Arteriovenous difference and tracer ([3-³H]glucose) techniques were used in 42-h-fasted conscious dogs to identify any insulin-like effects of intraportally administered glucagon-like peptide 1-(7–36)amide (GLP-1). Each study consisted of an equilibration, a basal, and three 90-min test periods (P1, P2, and P3) during which somatostatin, intraportal insulin (3-fold basal) and glucagon (basal), and peripheral glucose were infused. Saline was infused intraportally in P1. During P2 and P3, GLP-1 was infused intraportally at 0.9 and 5.1 pmol · kg⁻¹ · min⁻¹in eight dogs, at 10 and 20 pmol · kg⁻¹ · min⁻¹in seven dogs, and at 0 pmol · kg⁻¹ · min⁻¹in eight dogs (control group). Net hepatic glucose uptake was significantly enhanced during GLP-1 infusion at 20 pmol · kg⁻¹ · min⁻¹[21.8 vs. 13.4 μmol · kg⁻¹ · min⁻¹(control), P < 0.05]. Glucose utilization was significantly increased during infusion at 10 and 20 pmol · kg⁻¹ · min⁻¹[87.3 ± 8.3 and 105.3 ± 12.8, respectively, vs. 62.2 ± 5.3 and 74.7 ± 7.4 μmol · kg⁻¹ · min⁻¹(control), P < 0.05]. The glucose infusion rate required to maintain hyperglycemia was increased (P < 0.05) during infusion of GLP-1 at 5.1, 10, and 20 pmol · kg⁻¹ · min⁻¹(22, 36, and 32%, respectively, greater than control). Nonhepatic glucose uptake increased significantly during delivery of GLP-1 at 5.1 and 10 pmol · kg⁻¹ · min⁻¹(25 and 46% greater than control) and tended (P = 0.1) to increase during GLP-1 infusion at 20 pmol · kg⁻¹ · min⁻¹(24% greater than control). Intraportal infusion of GLP-1 at high physiological and pharmacological rates increased glucose disposal primarily in nonhepatic tissues.