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At least 19 recordsLinked to original sources

PubMed1992

Use of [3-3H]glucose and [6-14C]glucose to measure glucose turnover and glucose metabolism in humans.

[3-3H]glucose is frequently used to measure glucose turnover in humans. If fructose 6-phosphate-fructose 1,6-diphosphate cycling (Fpc) is negligible in both liver and muscle, then [3-3H]- and [6-14C]glucose (corrected for Cori cycle activity) should provide equivalent measures of glucose turnover. In addition, if glycogenolysis is fully suppressed, then [14C]lactate specific activity should equal that of [6-14C]glucose from which it was derived, and oxidation of [6-14C]glucose, as measured by rate of generation of 14CO2, should equal total glucose oxidation (i.e., that derived from intra- and extracellular pools) as measured by indirect calorimetry. To address these questions, glucose turnover was measured simultaneously with [3-3H]- and [6-14C]glucose in the basal state and in presence of low (approximately 200 pM) and high (approximately 750 pM) insulin concentrations. Glucose turnover rates measured with [3-3H]- and [6-14C]glucose were equivalent at all insulin concentrations, indicating that Fpc had no detectable effect on measurement of glucose appearance. [14C]lactate specific activity was lower (P less than 0.01) than that of [6-14C]glucose in the basal state but not during either low- or high-dose insulin infusion, implying that all lactate was derived from extracellular glucose. On the other hand, glucose oxidation as measured by rate of generation of 14CO2 was lower (P less than 0.05) than glucose oxidation as measured by indirect calorimetry during both insulin infusions, implying either that suppression of glycogenolysis was not complete in all tissues or that one or both of these techniques do not accurately measure glucose oxidation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1976

A comparative analysis of compartmentation of metabolism in the dorsal root ganglion and ventral spinal cord gray using [U-14C]glucose, [2-14C]glucose, [6-14C]glucose, [3,4-14C]glucose, NaH14CO3, and [2-14C]pyruvate.

A detailed temporal comparison of glucose metabolism, in the production of glutamate and glutamine as well as aspartate and alamine, was conducted in order to further define the uniqueness of the dorsal root ganglion compared to the ventral spinal cord gray. Experiments with injected labeled NaHCO3 and pyruvate were used in an attempt to clarify certain aspects of the above results with different [14C]glucose precursors. The glutamine/glutamate relative specific activity ratio (RSA) was consistently lower in the ganglion than in the ventral spinal cord gray, as was also true for glutamate specific activity from the same amount of injected [14C]glucose. The ganglion is characterized by a high level of alanine production from glucose and pyruvate. The NaH14CO3 experiments suggest that CO2 fixation from [3,4-14C]-glucose in the dorsal rool ganglion resul .ts in a higher glutamine/glutamate RSA when compared to results using either [6-14C] or [2-14C]glucose.

Alanine↗

PubMed1991

Intraportal glucose delivery enhances the effects of hepatic glucose load on net hepatic glucose uptake in vivo.

Although the importance of the hepatic glucose load in the regulation of liver glucose uptake has been clearly demonstrated in in vitro systems, the relationship between the hepatic glucose load and hepatic glucose uptake has yet to be defined in vivo. Likewise, the effects of the route of glucose delivery (peripheral or portal) on this relationship have not been explored. The aims of the present study were to determine the relationship between net hepatic glucose uptake (NHGU) and the hepatic glucose load in vivo and to examine the effects of the route of glucose delivery on this relationship. NHGU was evaluated at three different hepatic glucose loads in 42-h fasted, conscious dogs in both the absence (n = 7) and the presence (n = 6) of intraportal glucose delivery. In the absence of intraportal glucose delivery and in the presence of hepatic glucose loads of 50.5 +/- 5.9, 76.5 +/- 10.0, and 93.6 +/- 10.0 mg/kg/min and arterial insulin levels of approximately 33 microU/ml, NHGU was 1.16 +/- 0.37, 2.78 +/- 0.82, and 5.07 +/- 1.20 mg/kg/min, respectively. When a portion of the glucose load was infused into the portal vein and similar arterial insulin levels (approximately 36 microU/ml) and hepatic glucose loads (52.5 +/- 4.5, 70.4 +/- 5.6, and 103.6 +/- 18.4 mg/kg/min) were maintained, NHGU was twice that seen in the absence of portal loading (3.77 +/- 0.40, 4.80 +/- 0.59, and 9.62 +/- 1.43 mg/kg/min, respectively). Thus, net hepatic glucose uptake demonstrated a direct dependence on the hepatic glucose load that did not reach saturation even at elevations in the hepatic glucose load of greater than three times basal. In addition, the presence of intraportal glucose delivery increased net hepatic glucose uptake apparently by lowering the threshold at which the liver switched from net glucose output to net glucose uptake.

