[en] Diabetes Mellitus, Type 1/complications ; Diabetes Mellitus, Type 2/complications ; Dietary Carbohydrates/pharmacokinetics ; Enzyme Inhibitors/pharmacology ; Glucagon/secretion ; Humans ; Hyperglycemia/drug therapy/etiology/physiopathology ; Hypoglycemic Agents/pharmacology/therapeutic use ; Insulin/pharmacology ; Intestinal Absorption ; Postprandial Period ; alpha-Glucosidases/antagonists & inhibitors/pharmacology
[en] Besides dietary approaches, various pharmacological means have been recently developed in order to better control postprandial hyperglycaemia. This objective may be obtained: 1) by slowing down the intestinal absorption of carbohydrates; 2) by insuring a better insulin priming soon after the meal; and 3) by inhibiting post-prandial glucagon secretion or action. Some hormones (amylin, glucagon-like peptide-1) can slow gastric emptying while alpha-glucosidase inhibitors (acarbose, miglitol) retard intestinal digestion and resorption of complex carbohydrates. A more physiological post-meal profile of insulin may be obtained in type 2 diabetes by using new insulin secretagogues of the glinide family (repaglinide, nateglinide) with an earlier and shorter insulinotropic action or, mainly in type 1 diabetes but also in type 2 diabetes, by using short-acting insulin analogues (lispro. Asp B28) or inhated insulin the action of which is faster than that of subcutaneous insulin. Post-prandial glucagon secretion can be inhibited by amylin. GLP-1 or insulin while other glucagon antagonists are currently in development.