Effect of growth hormone on intestinal Na+/glucose cotransporter activity

Background: Growth hormone (GH) has been used alone or as part of a defined regimen in the treatment of patients with short bowel syndrome; however it s mode of action remains unclear. Growth hormone has been shown to increase amino acid, water, and electrolyte absorption from the small intestine. Th e acute effect of growth hormone on intestinal sugar transport has not been described previously. Methods: Mucosal preparations of rat jejunum were mo unted in the Ussing chamber. Growth hormone (2 x 10(-6) M or 8 x 10(-6) M) or vehicle was added to the serosal chamber 1, 3, or 5 hours later. Twenty or 40 minutes after growth hormone addition, 30 mmol/L 3-O-methylglucose wa s added to both chambers, and the change in short-circuit current (DeltaI(s c)) was recorded. In separate experiments, tissues were pretreated with phl oridzin, an inhibitor of Na+/glucose cotransport, before the addition of 3- O-methylglucose. In the final set of experiments, kinetic studies were perf ormed. Results: GH did not induce any alterations in baseline electrical pa rameters. Only tissues left in the chambers for 5 hours, but not 1 or 3 hou rs, before GH treatment displayed a greater 3-O-methylglucose-induced Delta I(sc) than controls (p < .05). The increase in I-sc induced by 3-O-methylgl ucose was 100% phloridzin-inhibitable. Kinetic analysis showed that growth hormone administration is associated with an increase in Na+/glucose cotran sporter maximal velocity (V-max) but no significant change in carrier affin ity for substrate (K-m). Conclusions: Growth hormone increases intestinal s ugar transport, but only in tissue that has not been exposed to endogenous GH for over 3 hours.