If this mechanism is physiologically relevant, our observation could be explained by increased glucose uptake in adipocytes during hyperinsulinemia in the saline experiment and decreased glucose uptake in adipocytes during hyperinsulinemia in the ghrelin experiment, leading to i) a compensatory reduction of RBP4 secretion in the saline experiment and ii) no change in RBP4 secretion in the ghrelin experiment. The gene discussed is GHRL; the disease is hyperinsulinism.