Insulin-induced Hypoglycemia In Humans Research Articles

Naloxone abolishes the inhibiting effect of somatostatin on the release of oxytocin evoked by insulin-induced hypoglycemia in humans

The effect of somatostatin (SRIH) on the release of oxytocin (OT) in response to hypoglycemia during insulin tolerance test (ITT) was studied in seven normal men. Subjects were injected intravenously with 0.15 U/kg insulin alone (control test) or together with SRIH (4.1 μg/min × 90 min), naloxone (10 mg in an IV bolus), or the combination of the two substances. Plasma OT concentrations rose significantly during ITT; the OT response was significantly reduced by the treatment with SRIH and increased in the presence of naloxone. When both SRIH and naloxone were given, the OT response to hypoglycemia did not differ from that observed in the control test. These findings provide evidence that the effect of hypoglycemia on plasma OT levels is sensitive to the inhibition by SRIH and by naloxone-sensitive endogenous opioids. Because naloxone reversed the inhibiting effects of SRIH, an involvement of opioid peptides in SRIH action might be supposed. Alternatively, SRIH and naloxone-sensitive opioids might produce their inhibiting effects on OT rise in response to hypoglycemia through independent pathways.

Maintenance of high-energy brain phosphorous compounds during insulin-induced hypoglycemia in men. 31P nuclear magnetic resonance spectroscopy study.

31P nuclear magnetic resonance (NMR) spectroscopy allows noninvasive studies of cerebral energy-rich phosphorous compounds in humans. In an attempt to characterize the relationship between peripheral blood glucose concentrations and whole-brain phosphate metabolism during insulin-induced hypoglycemia, 31P NMR spectra were obtained before and after intravenous injection of insulin (0.15 IU/kg body wt) in six men. Compared with prehypoglycemic measurements, no significant changes were found in brain content of Pi, sugar phosphates, phosphocreatine, phosphodiesters, and ATP, and brain pH remained constant during the experiment. These results show that the integrated brain profile of energy-rich phosphorous compounds is unaffected by experimental insulin-induced hypoglycemia in humans.

Bombesin inhibits growth hormone response to insulin-induced hypoglycemia in humans

Intravenous administration of bombesin (5ng/kg/min× 2.5h) significantly reduced growth hormone (GH) response to insulin-induced (0.15 U/kg, i.v.) hypoglycemia in 8 male volunteers without affecting its basal plasma levels. These data, together with the presence of bombesin-like immunoreactivity in the human brain, suggest that — as in experimental animals — this neurogastrointestinal peptide may be of physiological significance in the control of GH secretion also in man.

Pyloric pressure response to insulin-induced hypoglycemia in humans.

The pyloric pressure response to insulin-induced hypoglycemia was studied. Studies were performed in 102 experiments on 38 normal subjects. During insulin-induced hypoglycemia, pyloric pressure increased from 5.5 +/- 1.2 to 10.8 +/- 1.1 mmHg (P less than 0.02). This increase in pyloric pressure ws not due to a direct effect of insulin, duodenal acidification, or the release of corticosteroids or growth hormone. Glucagon doses of 2 and 5 micrograms . kg-1 . h-1 increased pyloric pressure from 4.7 +/- 1.1 to 6.7 +/- 0.5 mmHg (P less than 0.05) and from 4.7 +/- 1.1 to 8.5 +/- 1.1 mmHg (P less than 0.02), respectively. Pyloric pressures were increased to 10.8 +/- 0.9 (P less than 0.01) and 13.0 +/- 1.4 mmHg (P less than 0.01) at 0.1 and 0.2 micrograms . kg-1 . min-1 of epinephrine, respectively. Neither cholinergic blockade nor alpha-adrenergic blockade significantly affected the pyloric pressure response to insulin hypoglycemia. beta-Adrenergic blockade abolished the pyloric pressure responses to both insulin hypoglycemia and epinephrine. Neither beta- nor alpha-adrenergic stimulation altered the basal pyloric pressure. In contrast, the combination of isoproterenol and phenylephrine increased the pyloric pressure significantly from 4.2 +/- 0.8 to 12.0 +/- 1.7 mmHg ( P less than 0.01). These observations suggest that insulin hypoglycemia increases pyloric pressure by an adrenergic mechanism that requires stimulation of both alpha- and beta-receptors.