Enteroendocrine L-cells release GLP-1 in response to luminal nutrient (primarily carbohydrate and fat) stimulation, GLP-1 receptors (GLP-1R) are expressed in the periphery and in brain areas implicated in the regulation of energy homeostasis. GLP-1 has potent insulinotropic and gluco-regulatory effects, and peripheral administration of GLP-1 inhibits eating. This may reflect a physiological satiating function of endogenous GLP-1, but the exact stimuli of GLP-1's release and the site(s) and mechanism(s) of its action are unresolved. Here I present data indicating that: 1) high fat meals are a more potent stimulus for intestinal GLP-1 release in rats than isocaloric low fat meals, as measured by postprandial changes in active GLP-1 levels in intestinal lymph; 2) intestinal triglyceride re-synthesis directly or indirectly modulates dietary fat-induced GLP-1 release; 3) hepatic degradation appears to prevent a systemic increase in endogenous GLP-1 during chow meals in rats; 4) the area postrema and hindbrain GLP-1R activation are involved in mediating a possible endocrine eating-inhibitory effect of GLP-1, whereas abdominal vagal afferents are involved in its putative paracrine satiating action; and 5) GLP-1 can promote adipocyte proliferation and triglyceride synthesis through a direct, GLP-1R-mediated effect. Further studies should a) examine under which conditions a systemic endocrine or a local paracrine action of GLP-1 in the intestine is physiologically relevant for satiation, b) identify the neural mechanisms mediating these effects, and c) test whether GLP-1 released into the intestinal lymph may have direct access to intra-abdominal adipose tissue.