Idiopathic Reactive Hypoglycemia: Mechanisms of Onset and Remission with High Protein Low Carbohydrate Diet

Abstract

Objective: Idiopathic reactive hypoglycemia is defined as early postprandial hypoglycemia occur-ring on ingestion of high carbohydrate containing meal. Remission ensues with high protein low carbohydrate diet. This study assessed roles of insulin and glucagon in its onset and remission. Methods: Plasma glucose, insulin and glucagon were determined after an overnight fast and re-peatedly until 180 minutes on ingestion of 3 meals; 100 g glucose; 100 g pure protein liquid and mixture of 50 g each at 14 days' interval. Five adults with IRH and 6 age matched healthy volun-teers participated. Results: In IRH, glucose ingestion induced prompt rise in glucose (5.1 ± 0.8 to10.5 ± 1.2 mM/L) followed later by hypoglycemia (2.6 ± 0.4 mM/L). Insulin rose from 7 ± 2 to 90 ± 18 mU/L. Glucagon rose initially (10% ± 2%) from elevated basal concentration (373 ± 57 mU/L) followed by later decline (−43% ± 12%). On protein ingestion, glucose declined followed by a res-toration to basal level while both insulin and glucagon rose (28 ± 6 mU/L; 148% ± 38%, p < 0.01). However, insulin response was lower and glucagon rise was greater when compared to responses on glucose ingestion (p < 0.01). With mixed meal, glucose (8.2 ± 0.6 mM/L), insulin (65 ± 12 mU/L) and glucagon (48% ± 7%) responses were lesser than rises following glucose ingestion (p < 0.05) and hypoglycemia did not occur. Conclusion: In IRH, initial hyperglycemia on glucose ingestion may be exacerbated by paradoxical glucagon rise and hypoglycemia may be induced by increased insulin and declining glucagon responses. Resolution of hypoglycemia with high protein low car-bohydrate diet may be attributed to blunting of insulin response and concurrent glucagon rise.