GLP-1 (glucagon-like peptide-1), recently proposed as a new tool for the therapy of NIDDM [1], is a natural occurring glucose-dependent insulinotropic peptide, with incretin characteristics and insulin-independent antidiabetic properties [1, 2]. GLP-1 has insulin-like effects upon glucose metabolism in rat liver and skeletal muscle ą normal [3, 4] and diabetic [5] ą, where it seems to act throughout specific receptors [6, 8], apparently different in structure or signalling-pathway [9, 11] to that in the pancreas [12], as in these tissues GLP-1 does not increase adenylate cyclase activity [3, 4]. In the rat, where the presence of specific receptors has also been reported in adipose tissue [13], the peptide not only stimulates, in adipocytes, glycogen synthesis, glycogen synthase a activity, and other parameters involved in the glucose metabolism, but also exerts a dual action upon lipid metabolism ą lipogenic and lipolytic ą [14, 15], being already suggested a possible implication of inositolphosphoglycans at mediating the effects of GLP-1 in this tissue [9]. In this work we have studied the effect of GLP-1, as compared to that of insulin and glucagon, upon the lipid metabolism of human adipose tissue from normal subjects, where also the presence of specific receptors has been informed [16].