Altered adipokine signatures in obesity, especially with concurrent metabolic syndrome, are characterised by decreased levels of anti-inflammatory adipokines (e.g., adiponectin and omentin-1) and the upregulation of pro-inflammatory adipokines (e.g., leptin, resistin, and visfatin) and foster a pro-inflammatory milieu akin to inflammageing, driving metabolic syndrome-related chronic diseases, such as OA. This evidence concerns the gene LEP and metabolic syndrome.