<p>The involvement of adipose tissue in the development of cancer is currently the subject of an increasing number of research due to the growing relevance of lipid metabolism in tumor growth. Obesity influences the tumor immune microenvironment (TME) in oral cancer. Visceral white adipose tissue (WAT) consists of adipocytes, connective tissue, immune cells, and stromovascular cells. The metabolic processes of immune cells within the adipose tissue of individuals with obesity predominantly depend on oxidative phosphorylation (intrinsically) and are characterized by elevated levels of M2 macrophages, Treg cells, Th2 cells, and eosinophils from an extrinsic perspective. The adipokines secreted by adipocytes facilitate communication with adjacent tissues to regulate glucose and lipid metabolism. Obesity influences cancer progression through the dysregulation of adipocytokines, characterized by an augmented synthesis of the oncogenic adipokine leptin, coupled with a reduced secretion of adiponectin. Under standard physiological settings, these adipokines fulfill essential roles in sustaining homeostasis. This review analyzed the influence of adipocytes on oral cancer by detailing the mediators released by adipocytes. Comprehending the molecular foundations of the protumor roles of adipokines in oral cancers might provide novel treatment targets.</p> Graphical Abstract <p></p>