Improved glucose tolerance follows glucose challenges given in rapid succession, the Staub-Traugott effect. The cause for this facilitated glucose disposal is not clear. Augmented insulin release, prior "insulinization" of cells, and suppression of a pituitary factor or free fatty acids (FFA) are previously suggested mechanisms. For information bearing on the role of the pituitary in this phenomenon, study of the Staub effect was undertaken in hypopituitary patients receiving replacement thyroid, cortisone, and sex-steroid therapy and in normal untreated controls. All subjects received three intravenous injections of glucose (0.5 g/kg) at hourly intervals. Plasma glucose, FFA, and insulin were measured. Whereas a definite Staub effect was seen in each control subject, this phenomenon was conspicuously absent in seven hypopituitary patients similarly studied. Patterns of peripheral insulin response were similar for both groups: FFA levels fell more slowly in the hypopituitary subjects. Normal pituitary function appears to be required for the Staub effect. Incremental peripheral insulin levels do not explain the effect. Subnormal suppression of free fatty acids and impaired induction of key glycolytic and glycogenic enzymes are alternative explanations for the absence of the Staub effect in hypopituitary subjects.
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism