Cancer-associated cachexia is defined by systemic inflammation, bodyweight loss, adipose tissue remodeling, and muscle wasting. Interestingly, until nowadays, the etiology for this syndrome still unclear. It is well known that multiple factors can contribute to adipose tissue remodeling, and longitudinal studies show that adipose tissue is affected early in the course of this syndrome. During cancer cachexia, adipose tissue remodeling is associated with adipocyte atrophy, impairment of fatty acid turnover, inflammation, reorganization of the extracellular matrix, and increased thermogenic gene programming of adipose tissue. Another attractive pathway is the adipose tissue lipolysis, which is the catabolic process that is leading to the breakdown of triglycerides stored in adipocytes and the release of fatty acids and glycerol. This pathway is highly involved in the adipose tissue wasting during cancer cachexia. Whole-body deletion of the genes that encode the lipolytic enzymes attenuates the effects of the syndrome on the reduction of body fat and muscle mass. These sets of changes, in addition to metabolites derived from this process, may be the initial trigger of the sequence of events that result in the remodeling and consequent dysfunction of adipose tissue during cancer cachexia. Therefore, this review aimed to investigate the main morpho-functional events that are resulting in adipose tissue remodeling in the context of cancer-associated cachexia.