneous—it is often sold as a powder which must be reconstituted with bacteriostatic water (Habbema et al., 2017). Habbema et al. (2017) report the maximal effective dose to be 0.16 mg/kg per day. However, users were often reported using much higher doses.
Vagal Afferent Signaling and the Integration of Direct and Indirect Controls of Food Intake
Published in Ruth B.S. Harris, Appetite and Food Intake, 2017
Robert C. Ritter, Carlos A. Campos, Jason Nasse, James H. Peters
The fact that reduction of food intake by CCK-A receptor activation involves modulation of vagal afferent transmission via synapsin phosphorylation raises the possibility that activation of other peptide receptors expressed by vagal afferents also might modulate vagal synaptic function to control food intake. Vagal afferent MC4Rs are of special interest in this regard because of the key role played by this receptor in mediating leptin’s effects on food intake and body weight. Injection of MC4R agonist into the fourth ventricle or directly into the NTS triggers a rapid reduction of food intake that persists for hours following injection (Grill et al. 1998, Campos, Shiina, and Ritter 2014, Campos and Ritter 2015). Reduction of food intake following hindbrain MC4R activation is entirely due to reduction of meal size, with little if any effect on meal frequency. Significantly, reduction of food intake following injection of MC4R agonist into the NTS does not require peripheral vagal fibers (Williams, Kaplan, and Grill 2000) but does depend on the presence of intact vagal afferent endings in the NTS (Campos, Shiina, and Ritter 2014). Sectioning the vagus below the diaphragm, or just distal to the nodose ganglion, results in degeneration of vagal afferent innervation to peripheral organs. However, vagal afferent neurons in the nodose ganglia and vagal afferent terminals in the NTS survive. Unilateral nodose ganglion removal, however, results in degeneration of the majority of vagal afferent endings ipsilateral to nodose removal, while vagal endings in the NTS contralateral to ganglion removal are not diminished. When melanotan-II (MTII), an MC3/4 receptor agonist, is injected into the NTS, contralateral to nodose removal, food intake is reduced, as it is in intact rats. However, if MTII is injected ipsilateral to nodose removal, where vagal afferent endings have degenerated, food intake is not significantly decreased by MTII (Figure 11.6). These results suggest that vagal afferent endings in the NTS are necessary participants in reduction of food intake by MC4R activation. The possibility that reduction of food intake by hindbrain MC4R activation depends on release of glutamate, perhaps from vagal afferent endings, is supported by the finding that hindbrain injection of an NMDAR antagonist prevents reduction of food intake by MTII injection (Campos and Ritter 2015). Importantly (see Section 11.3.5) reduction of food intake following hindbrain injection of MC4R agonist is attenuated by pretreatment, either with U0126, which inhibits ERK1/2 phosphorylation (Sutton et al. 2005), or by pretreatment with an inhibitor of cyclic adenosine monophosphate (cAMP)-dependent protein kinase (PKA) (Campos, Shiina, and Ritter 2014). Collectively, these observations are consistent with the hypothesis that activation of MC4R on vagal afferent endings reduces food intake, at least in part, by enhancing vagal release of glutamate, thereby reducing meal size. The results also suggest that the mechanisms for reduction of feeding by hindbrain MC4R activation involve both mitogen-activated protein kinase (MAPK) and PKA.
Afamelanotide for prevention of phototoxicity in erythropoietic protoporphyria
Published in Expert Review of Clinical Pharmacology, 2021
Debby Wensink, Margreet A.E.M. Wagenmakers, Janneke G. Langendonk
In previous studies afamelanotide was also named NDP-MSH, CUV1647, or Melanotan-I. In this review we will use afamelanotide in all these cases. However, afamelanotide should not be confused with Melanotan-II (Ac-Nle-c[Asp, HisDPhe, Arg, Trp, Lys]-NH2) which is a smaller molecule than afamelanotide. Melanotan II is just as potent for skin pigmentation as afamelanotide and cheaper to manufacture, but can also cross the blood brain barrier and has more side effects including nausea and penile erections [57,58]. Both Melanotan-I and Melanotan-II are commercially available, not registered nor approved as medical drugs, and without regulatory oversight. However, there has been illegal supply of unlicensed and unregulated products claiming to be Melanotan-I or Melanotan-II that are possibly harmful, due to potential impurity of chemicals and transmission of bloodborne diseases from needle sharing [59].
An overview on performance and image enhancing drugs (PIEDs) confiscated in Italy in the period 2017–2019
Published in Clinical Toxicology, 2021
Sara Odoardi, Serena Mestria, Giulia Biosa, Valeria Valentini, Sofia Federici, Sabina Strano Rossi
Firstly, because the majority of these substances have their own toxicity and adverse effects [7–11,26–29], especially when taken without a therapeutic indication, no medical supervision or when the results of the clinical trials did not allow their release on the market. This is the case of Melanotan II, an oligopeptide used to enhance melanin production, the use of which has been associated with the onset of melanoma [27,28]. As a further example, the anorectic compound sibutramine, contained in two confiscations, was withdrawn from the EU market in 2010 for some deaths related to its use. In the case of AASs, most of the time the actual quantitative content of a single steroid was lower than stated, but the preparations were made of mixtures of different esters or different steroids (e.g., in the case of testosterone or trenbolone). This can lead to the intake of high amounts of AASs, with several possible health risks [7–11,29], as they mutually boost their activity.
Drug delivery options and therapeutic advances in the management of erectile dysfunction
Published in Expert Opinion on Drug Delivery, 2020
P.T. Grice, J. Liu, A.T. Gabrielson, I Pearce, T.J. Bivalacqua, V. Modgil
Melanocortin receptor agonists (MRAs) are centrally acting agents that are showing promise in the treatment of ED. As part of phase I trials studying the tanning properties of melanotan II erection-enhancing properties were incidentally discovered. Subsequently, in a small study of 20 men, melanotan II was administered as a solution for subcutaneous injection without any visual sexual stimulation. Erections were observed in 17 men. Side effects included nausea, lethargy, and yawning – an undesirable side effect profile for intercourse [60].