Beta-adrenergic contribution to glucagon-induced glucose production and insulin secretion in uremia

1986 ◽  
Vol 251 (3) ◽  
pp. E322-E327
Author(s):  
P. Baylor ◽  
S. Shilo ◽  
J. Zonszein ◽  
H. Shamoon
Keyword(s):  
Plasma Insulin ◽  
Insulin Response ◽  
Glucose Production ◽  
Adrenergic Blockade ◽  
Glucose Kinetics ◽  
Beta Adrenergic ◽  
Adrenergic Regulation ◽  
Insulin Secretory Response ◽  
Plasma Insulin Response ◽  
Normal Controls

Spontaneous or propranolol-induced hypoglycemia can occur in uremic humans. We studied glucose kinetics (using [3-3H]glucose) in five uremic humans 24 h after hemodialysis and in seven normal controls. The effect of glucagon infusion at rates of 3, 6, 12, and 18 ng X kg-1 X min-1 at 60-min intervals was compared with either saline or beta-adrenergic blockade (propranolol infusion). In uremics, plasma glucose increased by 20-25% and by 40-50% at the 3 and 6 ng X kg-1 X min-1 glucagon doses, respectively, with no further increases at higher infusion rates. Glucose production increased transiently and in tandem with glucose uptake at each glucagon increment (P less than 0.0001). During beta-adrenergic blockade, the effect of glucagon in stimulating glucose production was blunted by 14-24% at the 6-18 ng X kg-1 X min-1 doses (P less than 0.05). During saline infusion, plasma insulin concentrations increased progressively to peak levels fourfold above basal at the 18 ng X kg-1 X min-1 dose. This increase in plasma insulin was virtually abolished by concomitant beta-adrenergic blockade (P = 0.0002). In contrast to uremic subjects, normal controls exhibited lesser degrees of hyperglycemia and hyperinsulinemia at all glucagon infusion rates. Propranolol infusion had no effect on the increments in glucose production and uptake nor on the plasma insulin response. These results suggest that in uremic humans propranolol independently reduces the hepatic response to glucagon and the insulin secretory response to hyperglycemia and/or hyperglucagonemia. These observations provide a possible mechanism for the adrenergic regulation of glucose homeostasis in uremia.

Adrenergic blockade prevents endotoxin-induced increases in glucose metabolism

1988 ◽  
Vol 255 (5) ◽  
pp. E629-E635 ◽  
Author(s):  
D. M. Hargrove ◽  
G. J. Bagby ◽  
C. H. Lang ◽  
J. J. Spitzer
Keyword(s):  
Plasma Insulin ◽  
Lactate Concentration ◽  
Insulin Concentration ◽  
Adrenergic Blockade ◽  
Plasma Lactate ◽  
Glucose Kinetics ◽  
Plasma Insulin Concentration ◽  
Beta Adrenergic ◽  
Plasma Lactate Concentration ◽  
Adrenergic Antagonists

Combined alpha- and beta-adrenergic blockade was used to investigate the role of catecholamines in endotoxin-induced elevations in glucose kinetics. Glucose kinetics were measured before and for 4 h after the injection of endotoxin [100 micrograms/100 g body wt iv, 30% lethal dose (LD30) at 24 h]. Adrenergic blockade was achieved by the bolus injection of phentolamine and propranolol followed by their continuous infusion. Endotoxin-treated rats exhibited a transient hyperglycemia and sustained (greater than 4 h) increase in plasma lactate concentration, as well as elevated rates of glucose appearance (Ra, 83%), disappearance (Rd, 58%), recycling (160%), and metabolic clearance (23%). Adrenergic blockade prevented endotoxin-induced increases in plasma glucose concentration, Ra, Rd, and recycling but not glucose clearance. The increase in plasma lactate concentration was blunted by 35%. After 2 h, endotoxic animals infused with adrenergic antagonists developed hypoglycemia, which may have resulted from an increased plasma insulin concentration. The attenuation of elevated glucose turnover by adrenergic blockade in the endotoxin-treated animals was not due to a reduction in plasma glucagon level or differences in plasma insulin concentration. Administration of the alpha- or beta-adrenergic antagonists separately blunted but did not prevent endotoxin-induced changes in glucose kinetics, and therefore the efficacy of the adrenergic blockade could not be assigned to a single receptor class. These results indicate that catecholamines are important contributory factors to many of the early alterations in carbohydrate metabolism observed during endotoxemia.