Animals↗

PubMed1979

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.

To further characterize mechanisms of glucose counterregulation in man, the effects of pharmacologically inducd deficiencies of glucagon, growth hormone, and catecholamines (alone and in combination) on recovery of plasma glucose from insulin-induced hypoglycemia and attendant changes in isotopically ([3-(3)H]glucose) determined glucose fluxes were studied in 13 normal subjects. In control studies, recovery of plasma glucose from hypoglycemia was primarily due to a compensatory increase in glucose production; the temporal relationship of glucagon, epinephrine, cortisol, and growth hormone responses with the compensatory increase in glucose appearance was compatible with potential participation of all these hormones in acute glucose counterregulation. Infusion of somatostatin (combined deficiency of glucagon and growth hormone) accentuated insulin-induced hypoglycemia (plasma glucose nadir: 36+/-2 ng/dl during infusion of somatostatin vs. 47+/-2 mg/dl in control studies, P < 0.01) and impaired restoration of normoglycemia (plasma glucose at min 90: 73+/-3 mg/dl at end of somatostatin infusion vs. 92+/-3 mg/dl in control studies, P<0.01). This impaired recovery of plasma glucose was due to blunting of the compensatory increase in glucose appearance since glucose disappearance was not augmented, and was attributable to suppression of glucagon secretion rather than growth hormone secretion since these effects of somatostatin were not observed during simultaneous infusion of somatostatin and glucagon whereas infusion of growth hormone along with somatostatin did not prevent the effect of somatostatin. The attenuated recovery of plasma glucose from hypoglycemia observed during somatostatin-induced glucagon deficiency was associated with plasma epinephrine levels twice those observed in control studies. Infusion of phentolamine plus propranolol (combined alpha-and beta-adrenergic blockade) had no effect on plasma glucose or glucose fluxes after insulin administration. However, infusion of somatostatin along with both phentolamine and propranolol further impaired recovery of plasma glucose from hypoglycemia compared to that observed with somatostatin alone (plasma glucose at end of infusions: 52+/-6 mg/dl for somatostatin-phentolamine-propranolol vs. 72+/-5 mg/dl for somatostatin alone, P < 0.01); this was due to further suppression of the compensatory increase in glucose appearance (maximal values: 1.93+/-0.41 mg/kg per min for somatostatin-phentolamine-propranolol vs. 2.86+/-0.32 mg/kg per min for somatostatin alone, P < 0.05). These results indicate that in man (a) restoration of normoglycemia after insulin-induced hypoglycemia is primarily due to a compensatory increase in glucose production; (b) intact glucagon secretion, but not growth hormone secretion, is necessary for normal glucose counterregulation, and (c) adrenergic mechanisms do not normally play an essential role in this process but become critical to recovery from hypoglycemia when glucagon secretion is impaired.

Adrenergic alpha-Antagonists↗

PubMed1992

Concordant glucose induction of glucokinase, glucose usage, and glucose-stimulated insulin release in pancreatic islets maintained in organ culture.

Using cultured islets as the experimental system, this study established dosage-response and time-dependency curves of the inductive glucose effect on glucose-stimulated insulin release, glucose usage, and glucokinase activity. Glucose-stimulated insulin release in islets cultured for 1, 2, or 7 days was increased as a function of glucose concentration in the culture medium and as a function of time. Glucose usage in the cultured islets showed a close relationship with glucose concentration in the culture medium at both 2 and 7 days of culture. Glucokinase activity increased in islets cultured for 1, 2, or 7 days as a function of increasing glucose concentrations in the culture medium and as a function of time. The V(max) of glucokinase in islets cultured for 7 days in medium containing 30 mM glucose was twice the value of freshly isolated islets and was almost fivefold higher than that in islets cultured for 7 days in 3 mM glucose. The glucose induction of glucose-stimulated insulin release, of glucose usage, and of glucokinase activity were tightly correlated. The biochemical mechanisms of glucose induction of islet glucokinase were further studied. Immunoblotting with an antibody against C-terminal peptide of glucokinase showed that densities of a 52,000-kD protein band from tissue extracts of islets cultured for 7 days in 3, 12, and 30 mM glucose were 25, 44, and 270% compared with that of extract from freshly isolated islets (100%). RNA blot analysis of glucokinase mRNA demonstrated virtually the same levels in fresh islets and islets after 7 days of culture in 3 or 30 mM glucose. The adaptive response of glucokinase to glucose appears therefore to be occurring at a translational or posttranslational site in cultured islets. These data greatly strengthen the concept that glucose is the regulator that induces the activity of glucokinase, which in turn determines the rate change of glucose usage as well as glucose-stimulated insulin release from beta-cells. Thus, the hypothesis that glucokinase is the glucose sensor of beta-cells is strengthened further.

