Effect of phentolamine on the insulin, glucagon, and glucose responses to exercise in adrenal-denervated sheep

1985 ◽  
Vol 63 (4) ◽  
pp. 346-349 ◽  
Author(s):  
Ronald P. Brockman
Keyword(s):  
Sympathetic Innervation ◽  
Adrenergic Innervation ◽  
Metabolic Responses ◽  
Metabolic Clearance ◽  
Adrenergic Stimulation ◽  
Hepatic Glucose Output ◽  
Optimal Response ◽  
Hepatic Glucose ◽  
Alpha Blockade ◽  
Glucose Output

Hyperglycemia and increased hepatic glucose output are characteristic responses to exercise in sheep. They appear to be due in part to α-adrenergic stimulation. To delineate the contributions of sympathetic innervation and adrenal catecholamines to the hormonal and metabolic responses to exercise, adrenal-denervated sheep were exercised with and without α-blockade (phentolamine treatment). Alpha blockade exaggerated the hyperinsulinemia during exercise (increment of 61 ± 8 vs. 34 ± 7 μU/mL for the control). This was associated with a reduction in glucose appearance (increments of 63 ± 8 vs. 236 ± 23 μmol/min, respectively). The metabolic clearance rates were not altered by α-blockade. It appears that both the adrenal catecholamines and adrenergic innervation to the pancreas contribute to the prevention of a rise in insulin concentrations during exercise in sheep. While this may not be essential for glucose appearance to rise during exercise, it appears necessary for an optimal response.

Effect of Catecholamines and Dibutyryl-cyclic-AMP on Glucose Turnover, Plasma Free Fatty Acids, and Insulin in Dogs Treated with Methylprednisolone

1972 ◽  
Vol 50 (10) ◽  
pp. 999-1006 ◽  
Author(s):  
Bela Issekutz Jr. ◽  
Ingrid Borkow
Keyword(s):  
Cyclic Amp ◽  
Treated Group ◽  
Glucose Turnover ◽  
Immunoreactive Insulin ◽  
Metabolic Clearance ◽  
Hepatic Glucose Output ◽  
Hepatic Glucose ◽  
Lactate Levels ◽  
Glucose Output ◽  
Hyperglycemic Effect

The turnover rate of glucose was measured in dogs with indwelling arterial and venous catheters, according to the primed constant rate infusion techniques, using 2-3H-glucose as tracer. The effects of adrenalin (A), noradrenalin (NA), and dibutyryl-cAMP (DBcAMP) infusions were tested on normal dogs and on dogs treated for 3 days with methylprednisolone (MP, 3–3.5 mg/kg day). MP potentiated the hyperglycemic effect of A (0.5 μg/kg min) six- to sevenfold, and the increase of hepatic glucose output (Ra) 11-fold. In addition, the free fatty acid (FFA) increasing and lactacidemic effects of A were significantly potentiated by MP. A prevented the rise of immunoreactive insulin even though plasma glucose reached values of 400–450 mg%. The metabolic clearance rate was significantly decreased by A. NA (0.5 μg/kg min) had no hyperglycemic effect in the controls, but it increased the blood sugar by 120 mg% in the treated group. This was caused by a more than twofold increase in the hepatic glucose output. MP treatment did not alter the NA induced rise of FFA and no effect was seen on plasma lactate levels. NA caused a transient rise of insulin in the controls and a greater and more sustained one in treated dogs. Following MP treatment, DBcAMP (0.1 or 0.2 mg/kg min) also caused a much greater hepatic glucose output and hyperglycemia than what had been obtained on the same animals prior to treatment. DBcAMP increased plasma insulin and decreased FFA. It is concluded that the cyclic-AMP sensitivity of hepatic enzyme systems involved in glucose output was greatly increased by MP treatment.

