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.

Does a glucose load inhibit hepatic sugar output? C14 glucose studies in eviscerated dogs

1959 ◽  
Vol 197 (1) ◽  
pp. 60-62 ◽  
Author(s):  
Robert Steele ◽  
Jonathan S. Bishop ◽  
Rachmiel Levine
Keyword(s):  
Plasma Glucose ◽  
Glucose Concentration ◽  
Alternative Explanation ◽  
Specific Activity ◽  
The Body ◽  
Glucose Load ◽  
Hepatic Glucose Output ◽  
Minute Amount ◽  
Hepatic Glucose ◽  
Glucose Output

A sequence of changes in plasma glucose specific activity is observed in intact dogs when a large amount of C12 glucose is injected intravenously following the tagging of the circulating glucose by injection of a minute amount of C14 glucose. Similar changes are observed when the same procedure is applied to eviscerated dogs in which the plasma glucose concentration is being maintained by a continuous infusion of C12 glucose, this infusion being continued unchanged after the C12 glucose load is given. These results show that inhibition of hepatic glucose output is not the only or the necessary explanation for the cessation in the exponential fall of plasma glucose specific activity which is seen in the intact dog following an intravenous C12 glucose load. An alternative explanation of the effect is offered which is based on the slowness of mixing of the injected C12 glucose load with a part of the body glucose pool.

Plasma glucose and insulin responses to oral and intravenous glucose in cold-exposed humans

1988 ◽  
Vol 65 (6) ◽  
pp. 2395-2399 ◽  
Author(s):  
A. L. Vallerand ◽  
J. Frim ◽  
M. F. Kavanagh
Keyword(s):  
Glucose Tolerance ◽  
Glucose Uptake ◽  
Carbohydrate Metabolism ◽  
Cold Exposure ◽  
Plasma Glucose ◽  
Hepatic Glucose Output ◽  
Hepatic Glucose ◽  
Oral Gtt ◽  
Glucose Output ◽  
Insulin Responses

Although glucose tolerance and skeletal muscle glucose uptake are markedly improved by cold exposure in animals, little is known about such responses in humans. This study used two variations of a glucose tolerance test (GTT) to investigate changes in carbohydrate metabolism in healthy males during nude exposure to cold. In experiment 1, an oral GTT was performed in the cold and in the warm (3 h at 10 or 29 degrees C). To bypass the gastrointestinal tract, and to suppress hepatic glucose output, a second experiment was carried out as described above, using an intravenous GTT. Even though cold exposure raised metabolic rate greater than 2.5 times, plasma glucose and insulin responses to an oral GTT remained unaltered. In contrast, cold exposure reduced the entire plasma glucose profile as a function of time during the intravenous GTT (P less than 0.05), as plasma glucose was returned to basal levels within 1 h in comparison to a full 2 h in the warm, despite low insulin levels. The results of the intravenous GTT demonstrate that even with low insulin levels, carbohydrate metabolism is increased in cold-exposed males. This effect could be masked in the oral GTT by gastrointestinal factors and a high hepatic glucose output. Cold exposure may enhance insulin sensitivity and/or responsiveness for glucose uptake, mainly in shivering skeletal muscles.

Mechanisms of postabsorptive hyperglycemia in streptozotocin diabetic rats

1996 ◽  
Vol 270 (5) ◽  
pp. E752-E758 ◽  
Author(s):  
J. K. Wi ◽  
J. K. Kim ◽  
J. H. Youn
Keyword(s):  
Glucose Uptake ◽  
Plasma Glucose ◽  
Diabetic Rats ◽  
Normal Rate ◽  
Hepatic Glucose Output ◽  
Hepatic Glucose ◽  
Glucose Clearance ◽  
Streptozotocin Diabetic Rats ◽  
Acute Changes ◽  
Glucose Output

Postabsorptive hepatic glucose output (HGO) was estimated in normal (n = 9) and streptozotocin (STZ) diabetic rats after a 6-h [3-3H]glucose infusion. In diabetic rats, HGO was estimated at ambient (n = 12) or normal (achieved via phlorizin infusion; n = 9) glucose concentrations. HGO was not statistically different between normal and diabetic rats (63 +/- 3 vs. 77 +/- 10 mumol.kg-1.min-1; P> 0.05). HGO was also normal in diabetic rats even when plasma glucose was normalized with phlorizin infusion (71 +/- 5 vs. 63 +/- 3 mumol.kg-1.min-1; P> 0.05). In contrast, peripheral glucose uptake, when estimated at matched euglycemia, was lower by approximately 25% in diabetic than in normal rate (46 +/- 6 vs. 62 +/- 3 mumol.kg-1.min-1; P < 0.01). In addition, acute changes in plasma glucose concentrations did not have significant effects on HGO or peripheral glucose uptake in diabetic rats (P> 0.05), resulting in markedly decreased glucose clearance at ambient hyperglycemia (P < 0.001). In conclusion, postabsorptive HGO was not elevated in a majority (17 of 21) of STZ diabetic rats with severe hyperglycemia and therefore was not responsible for postabsorptive hyperglycemia. Our data suggest that an impairment in the ability of glucose to regulate peripheral glucose uptake or HGO develops in STZ diabetes and contributes to postabsorptive hyperglycemia.

Contributions of gluconeogenesis and glycogenolysis during glucose counterregulation in normal humans

1989 ◽  
Vol 256 (6) ◽  
pp. E844-E851 ◽  
Author(s):  
L. Lecavalier ◽  
G. Bolli ◽  
P. Cryer ◽  
J. Gerich
Keyword(s):  
Plasma Glucose ◽  
Hepatic Glucose Output ◽  
Insulin Hypoglycemia ◽  
Isotopic Method ◽  
Exogenous Glucose ◽  
Primary Mechanism ◽  
Hepatic Glucose ◽  
Normal Humans ◽  
Predominant Factor ◽  
Glucose Output

To estimate the relative contributions of gluconeogenesis and glycogenolysis to the increase in hepatic glucose output (HGO) during glucose counterregulation under conditions simulating clinical insulin hypoglycemia, we induced moderate hypoglycemia (approximately 55 mg/dl) with a continuous infusion of insulin that resulted in physiological hyperinsulinemia (approximately 20 microU/ml) in eight normal volunteers and estimated gluconeogenesis by two methods: an isotopic approach in which appearance of plasma glucose derived from lactate was determined and another approach in which we infused alcohol along with insulin to block gluconeogenesis and used the exogenous glucose required to prevent greater hypoglycemia as an index of gluconeogenesis. Both methods gave similar results. Initially glycogenolysis accounted for approximately 85% of HGO; however, once hypoglycemia became established, the contribution of gluconeogenesis increased progressively to 77 +/- 10 (isotopic method) and 94 +/- 10% (alcohol method) of overall HGO. We conclude that in normal humans during moderate protracted hypoglycemia induced by physiological hyperinsulinemia, gluconeogenesis is the predominant factor responsible for the counterregulatory increase in HGO and that increased gluconeogenesis rather than increased glycogenolysis is the primary mechanism preventing development of greater hypoglycemia.

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.

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.

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