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.

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.

Effect of phlorizin on hepatic glucose output

1962 ◽  
Vol 202 (1) ◽  
pp. 149-154 ◽  
Author(s):  
Edwin H. Kolodny ◽  
Robert Kline ◽  
Norman Altszuler
Keyword(s):  
Plasma Glucose ◽  
Vena Cava ◽  
The Body ◽  
Hepatic Veins ◽  
Hepatic Glucose Output ◽  
Direct Stimulation ◽  
Indwelling Catheters ◽  
Glucose Levels ◽  
Hepatic Glucose ◽  
Glucose Output

Using phlorizin as an experimental tool, an investigation of the mechanisms responsible for the maintenance of plasma glucose levels was undertaken. Infusion of phlorizin has been shown to produce a prompt glucosuria and increase in hepatic glucose output (HGO), but without discernable hypoglycemia. This raises the question as to the nature of the stimulus for the increased HGO. The effect of phlorizin on net HGO was studied in anesthetized dogs with indwelling catheters in the portal and hepatic veins. Infusion of phlorizin into normal dogs produced a prompt glucosuria and a concomitant increase in HGO, without significant changes in the plasma glucose concentration in the portal vein. In functionally nephrectomized dogs, phlorizin did not change HGO nor circulating glucose levels. In dogs with intact kidneys, when glucosuria was prevented by urine recirculation into the inferior vena cava, the infusion of phlorizin again failed to alter HGO or circulating glucose levels. The data indicate that the phlorizin-induced increase in HGO is dependent on loss of glucose from the body. The enhancement of HGO could not be ascribed to a direct stimulation of the liver, kidney, or endocrine glands, or to an impairment of glucose utilization. Possible mechanisms to explain this effect of phlorizin are discussed.

Insulin as a mediator of hepatic glucose uptake in the conscious dog

1982 ◽  
Vol 242 (2) ◽  
pp. E97-E101 ◽  
Author(s):  
A. D. Cherrington ◽  
P. E. Williams ◽  
N. Abou-Mourad ◽  
W. W. Lacy ◽  
K. E. Steiner ◽  
...  
Keyword(s):  
Glucose Uptake ◽  
Plasma Insulin ◽  
Marked Effect ◽  
Glucose Infusion ◽  
Hepatic Glucose Output ◽  
Intravenous Glucose ◽  
Conscious Dog ◽  
Hepatic Glucose ◽  
Glucose Output ◽  
Hepatic Glucose Uptake

The aim of this study was to determine whether a physiological increment in plasma insulin could promote substantial hepatic glucose uptake in response to hyperglycemia brought about by intravenous glucose infusion in the conscious dog. To accomplish this, the plasma glucose level was doubled by glucose infusion into 36-h fasted dogs maintained on somatostatin, basal glucagon, and basal or elevated intraportal insulin infusions. In the group with basal glucagon levels and modest hyperinsulinemia (33 +/- 2 micro U/ml), the acute induction of hyperglycemia (mean increment of 120 mg/dl) caused marked net hepatic glucose uptake (3.7 +/- 0.5 mg . kg-1 . min-1). In contrast, similar hyperglycemia brought about in the presence of basal glucagon and basal insulin levels described net hepatic glucose output in 56%, but did not cause net hepatic glucose uptake. The length of fast was not crucial to the response because similar signals (insulin, 38 +/- 6 micro U/ml; glucose increment, 127 mg/dl) promoted identical net hepatic glucose uptake (3.8 +/- 0.6 mg . kg-1 . min-1) in dogs fasted for only 16 h. In conclusion, in the conscious dog, a) physiologic increments in plasma insulin have a marked effect on the ability of hyperglycemia to stimulate net hepatic glucose uptake, and b) it is not necessary to administer glucose orally to promote substantial net hepatic glucose uptake.

Impaired Modulation of Hepatic Glucose Output Overnight after a 72-h Fast in Normal Man*

1990 ◽  
Vol 70 (4) ◽  
pp. 865-868 ◽  
Author(s):  
J. N. CLORE ◽  
S. T. HELM ◽  
J. E. NESTLER ◽  
W. G. BLACKARD
Keyword(s):  
Hepatic Glucose Output ◽  
Hepatic Glucose ◽  
Normal Man ◽  
Glucose Output

scholarly journals Measurement of Hepatic Glucose Output, Krebs Cycle, and Gluconeogenic Fluxes by NMR Analysis of a Single Plasma Glucose Sample

1998 ◽  
Vol 263 (1) ◽  
pp. 39-45 ◽  
Author(s):  
John G. Jones ◽  
Rui A. Carvalho ◽  
Byron Franco ◽  
A.Dean Sherry ◽  
Craig R. Malloy
Keyword(s):  
Plasma Glucose ◽  
Krebs Cycle ◽  
Nmr Analysis ◽  
Hepatic Glucose Output ◽  
Hepatic Glucose ◽  
Glucose Output ◽  
Single Plasma

Influence of somatostatin on glucagon- and epinephrine-stimulated hepatic glucose output in the dog.

