Summary Aims Hepatic glycogen stores have been shown to be depleted, and glucagon stimulated hepatic glucose production reduced, in Type 1 diabetic subjects. Co‐administration of amylin and insulin has been shown to replete hepatic glycogen stores in diabetic animal models. The aim of the present study was to investigate the effect of amylin replacement on hepatic glucagon responsiveness in humans. Methods Thirteen Type 1 diabetic men were studied in a double‐blind, placebo‐controlled, cross‐over study after 4 weeks of subcutaneous pramlintide (30 μg q.i.d.) or placebo administration. Following an overnight fast, plasma glucose was kept above 5 mmol/l (baseline 210–240 min) with an insulin infusion rate of 0.25 mU.kg–1.min–1. To control portal glucagon levels, somatostatin was infused at a rate of 200 μg/h. Basal growth hormone (2 ng.kg–1.min–1) and glucagon (0.7 ng.kg–1.min–1) were replaced. Glucagon infusion was increased to 2.1 ng.kg–1.min–1 at 240–360 min (step 1) and to 4.2 ng.kg–1.min–1 at 360–420 min (step 2). Results Baseline plasma glucose (5.59 ± 0.16 vs. 5.67 ± 0.25 mmo/l) and endogenous glucose production (EGP) (1.32 ± 0.22 vs. 1.20 ± 0.13 mg.kg–1. min–1) were similar a
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