期刊
DIABETES
卷 54, 期 10, 页码 2946-2951出版社
AMER DIABETES ASSOC
DOI: 10.2337/diabetes.54.10.2946
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资金
- NIDDK NIH HHS [DK-52771, DK-67571] Funding Source: Medline
The mechanisms involved in the release of glucagon in response to hypoglycemia are unclear. Proposed mechanisms include the activation of the autonomic nervous system via glucose-sensing neurons in the central nervous system, via the regulation of glucagon secretion by intraislet insulin and zinc concentrations, or via direct ionic control, all mechanisms that involve high-affinity sulfonylurea receptor/inwardly rectifying potassium chanhel-type ATP-sensitive K+ channels. Patients with congenital hyperinsulinism provide a unique physiological model to understand glucagon regulation. In this study, we compare serum glucagon responses to hyperinsulinemic hypoglycemia versus nonhyperinsulinemic hypoglycemia. In the patient group (n = 20), the mean serum glucagon value during hyperinsulinemic hypoglycemia. was 17.6 +/- 5.7 ng/l compared with 59.4 +/- 7.8 ng/l ,in the control group (n = 15) with nonhyperinsulineihic hypoglycemia (P < 0.01). There was no difference between the serum glucagon responses in children with diffuse, focal,, and diazoxide-rerponsive forms of hyperinsulinism. The mean serum epinephrine and norepinephrine concentrations in the hyperinsulinemic group were 2,779 +/- 481 pmol/l And 2.9 +/- 0.7 nmol/l and appropriately rose despite the blunted glucagon response. In conclusion, the loss of ATP-sensitive K+ channels and or elevated intraislet insulin cannot explain the blunted glucagon release in all patients with congenital hyperinsulinism. Other possible mechanisms such As the suppressive effect of prolonged hyperinsulinemia on a-cell, secretion should be considered.
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