Effect of alpha-adrenergic stimulation and its blockade on glucose turnover in man

1980 ◽  
Vol 238 (5) ◽  
pp. E467-E472 ◽  
Author(s):  
R. A. Rizza ◽  
M. W. Haymond ◽  
J. M. Miles ◽  
C. A. Verdonk ◽  
P. E. Cryer ◽  
...  
Keyword(s):  
Plasma Glucose ◽  
Plasma Insulin ◽  
Glucose Production ◽  
Glucose Turnover ◽  
Adrenergic Blockade ◽  
Plasma Epinephrine ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Glucose Clearance ◽  
Adrenergic Effects

Epinephrine (50 ng . kg-1 . min-1) was infused for 120 min in seven normal volunteers alone (combined alpha- and beta-adrenergic stimulation), with propranolol (alpha-adrenergic stimulation), and with propranolol plus phentolamine (alpha-adrenergic blockade superimposed on alpha-adrenergic stimulation). During alpha-adrenergic stimulation, plasma glucose and glucose production increased 32 and 42% less, respectively, than during infusion of epinephrine alone, whereas glucose clearance was suppressed comparably. Plasma insulin decreased during alpha-adrenergic stimulation but increased during infusion of epinephrine alone. Plasma epinephrine was threefold greater during infusion of epinephrine plus propranolol than during infusion of epinephrine alone. When alpha-adrenergic blockade was superimposed on alpha-adrenergic stimulation, the increases in plasma glucose and glucose production as well as the decreases in plasma insulin and glucose clearance observed during alpha-adrenergic stimulation were virtually abolished, whereas plasma epinephrine levels were unaltered. These results indicate that in man epinephrine can cause hyperglycemia via both alpha- and beta-adrenergic stimulation of glucose production and suppression of glucose clearance, either directly or indirectly. alpha-Adrenergic effects on glucose production and clearance may be mediated by inhibition of insulin secretion.

Effects of adrenergic blockade on glucose kinetics in septic and burned guinea pigs

1981 ◽  
Vol 241 (3) ◽  
pp. R222-R227
Author(s):  
M. J. Durkot ◽  
R. R. Wolfe
Keyword(s):  
Guinea Pigs ◽  
Glucose Production ◽  
Constant Infusion ◽  
Adrenergic Blockade ◽  
Glucose Kinetics ◽  
Counterregulatory Hormones ◽  
Beta Adrenergic ◽  
Glucoregulatory Hormones ◽  
Adrenergic Blocker ◽  
Septic Group

We have used the primed-constant infusion of [6-3H]glucose to study the effects of phentolamine, an alpha-adrenergic blocker, and propranolol, a beta-adrenergic blocker, on glucose production and clearance in gastrostomy-fed control, septic (repeated sub-Q Escherichia coli injections), and burned (25-30% BSA) guinea pigs. Hypermetabolism and elevated glucoregulatory hormones were evident in both traumatized models, whereas their glucose kinetic response was different. Basal glucose production and clearance were elevated in the burned group and were depressed in the septic group when compared to control values. Propranolol caused a further increase in glucose production and clearance in the burned group, whereas it depressed glucose production and clearance to an even greater extent in the septic group. Phentolamine also produced an increase in glucose production and clearance in the burned group. In the septic group, phentolamine had no significant effect on glucose production, but clearance was significantly elevated. Thus, although alpha- or beta-adrenergic blockade normalized metabolic rate in both groups with respect to control animals, glucose kinetics remained different despite similar changes in counterregulatory hormones.

Plasma insulin response among Nauruans. Prediction of deterioration in glucose tolerance over 6 yr

Diabetes ◽  
1987 ◽  
Vol 36 (2) ◽  
pp. 179-186 ◽  
Author(s):  
R. A. Sicree ◽  
P. Z. Zimmet ◽  
H. O. King ◽  
J. S. Coventry
Keyword(s):  
Glucose Tolerance ◽  
Plasma Insulin ◽  
Insulin Response ◽  
Plasma Insulin Response

THE USE OF CHLORPROPAMIDE IN DIABETES INSIPIDUS IN CHILDREN

PEDIATRICS ◽  
1970 ◽  
Vol 45 (2) ◽  
pp. 236-245
Author(s):  
Robert M. Ehrlich ◽  
Sang Whay Kooh
Keyword(s):  
Diabetes Insipidus ◽  
Water Deprivation ◽  
Plasma Insulin ◽  
Urine Volume ◽  
Insulin Response ◽  
Urine Osmolality ◽  
Post Traumatic ◽  
Term Management ◽  
Plasma Insulin Response

Oral chlorpropamide was administered to 17 children with diabetes insipidus (D.I.). The cause of the D.I. was idiopathic, six; histiocytosis, five; craniopharyngioma, three; pinealoma, two, and post-traumatic, one. Twenty-four-hour urine volume and measurements of serum and urine osmolality at the beginning and end of a 7-hour water deprivation test were used to evaluatechlorpropamide therapy. Administration of 150 to 400 mg of chlorpropamide per day by mouth caused a reduction in urine volume in all patients (range 8 to 67%). No change in aldosterone, 17-hydroxycorticoids, or electrolyte excretion was noted. Serum electrolytes and glomerular filtration rate were not affected by therapy. Glucose tolerance and plasma insulin response remained normal in those patients tested. Mild leucine sensitivity without significant change in plasma insulin was induced in four children. During water deprivation, seven patients with secondary D.I. but only one with idiopathic D.I. produced hypertonic urine. Hypoglycemia developed in seven children and is the major hazard of treatment. Long-term management of D.I. has been possible in nine children. Oral chlorpropamide is a useful drug in children with vasopressin-sensitive diabetes insipidus.

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