Abstract

The effect of an insulin-induced hypoglycemia was examined in 14 type I diabetic patients. After an overnight blood glucose normalization, each patient received an additional intravenous bolus of 3 U regular insulin at 0900 h (time 0). Blood glucose was continuously recorded up to 180 min. Plasma samples were assayed for beta-thromboglobulin (beta TG, ng/ml), pancreatic glucagon (pg/ml), cortisol (microgram/dl), and growth hormone (ng/ml) 30 min before the insulin stress, at time 0, at blood glucose nadir, and at 180 min. The blood glucose fell from a baseline level of 85.0 +/- 3.2 mg/dl to a nadir value of 39.2 +/- 1.9 mg/dl (P less than 0.001) reached at an average time of 41.4 +/- 4.9 min. Plasma beta TG increased significantly (P less than 0.05) during the insulin stress: 93.4 +/- 23.7 ng/ml at nadir versus 42.5 +/- 5.9 at time 0. Plasma cortisol and growth hormone were significantly increased (P less than 0.02 and P less than 0.01) at nadir compared with time 0 values. Plasma pancreatic glucagon was higher at nadir than at time 0, but the difference was not significant. The present results indicate that in vivo platelet activation can be triggered by hypoglycemic episodes in insulin-treated diabetic patients.

Highlights

  • The blood glucose nadir was reached at an average time of 41.4 ± 4.9 min

  • Plasma cortisol rose from 11.6 ± 0.7 (0-value) to 15.1 ± 1.3 |xg/dl at blood glucose nadir (P < 0.01)

  • Plasma growth hormone increased from a baseline value of 5.8 ± 1.3 to 14.1 ± 2.6 ng/ml at blood glucose nadir (P < 0.02)

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Summary

Methods

SUBJECTS Fourteen insulin-requiring diabetic patients, 16-52 yr old (mean, 27 yr), were studied after their informed consent had been obtained. The mean percentage ideal body weight of the patients was 102% (range, 81-130%). Mean ideal body weight was estimated from the tables of the Metropolitan Life Insurance Co. In order to avoid any interference from treatment on platelet function, the patients selected for the study received no medication other than insulin. Glycosylated hemoglobin percentages at the time of the investigation ranged from 8% to 12.5% (mean, 10.2%). In the patients, plasma pTG levels at time 0 were between and 80 ng/ml. All patients except one (pTG = 80 ng/ml) had (3TG levels within the normal range (9-68 ng/ml) determined in a group of 17 age-matched control subjects. Twelve patients had no diabetic complications while the other two suffered from peripheral neuropathy and/or retinal complications

Results
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Conclusion

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