1979 ◽  
Vol 236 (2) ◽  
pp. E113
Author(s):  
L Saccà ◽  
R Sherwin ◽  
P Felig
Keyword(s):  
Plasma Glucose ◽  
Glucose Production ◽  
Conscious Dogs ◽  
Insulin Deficiency ◽  
Hepatic Glucose Output ◽  
Glucose Kinetics ◽  
Insulin Levels ◽  
Hepatic Glucose ◽  
Glucose Output ◽  
Insulin Replacement

Glucose kinetics were measured using [3-3H]glucose in conscious dogs during the infusion of: 1) glucagon alone; 2) glucagon plus somatostatin with insulin replacement; 3) epinephrine alone; and 4) epinephrine plus somatostatin with insulin and glucagon replacement. Infusion of glucagon alone resulted in a 10-15 mg/dl rise in plasma glucose and a transient 45% rise in glucose production. When somatostatin and insulin were added, a four- to fivefold greater rise in plasma glucose and glucose production was observed. Glucagon levels were comparable to those achieved with infusion of glucagon alone, whereas peripheral insulin levels increased three- to fourfold above baseline, suggesting adequate replacement of preinfusion portal insulin levels. Infusion of epinephrine alone produced a 40% rise in plasma glucose and a 100% rise in glucose production. When somatostatin, insulin, and glucagon were added to epinephrine, the rise in glucose production was reduced in 65% despite replacement of glucagon levels and presumably mild portal insulin deficiency. These findings suggest that somatostatin: 1) potentiates the stimulatory effect of physiologic hyperglucagonemia on glucose production independent of insulin availability and 2) blunts the stimulatory effect of physiologic increments of epinephrine independent of glucagon availability.

Regulation of hepatic glucose output during exercise by circulating glucose and insulin in humans

1986 ◽  
Vol 250 (3) ◽  
pp. R411-R417 ◽  
Author(s):  
A. B. Jenkins ◽  
S. M. Furler ◽  
D. J. Chisholm ◽  
E. W. Kraegen
Keyword(s):  
Plasma Glucose ◽  
Insulin Infusion ◽  
Cycle Ergometer ◽  
Constant Infusion ◽  
Hepatic Glucose Output ◽  
Fixed Rate ◽  
Ergometer Exercise ◽  
Hepatic Glucose ◽  
Glucose Output ◽  
Simple Difference

We have tested the hypothesis that hepatic glucose output (Ra) during exercise in humans is subject to feedback control by circulating glucose within a control range that is determined by the circulating insulin concentration. Three exercise protocols based on 60-min cycle ergometer exercise at 55% maximal O2 consumption were used: 1) control, 2) insulin infusion with a euglycemic clamp, and 3) insulin infusion with a fixed-rate glucose infusion. Ra was measured using a constant infusion of [3H]glucose. During the glucose clamp there was no Ra response to exercise. There were significant inverse relationships between Ra and plasma glucose during control exercise (r = -0.73, P less than 0.001) and exercise with fixed-rate glucose and insulin infusion (r = -0.96, P less than 0.001). During the fixed-rate glucose and insulin infusion, plasma glucose fell from the commencement of exercise but stabilized at a lower level. These results are interpreted in terms of a simple difference controller where Ra is proportional to the deviation of plasma glucose from a defined set point. Insulin affects Ra and regulates the steady-state glucose level by altering the sensitivity of this control system.

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.

Pentobarbital reduces basal liver glucose output and its insulin suppression in rats

1990 ◽  
Vol 258 (4) ◽  
pp. E701-E707 ◽  
Author(s):  
P. W. Clark ◽  
A. B. Jenkins ◽  
E. W. Kraegen
Keyword(s):  
Plasma Glucose ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Conscious State ◽  
Hepatic Insulin Resistance ◽  
Glucose Turnover ◽  
Pentobarbital Anesthesia ◽  
Hepatic Glucose ◽  
Glucose Output ◽  
Conscious Animals

Recent reports conflict on the effect that pentobarbital anesthesia has on basal glucose turnover in the rat. It is also unclear whether pentobarbital alters insulin suppressibility of hepatic glucose production (Ra). We examined these issues by performing basal and hyperinsulinemic euglycemic clamp studies in anesthetized and conscious animals. Ra and glucose utilization (Rd) were estimated using a steady-state infusion of 3-[3H]glucose. Pentobarbital anesthesia in normothermic rats transiently elevated plasma glucose but resulted in a sustained suppression of basal Ra (10.4 +/- 0.3 vs. conscious 13.2 +/- 0.9 mg.kg-1.min-1, P less than 0.05). In the insulin-stimulated state (110 mU/l), despite similar plasma glucose and insulin levels, clamp glucose infusion rate was significantly reduced in anesthetized animals (11.1 +/- 0.9 vs. conscious 23.6 +/- 1.3 mg.kg-1.min-1, P less than 0.001). This can be attributed to both a significantly lower insulin-stimulated Rd (15.4 +/- 1.3 vs. conscious 22.8 +/- 1.4 mg.kg-1.min-1, P less than 0.005) and reduced insulin suppression of Ra (4.3 +/- 0.8 vs. conscious -0.8 +/- 0.5 mg.kg-1.min-1, P less than 0.001; i.e., anesthetized 59% vs. conscious 100% reduction of basal Ra). Thus pentobarbital anesthesia significantly reduces basal Ra and induces hepatic insulin resistance (reduces Ra suppressibility). Pentobarbital effects are not dependent on induced hypothermia, but this exacerbates the metabolic perturbation. Caution should be used in extrapolating from the anesthetized to the conscious state.

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