Immunoreactive insulin (IRI) responses to oral and/or intravenous (IV) glucose were measured in kwashiorkor and marasmus. Responses were expressed either as peak IRI levels attained or as insulin-glucose ratios. Similar measurements were made in normal controls.
After oral glucose, insulin secretion was abnormally low in every patient with kwashiorkor and in most of the marasmic cases. After IV glucose, normal insulin responses were noted more often, presumably associated with the greater glycemic stimulus. This was particularly noticeable in marasmus.
In both groups of subjects there was improvement after three to six weeks therapy, but this was much more striking after oral glucose. However, in many patients, insulin secretion remained subnormal or even deteriorated at this time, when nutritional status had greatly improved. Two to ten months later however, insulin levels were judged to be within normal limits in these cases. Children known to have suffered from kwashiorkor ten years previously likewise had normal insulin responses in 90 per cent of cases.
Augmented stimulation by glucose plus glucagon revealed some pancreatic insulin reserve in half the untreated patients studied. Yet the responses to augmented testing improved still further in three of five cases after therapy.
Insulin secretion is grossly impaired in kwashiorkor and marasmus. However, it is increased in many cases either by a greater glycemic stimulus or by adding glucagon to the glucose load. This suggests a “sluggishness” of insulin release after glucose under conventional conditions of testing in these cases. The disproportionate improvement after therapy in the insulin response to oral, as opposed to IV, glucose, may provide some evidence that an impaired gut betacytotrophic mechanism is partly responsible for the altered release mechanisms.