Animals↗

PubMed1991

Contribution to postprandial hyperglycemia and effect on initial splanchnic glucose clearance of hepatic glucose cycling in glucose-intolerant or NIDDM patients.

Excessive amounts of glucose enter the systemic circulation when patients with non-insulin-dependent diabetes mellitus (NIDDM) eat a carbohydrate-containing meal. To determine the contribution of hepatic glucose cycling (defined as the net effect of glucose/glucose-6-phosphate cycling and uptake and release of glucose from hepatic glycogen) to postprandial hyperglycemia, diabetic, glucose-intolerant, and nondiabetic subjects were fed mixed meals. The meal contained both [2-3H]glucose (an isotope that is extensively detritiated during hepatic glucose cycling) and [6-3H]glucose (an isotope that is not detritiated during hepatic glucose cycling). Of the 50 g of carbohydrate contained in the meal, approximately 4-8 g underwent hepatic glucose cycling. Although total cycling of ingested glucose did not differ between diabetic, glucose-intolerant, and nondiabetic subjects (361 +/- 67 vs. 494 +/- 106 vs. 322 +/- 44 mumol.kg-1.5 h-1, respectively), the data suggested that hepatic cycling was increased in the diabetic and glucose-intolerant individuals but not in the nondiabetic subjects during the first 2 h after eating. Hepatic cycling during the first 2 h after eating was correlated with the prevailing glucagon concentration (r = 0.6, P less than 0.01) and increased (P less than 0.05) as hepatic glucose release increased. Hepatic glucose cycling had a marked effect on the measurement of so-called initial splanchnic glucose uptake. Nevertheless, however measured, initial splanchnic glucose uptake was not decreased and, if anything, was increased in diabetic and glucose-intolerant patients. Integrated postprandial hepatic glucose release increased (r less than 0.01) with the severity of fasting hyperglycemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Glucose↗

PubMed1992

Calibration in dogs of a subcutaneous miniaturized glucose sensor using a glucose meter for blood glucose determination.

The feasibility of calibrating a glucose sensor by using a wearable glucose meter for blood glucose determination and moderate variations of blood glucose concentration was assessed. Six miniaturized glucose sensors were implanted in the subcutaneous tissue of conscious dogs, and the parameters used for the in vivo calibration of the sensor (sensitivity coefficient and extrapolated current in the absence of glucose) were determined from values of blood glucose and sensor response obtained during glucose infusion. (1) Venous plasma glucose level and venous total blood glucose level were measured simultaneously on the same sample, using a Beckman analyser and a Glucometer II, respectively. The regression between plasma glucose (x) and whole blood glucose (y) was y = 1.12x-0.08 mM (n = 114 values, r = 0.96, p = 0.0001). The error grid analysis indicated that the use of a Glucometer II for blood glucose determination was appropriate in dogs. (2) The in vivo sensitivity coefficients were 0.57 +/- 0.11 nA mM-1 when determined from plasma glucose, and 0.51 +/- 0.07 nA mM-1 when determined from whole blood glucose (t = 1.53, p = 0.18, n.s.). The background currents were 0.88 +/- 0.57 nA when determined from plasma glucose, and 0.63 +/- 0.77 nA when determined from whole blood glucose (t = 0.82, p = 0.45, n.s.). (3) The regression equation of the estimation of the subcutaneous glucose level obtained from the two methods was y = 1.04x + 0.56 mM (n = 171 values, r = 0.98, p = 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

Glucose as regulator of glucose transport activity and glucose-transporter mRNA in hamster beta-cell line.

To investigate the role of glucose in regulating glucose transporters in pancreatic beta-cells, we studied the hamster clonal beta-cell line HIT-T15, which retains responsiveness to glucose. Northern blot analysis demonstrates that GLUT2 and GLUT1 mRNA are abundant in HIT cells. After a 24-h culture with various concentrations of glucose (0-22.2 mM [0-400 mg/dl]), the GLUT2 mRNA level in HIT cells increased by 40% at 22.2 mM (400 mg/dl) glucose compared with 11.1 mM (200 mg/dl) without a change in mRNA stability. It also decreased proportionally to the reduction of glucose concentration. Glucose deprivation resulted in a decrease of GLUT2 mRNA to an almost undetectable level, with a marked increase in the degradation rate of mRNA. In contrast, the GLUT1 mRNA was not affected by glucose. We show that glucose uptake is highest in HIT cells incubated at 2.8-5.5 mM (50-99 mg/dl) glucose for 24 h, and that levels in cells cultured at 0 mM (0 mg/dl) and 22.2 mM (400 mg/dl) glucose decrease to approximately 20% of the maximum level. This decrease is consistent with the effects of glucose on glucose-stimulated insulin secretion in HIT cells. Our results indicate that glucose is involved in regulating GLUT2 mRNA and glucose uptake activity and that the glucose responsiveness of the insulin secretion correlates with the glucose-induced change in glucose uptake activity in HIT cells.

