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,
PETER H. BAYLIS,
STEVE THORNTON and
BRIAN M. FRIER
Diabetic Department, Western Infirmary/Gartnavel General Hospital Glasgow, Scotland
The Endocrine Unit, Royal Victoria Infirmary, Newcastle-Upon-Tyne England, United Kingdom
Address requests for reprints to: Dr. B. Miles Fisher, Diabetic Department, Ward 4/5, Royal Infirmary, Glasgow, Scotland G4 OSF, United Kingdom.
In normal humans, arginine vasopressin and oxytocin are released acutely from the posterior pituitary gland in response to hypoglycemia, and their release may assist coun-terregulation. The responses of these hormones to insulin-induced hypoglycemia were measured in 16 insulin-dependent diabetic patients with no autonomic neuropathy (8 patients who had been diabetic <5 yr and 8 patients who had been diabetic >15 yr) and in 6 normal subjects. The time of the onset of hypoglycemia and the mean blood glucose nadirs were similar in all groups, but the blood glucose recovery was delayed in the diabetic patients. In the normal subjects plasma arginine vasopressin rose from a mean basal value of 0.4 ± 0.2 (±SE) pmol/L t o a maximum of 1.3 ± 0.6 pmol/L, and plasma oxytocin rose from 0.7 ± 0.1 pmol/L to a maximum of 1.2 ± 0.2 pmol/L 30 min after the onset of hypoglycemia. The plasma arginine vasopressin and oxytocin concentrations after hypoglycemia were significantly higher in both of the diabetic groups compared with those in the normal group. Arginine vasopressin and oxytocin rose in all control subjects after hypoglycemia. The individual hormonal profiles in the diabetic patients were variable, with an exaggerated rise of oxytocin in some diabetic patients and no rise in others. The arginine vasopressin responses were exaggerated in all of the diabetic patients. There was no correlation between the hormonal responses and the duration of diabetes. The exaggerated plasma arginine vasopressin and oxytocin responses to hypoglycemia in diabetic patients may indicate the failure of a normal inhibitory mechanism which modulates hormonal secretion or a compensatory response to impaired glucose recovery.
* This work was supported by an equipment grant from Nordisk-UK.
Supported by a research fellowship from Eli Lilly Co.
Received July 6, 1988.
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