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Funding sources: no external funding.

Conflicts of interest: None.

Madam, I welcome de Giorgi et al.’s1 constructive letter, outlining further ways in which obesity might be implicated in the pathophysiology of melanoma. They rightly mention that we did not discuss in too much detail possible links between hyperleptinaemia and cutaneous malignant melanoma in a recent review article published in the BJD.2 Therefore, I appreciate the opportunity to discuss this specific issue further, particularly given that there is increasing evidence that the issue of exposure to ultraviolet radiation, and its relationship to melanoma, is complex.3, 4

Leptin (LEP) is a cytokine produced from adipose tissues.2, 5 It acts as a circulating satiety factor, with its target being discrete feeding centres within the central nervous system, mostly in the hypothalamus, where its actions are mediated via LEPR receptors.5 Homozygous LEP deficiency and LEPR deficiency has been described in both natural mouse mutants and humans.5 Both human and mouse leptin mutants are obese with pubertal failure, responding to leptin therapy.5 In LEPR deficiency, there is a similar phenotype, but with hyperleptinaemia – in other words absolute leptin resistance.5 In common obesity, leptin levels rise relative to body fat, which together with the minimal response to leptin therapy suggests leptin resistance too.5

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