Knowing that, in obesity, and in parallel with the increased secretion of leptin from adipose tissue, there is a disturbed adipose tissue secretory pattern characterized by an increased release of pro-inflammatory factors and decreased production of anti-inflammatory adipokines [42] and associated with the development of obesity-associated comorbidities, we hypothesize that inflammation can also contribute to the CB dysfunction that is involved in the genesis of metabolic diseases. Here, LEP is linked to obesity due to melanocortin 4 receptor deficiency.