Severe insulin-induced hypoglycemia associated with deficiencies in the release of counterregulatory hormones.

A FALL in blood glucose to hypoglycemic levels usually triggers a prompt release of catecholamines, glucagon, growth hormone, and cortisol. These so-called counterregulatory hormones are believed to restore blood glucose to normal concentrations by increasing hepatic glucose production (in the cases of glucagon, epinephrine, and cortisol) or by decreasing peripheral use of glucose (in the cases of epinephrine and growth hormone). The relative contributions of the individual hormones in counteracting insulin-induced hypoglycemia, however, have not been established. In this paper, we report the case of an insulin-dependent diabetic patient who was capable of synthesizing and releasing all the counterregulatory hormones . . .

[1]  P. Cryer Glucose Counterregulation in Man , 1981, Diabetes.

[2]  I. Kopin,et al.  The adrenal medullary response to hypoglycemia in patients with orthostatic hypotension. , 1980, The Journal of clinical endocrinology and metabolism.

[3]  P. Cryer,et al.  Epinephrine, norepinephrine, glucagon, and growth hormone release in association with physiological decrements in the plasma glucose concentration in normal and diabetic man. , 1980, The Journal of clinical endocrinology and metabolism.

[4]  P. Cryer,et al.  Epinephrine plasma metabolic clearance rates and physiologic thresholds for metabolic and hemodynamic actions in man. , 1980, The Journal of clinical investigation.

[5]  W. Tamborlane,et al.  Normalization of the Growth Hormone and Catecholamine Response to Exercise in Juvenile-Onset Diabetic Subjects Treated with a Portable Insulin Infusion Pump , 1979, Diabetes.

[6]  R. Rizza,et al.  Role of glucagon, catecholamines, and growth hormone in human glucose counterregulation. Effects of somatostatin and combined alpha- and beta-adrenergic blockade on plasma glucose recovery and glucose flux rates after insulin-induced hypoglycemia. , 1979, The Journal of clinical investigation.

[7]  H. Grill,et al.  The forebrain is not essential for sympathoadrenal hyperglycemic response to glucoprivation. , 1979, Science.

[8]  D. Johnson,et al.  Glucagon and catecholamine secretion during hypoglycemia in normal and diabetic man. , 1977, Journal of Clinical Endocrinology and Metabolism.

[9]  P. Cryer,et al.  The role of adrenergic mechanisms in the substrate and hormonal response to insulin-induced hypoglycemia in man. , 1976, The Journal of clinical investigation.

[10]  D. Johnson,et al.  Glucagon response to hypoglycemia in sympathectomized man. , 1976, The Journal of clinical investigation.

[11]  P. Cryer,et al.  Measurement of norepinephrine and epinephrine in small volumes of human plasma by a single isotope derivative method: response to the upright posture. , 1974, The Journal of clinical endocrinology and metabolism.

[12]  N. Christensen Plasma Norepinephrine and Epinephrine in Untreated Diabetics, During Fasting and After Insulin Administration , 1974, Diabetes.

[13]  D. Ewing,et al.  Vascular reflexes in diabetic autonomic neuropathy. , 1973, Lancet.

[14]  P. Watkins,et al.  Cardiac Denervation in Diabetes , 1973, British medical journal.

[15]  J. Gerich,et al.  Lack of Glucagon Response to Hypoglycemia in Diabetes: Evidence for an Intrinsic Pancreatic Alpha Cell Defect , 1973, Science.

[16]  F. Pi‐Sunyer,et al.  Neural control of counter-regulatory events during glucopenia in man. , 1973, The Journal of clinical investigation.

[17]  J. Peuler,et al.  A simplified radiometric assay for plasma norepinephrine and epinephrine. , 1973, Analytical biochemistry.

[18]  R. Himsworth Hypothalamic control of adrenaline secretion in response to insufficient glucose , 1970, The Journal of physiology.

[19]  S. Weinhouse,et al.  Quantitative Estimation of the Cori Cycle in the Human , 1963 .