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    How Melanotan 2 Affects Melanogenesis and Hunger

    Scientists in the US have developed a synthetic peptide, Melanotan 2, which can cause skin tan without sunlight. But how does it relate to hunger and metabolism?

    The peptide hormone α-MSH exists and works in the body. Its task is to stimulate melanogenesis, the process of skin pigmentation. Melanotan 2 is a synthetic variant of this natural hormone. The hormone α-MSH activates melanocortin receptors and through them also has a strong influence on fat metabolism, appetite or sexual libido. Melanotan 2 was developed at the University of Arizona in order to find a synthetic variant of the hormone α-MSH so that it can be researched and used for therapeutic purposes, as the natural hormone α-MSH has a very short half-life. Melanotan 2 has been investigated in many clinical studies, both as a protection against the negative effects of UV radiation, and also as a potential drug for the treatment of sexual dysfunction. In addition to these two effects, studies have shown that Melanotan 2 suppresses appetite and has lipolytic effects.

    The Role Of Leptin In Relation To Hunger

    Simply said, leptin is a hormone that regulates satiety and hunger. It controls food intake and energy expenditure of the body, even if the exact mechanism of satiety regulation is not fully understood. Most of the effects of leptin are mediated through POMC neurons in the central nervous system. By stimulating these neurons, leptin creates a feeling of satiety [1].

    Research has found that leptin and melanocortin receptors affect the same areas of the brain that are associated with hunger and metabolic processes. This led to new insights into the physiology of leptin and the effects of melanocortin analogs such as the Melanotan 2 peptide.

    Melanotan 2 and Leptin

    Since the development of Melanotan 2, this synthetic variant of the peptide hormone, an agonist of the melanocortin receptor, has been the subject of various researches and studies. Many came and are coming with interesting and important knowledge. Animal studies of Melanotan 2 have shown that the hormone can reduce fat storage and reduce hunger. Activation of the MC-4R receptor by Melanotan 2 altered food intake preferences in rodents. MC-4R-deficient subjects tended to prefer fatty foods and consume up to 95% more of them than control subjects [2]. On the other hand, subjects receiving Melanotan 2 avoided fatty and heavy foods and ate considerably less.

    Leptin and Melanotan 2 affect different aspects of the same neural pathway. Leptin administration leads to melanocortin signaling, which leads to activation of POMC neurons. The hormone α-MSH, an analogue of Melanotan 2, is produced precisely by POMC neurons and acts as a negative regulator of food intake [3]. Some of leptin's effects have been shown to result from its effect on melanocortin levels [4].

    Since exogenously administered leptin has never been a particularly effective treatment for obesity, the knowledge that melanocortin signaling is precisely the mechanism where leptin also has its influence led to an extraordinary discovery. The latter showed that there are leptin-dependent and -independent melanocortin signaling systems. So you could say that melanocortin works in conjunction with leptin to reduce hunger, but it works also only by itself and without leptin. This breakthrough discovery caused interest and more and more clinical studies in connection with Melanotan 2 and its derivatives.

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    [1] H. Pan, J. Guo, and Z. Su, "Advances in understanding the interrelations between leptin resistance and obesity," Physiol. Behav., vol. 130, pp. 157-169, May 2014.
    [2] A. van der Klaauw, J. Keogh, E. Henning, C. Stephenson, V. M. Trowse, P. Fletcher, and S. Farooqi, "Role of melanocortin signalling in the preference for dietary macronutrients in human beings," Lancet Lond. Engl., vol. 385 Suppl 1, p. S12, Feb. 2015.
    [3] C. Bjørbaek and A. N. Hollenberg, "Leptin and melanocortin signaling in the hypothalamus," Vitam. Horm., vol. 65, pp. 281-311, 2002.
    [4] H. Shimizu, K. Inoue, and M. Mori, "The leptin-dependent and -independent melanocortin signaling system: regulation of feeding and energy expenditure," J. Endocrinol., vol. 193, no. 1, pp. 1-9, Apr. 2007.