There is increasing evidence of close interactions between the adipose and the immune systems. Adipocytes secrete multiple factors, including adipokines such as leptin and adiponectin that have both pro- and anti-inflammatory effects, and influence diseases involving the immune system. Further, adipose tissue also secretes various chemokines and cytokines, derived from either the adipocytes themselves, or the neighbouring cells including both resident and infiltrating macrophages. This close physical and paracrine interaction results in reciprocal actions of adipocytes, preadipocytes and macrophages within the microenvironment of the adipose tissue. Adipose tissue is a source of Acylation Stimulating Protein (ASP)/C3adesArg which interacts with the receptor C5L2 to stimulate triglyceride synthesis and glucose transport. C5L2, present on adipocytes, preadipocytes, macrophages, and numerous other myeloid and non-myeloid cells is also postulated to be a decoy receptor for C5a in immune cells. Several reviews within the past year have recently examined the role of C5L2 in C5a-mediated physiology. The present mini-review is an adipocentric view with emphasis on the role of ASP and C5L2 in lipid metabolism. C5L2 may play a role in mediating, on one hand, ASP stimulation of triglyceride synthesis in adipose, and, on the other hand, a role as mediator of C5a immune function. Both roles remain controversial, and will only be resolved with further studies.