Chronic inflammation can be considered as another mechanism that may promote the suppression of hypothalamic-pituitary-gonadal axis and HH in T2DM, as documented by studies in experimental animals and in vitro reporting that inflammatory mediators, such as tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β), which are generally increased in T2DM, obesity, and MetS, are able to suppress hypothalamic gonadotrophin-releasing hormone and LH secretion (33, 34). This evidence concerns the gene TNF and metabolic syndrome.