Pregnancy impairs the counterregulatory response to insulin-induced hypoglycemia in the dog

2004 ◽  
Vol 287 (3) ◽  
pp. E480-E488 ◽  
Author(s):  
Cynthia C. Connolly ◽  
Lisa N. Aglione ◽  
Marta S. Smith ◽  
D. Brooks Lacy ◽  
Mary Courtney Moore
Keyword(s):  
Steady State ◽  
Late Pregnancy ◽  
Conscious Dogs ◽  
Metabolic Responses ◽  
Hepatic Glucose Output ◽  
Hepatic Glucose ◽  
Glucose Output ◽  
The Impact ◽  
Arteriovenous Difference ◽  
Arterial Glucose

The impact of pregnancy on the counterregulatory response to insulin-induced hypoglycemia was examined in six nonpregnant (NP) and six pregnant (P; 3rd trimester) conscious dogs by tracer and arteriovenous difference techniques. After basal sampling, insulin was infused intraportally at 30 pmol·kg−1·min−1 for 180 min. Insulin rose from 70 ± 15 to 1,586 ± 221 pmol/l and 27 ± 4 to 1,247 ± 61 pmol/l in the 3rd h in NP and P, respectively. Arterial glucose fell from 5.9 ± 0.2 to 2.3 ± 0.2 mmol/l in P. Glucose was infused in NP to equate the rate of fall of glucose and the steady-state concentrations in the groups (5.9 ± 0.2 to 2.3 ± 0.1 mmol/l in NP). Glucagon was 32 ± 6, 69 ± 11, and 48 ± 10 ng/l (basal and 1st and 3rd h) in NP, but the response was attenuated in P (34 ± 5, 46 ± 6, 41 ± 9 ng/l). Cortisol and epinephrine rose similarly in both groups, but norepinephrine rose more in NP (Δ3.01 ± 0.46 and Δ1.31 ± 0.13 nmol/l, P < 0.05). Net hepatic glucose output (NHGO; μmol·kg−1·min−1) increased from 10.6 ± 1.8 to 21.2 ± 3.3 in NP (3rd h) but did not increase in P (15.1 ± 1.5 to 15.3 ± 2.8 μmol·kg−1·min−1, P < 0.05 between groups). The glycogenolytic contribution to NHGO in NP increased from 5.8 ± 0.7 to 10.4 ± 2.5 μmol·kg−1·min−1 by 90 min but steadily declined in P. The increase in glycerol levels and the gluconeogenic contribution to NHGO were 50% less in P than in NP, but ketogenesis did not differ. The glucagon and norepinephrine responses to insulin-induced hypoglycemia are blunted in late pregnancy in the dog, impacting on the magnitude of the metabolic responses to the fall in glucose.

Hepatic glycerol flux after E. coli endotoxin administration

1984 ◽  
Vol 247 (4) ◽  
pp. R687-R692 ◽  
Author(s):  
O. P. McGuinness ◽  
J. J. Spitzer
Keyword(s):  
Blood Flow ◽  
Clearance Rate ◽  
Arterial Blood Flow ◽  
Metabolic Clearance ◽  
Hepatic Glucose Output ◽  
Metabolic Clearance Rate ◽  
Endotoxin Administration ◽  
Arterial Blood ◽  
Hepatic Glucose ◽  
Glucose Output

Hepatic glycerol flux was examined in dogs after the administration of Escherichia coli endotoxin (0.4 mg/kg) to determine the contribution of the liver to the previously observed decline in the metabolic clearance rate of glycerol. Hepatic glycerol flux was estimated by determining hepatic arterial and portal venous blood flows with electromagnetic flow probes and by measuring arteriovenous difference of glycerol across the liver. Administration of endotoxin significantly decreased total hepatic blood flow (by approximately 20%) but did not alter hepatic arterial blood flow. Hepatic glycerol clearance decreased by 25–30% after endotoxin administration. Hepatic glycerol extraction also decreased. Under control conditions, 60% of the metabolic clearance rate of glycerol was attributable to the liver, whereas in the postendotoxin state approximately 72% of the glycerol clearance could be accounted for by hepatic clearance. Thus changes in transhepatic glycerol flux are only partially responsible for the previously observed alterations in glycerol clearance after endotoxin administration. Although hepatic glycerol clearance decreased, net hepatic glycerol, as well as lactate and alanine, uptake did not decrease, indicating that gluconeogenic precursor availability to the hepatocytes was not diminished. Hepatic glucose output was elevated after endotoxin administration. Changes in hepatic glucose output and gluconeogenic precursor uptake help explain the endotoxin-induced alternations in the fluxes of these metabolites.

