Transient insulin increase in reactive hypoglycemia in obese and non-obese subjects.

(1). Insulin levels at the moment of glucose-induced reactive hypoglycemia have been compared with zero-hour insulin levels in 108 subjects in whom the blood glucose had decreased to 50 mg percent or less (50 to 31 mg) at the third, fourth, or fifth hour in the course of an oral glucose tolerance test (1.75 g/kg of body weight). (2). Of the 47 obese subjects, insulin levels at the time of the reactive hypoglycemia were inappropriately high, ie exceeded the fasting insulin level by 20 uU/ml or more in 38 percent and by 40 microunits/ml or higher in 26 percent of the tests. (3). In 61 non-obese subjects, employing the same criteria, inappropriately high insulinemia at the time of reactive hypoglycemia was recorded with about the same frequency. (4). In each instance of reactive hypoglycemia of 50 mg percent or less with concomitant insulin levels above the starting value to the degree stipulated, the so-termed inappropriate hyperinsulinemia was transient. In other words, judging by levels preceding and/or following the reactive hypoglycemia, insulin titers were decreasing and hence, the inappropriately high insulin level at the moment of hypoglycemia represented a lag phenomenon. (5). The above data suggest that insulin levels elevated above the starting value may play a role in reactive hypoglycemia. In subjects with insulin levels at the time of reactive hypoglycemia equal to or below the starting value, the low blood glucose level cannot be attributed to insulin. In such instances, delay or lag in hepatic glucose output and/or counter-regulatory responses probably play the dominant or sole role in the reactive hypoglycemia.