A lack of suppression of hyperglucagonemia has also been shown to contribute to postprandial glucose intolerance in type 1 diabetes (26). Although hyperglucagonemia results in glucose intolerance in diabetic subjects with impaired insulin secretion or in normal subjects whose insulin secretion is experimentally blocked, it does not produce the same effects when insulin secretion is intact (i.e., in normal healthy subjects) (77, 79, 84). Taken as a whole, the discussion above indicates that hyperglucagonemia plays an important role in initiating and maintaining hyperglycemia when combined with delayed or deficient insulin secretion, as in the cases of type 1 and type 2 diabetes.