Effects of oxytocin upon the endocrine pancreas secretion and glucose turnover in normal man

1990 ◽  
Vol 123 (5) ◽  
pp. 504-510 ◽  
Author(s):  
Giuseppe Paolisso ◽  
Gennaro Pizza ◽  
Stefano De Riu ◽  
Giuseppe Marrazzo ◽  
Saverio Sgambato ◽  
...  
Keyword(s):  
Plasma Glucose ◽  
Glucose Infusion ◽  
Glucose Turnover ◽  
Metabolic Clearance ◽  
Hepatic Glucose Output ◽  
Glucose Levels ◽  
Glucose Disappearance ◽  
Hepatic Glucose ◽  
Normal Man ◽  
Glucose Output

Abstract. In normal man oxytocin infusion under basal conditions and at pharmacological doses evoked a rapid surge in plasma glucose and glucagon levels followed by a later increase in plasma insulin levels. Simultaneous [D-3H]glucose infusion indicated that oxytocin also produced a prompt and significant increase in hepatic glucose output with a secondary increase in glucose disappearance rate. Eight healthy volunteers were studied during euglycemic glucose clamp and simultaneous [D-3H]glucose infusion, during suppression of endogenous pancreatic secretion by cyclic somatostatin (250 μg/h) and during exogenous glucagon (67 ng/min) and insulin (0.15 mU · kg−1 · min−1 from 0 to 120 min and 0.40 mU · kg−1 · min−1 from 121 to 240 min) replacement. During the first 60 min oxytocin (0.2 U/min) evoked a transient but significant increase in plasma glucose levels and hepatic glucose output with a simultaneous suppression of the glucose infusion rate. No difference in glucose disappearance and metabolic clearance rates were recorded throughout the clamp irrespective of whether oxytocin was infused or not. So we conclude that oxytocin exerts a hyperglycemic effect through an A-cell stimulation and a glycogenolytic action.

Effects of epinephrine on the net hepatic uptake of lactate, pyruvate, and glycerol in sheep

1991 ◽  
Vol 69 (4) ◽  
pp. 475-479 ◽  
Author(s):  
Ronald P. Brockman
Keyword(s):  
Blood Vessels ◽  
Glucose Production ◽  
Hepatic Uptake ◽  
Metabolic Clearance ◽  
Hepatic Extraction ◽  
Hepatic Glucose Output ◽  
Epinephrine Infusion ◽  
Hepatic Gluconeogenesis ◽  
Hepatic Glucose ◽  
Glucose Output

Epinephrine causes hyperglycemia in part by increasing gluconeogenesis. However, the mechanism of its gluconeogenic effects has not been studied in ruminants. This study was undertaken to examine the effect of epinephrine on the net hepatic uptake of selected glucose precursors in sheep. The major abdominal blood vessels of the sheep were catheterized in normal and alloxan diabetic sheep. Glucose production, metabolic clearance of glucose, and the hepatic removal of certain glucose precursors were determined before, during, and after epinephrine infusion. Epinephrine increased the hepatic glucose output, the concentrations of lactate and glycerol in plasma, and the net hepatic uptake and fractional hepatic extraction of lactate and glycerol. These effects were independent of changes in the concentrations of insulin and glucagon in plasma. These results show that epinephrine directly stimulates hepatic gluconeogenesis in sheep.Key words: epinephrine, hepatic gluconeogenesis, sheep.

Evidence for dual control mechanism regulating hepatic glucose output in nondiabetic men

Diabetes ◽  
1991 ◽  
Vol 40 (8) ◽  
pp. 1033-1040 ◽  
Author(s):  
J. N. Clore ◽  
P. S. Glickman ◽  
S. T. Helm ◽  
J. E. Nestler ◽  
W. G. Blackard
Keyword(s):  
Control Mechanism ◽  
Dual Control ◽  
Hepatic Glucose Output ◽  
Hepatic Glucose ◽  
Glucose Output
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