Glucagon and Catecholamine Secretion During Hypoglycemia in Normal and Diabetic Man
| Autor: | Phillip L. Werner, David Johnson, John W. Ensinck, J W Benson, Jerry P. Palmer |
|---|---|
| Rok vydání: | 1977 |
| Předmět: |
Adult
Male medicine.medical_specialty Adolescent Epinephrine Endocrinology Diabetes and Metabolism medicine.medical_treatment Clinical Biochemistry Blood sugar Hypoglycemia Biochemistry Glucagon Alpha cell Catecholamines Endocrinology Internal medicine Diabetes Mellitus medicine Humans Insulin business.industry Biochemistry (medical) Glucagon secretion medicine.disease Catecholamine Female business medicine.drug |
| Zdroj: | The Journal of Clinical Endocrinology & Metabolism. 44:459-464 |
| ISSN: | 1945-7197 0021-972X |
| DOI: | 10.1210/jcem-44-3-459 |
| Popis: | To examine the role of catecholamines in glucopenia-induced glucagon secretion, urinary epinephrine and norepinephrine and plasma immunoreactive glucagon (IRG) were measured during insulin-induced hypoglycemia in normal and insulin-dependent diabetic-man. Despite equivalent levels of hypoglycemia the mean plasma IRG increment in diabetes was only 15% of normals. The increases in epinephrine and norepinephrine were comparable in diabetics and normals; thus, the blunted response in plasma IRG to the stimulus of low blood sugar in diabetics cannot be explained by a generalized defect in catecholamine secretion. It is suggested that an alpha-cell glucoreceptor defect may account for the abnormal response to glucopenia in diabetics. To evaluate the possibility that impaired sensitivity to circulating catecholamines could explain the alpha cell dysfunction in diabetics, exogenous epinephrine was infused in normals and insulin-dependent diabetics. Elevated plasma IRG during epinephrine infusion was observed in only 50% of normals. The diabetics were hyperresponsive; mean increment in plasma IRG 3 times that of normals. The data demonstrate enhanced rather than impaired sensitivity to catecholamines in diabetes mellitus. |
| Databáze: | OpenAIRE |
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