Abstract: Obesity (OB) and type 2 diabetes mellitus (T2DM) are two common metabolic diseases that are closely related to intervertebral disc degeneration (IDD). OB may lead to the occurrence of IDD by increasing the spinal mechanical stress and promoting the secretion of adipokines by white adipose tissue. T2DM accelerates the pathological process of IDD by affecting the blood supply and nutrition of the intervertebral disc and evoking inflammatory reactions through advanced glycation end products (AGEs). Various adipokines, such as IL-6, TNF-α, leptin, resistin, and adiponectin, are secreted by adipocytes and may participate in the pathophysiology of IDD. In addition, AGEs cause intervertebral disc cell apoptosis by activating RAGE receptors and NLRP3 inflammasome. Therefore, further elucidating the effects and mechanisms of OB and T2DM in the initiation and progression of IDD will provide more strategies for the prevention and treatment of IDD.