Animals↗

PubMed1991

Normalization of blood glucose in diabetic rats with phlorizin treatment reverses insulin-resistant glucose transport in adipose cells without restoring glucose transporter gene expression.

Evidence is emerging for a direct role of glucose, independent of changes in insulin, in the regulation of cellular glucose transport and glucose utilization in vivo. In this study we investigate potential cellular and molecular mechanisms for this regulatory effect of glucose by determining how normalization of glycemia without insulin therapy in diabetic rats influences 3-O-methylglucose transport and the expression and translocation of two genetically distinct species of glucose transporters (GTs) in adipose cells. These results are compared with alterations in glucose disposal in vivo measured by euglycemic clamp. In rats rendered diabetic by 90% pancreatectomy, insulin-stimulated glucose transport in adipose cells is decreased 50% in parallel with reduced insulin-mediated glucose disposal in vivo. Levels of adipose/muscle GTs measured by immunoblotting are decreased in adipose cell subcellular membrane fractions, as are the corresponding mRNA levels assessed by Northern blotting of total adipose cell RNA. Normalization of blood glucose in diabetic rats with phlorizin, which impairs renal tubular glucose reabsorption and thus enhances glucose excretion, restores insulin-stimulated glucose transport in adipose cells and insulin-mediated glucose disposal in vivo. Importantly, levels of the adipose/muscle GT protein remain 43% reduced in the low-density microsomes in the basal state and 46% reduced in the plasma membranes in the insulin-stimulated state. Adipose/muscle GT mRNA levels remain approximately 50% depressed. Levels of the HepG2/brain GT protein and mRNA are unaltered by diabetes or phlorizin treatment. Thus, changes in ambient glucose independent of changes in ambient insulin can regulate the glucose transport response to insulin in isolated adipose cells and changes in responsiveness parallel alterations in glucose uptake in vivo. Since this effect can occur without alteration in the expression of the two species of glucose transporters present in adipose cells or in their translocation to the plasma membrane in response to insulin, it may result from changes in GT functional activity.

Adipose Tissue↗

PubMed1992

Assessment of glucose turnover rates in euglycaemic clamp studies using primed-constant [3-3H]-glucose infusion and labelled or unlabelled glucose infusates.

Underestimation of glucose turnover rates has been a problem in clamp studies using primed-constant [3-3H]-glucose infusion technique. Due to slow mixing in interstitial compartments concealed specific activity gradients may arise between plasma and interstitial compartments during intravenous unlabelled glucose infusion. Such specific activity gradients, however, can be prevented if plasma specific activity is maintained constant. Two euglycaemic clamp studies (insulin infusion 40 mU m-2 min-1) were performed in six lean normal subjects. Using conventional unlabelled glucose infusates plasma specific activity declined by 74%, tracer determined glucose appearance was smaller than actual glucose infusion rates (317 +/- 11 vs 366 +/- 15 mg m-2 min-1, p < 0.001), and erroneous negative values were calculated for glucose production (- 49 +/- 7 mg m-2 min-1). Average underestimation during the first 2 h correlated with glucose infusion rates (r = 0.88, p < 0.02). In contrast, when plasma specific activity was maintained constant, using appropriately labelled glucose infusates, tracer determined glucose appearance and glucose infusion rates were similar (385 +/- 16 vs 385 +/- 17 mg m-2 min-1), and negative errors for glucose production were avoided. In conclusion, using unlabelled glucose infusates, as in previous studies, suppression of glucose production is overestimated and stimulation of glucose utilization is underestimated. As errors were greater with larger glucose infusions, the mistakes may have been greatest in insulin sensitive control subjects, and smaller in insulin resistant subjects. Therefore, re-evaluation of hepatic insulin sensitivity seems appropriate in diabetes, obesity, and other insulin resistant states.

Adult↗

PubMed1991

Glucose regulates both glucose transport and the glucose transporter gene expression in a hamster-derived pancreatic beta-cell line (HIT).

We studied the effect of chronic exposure to high glucose on the glucose transport regulation in hamster pancreatic Beta cells in permanent culture (HIT). Cells were exposed to either 5.5 mmol/l or 16.7 mmol/l glucose for 48 h and then glucose transport was studied by measuring the (3H)-2-deoxyglucose uptake for 5 and 10 min at 37 degrees C. The 2-deoxyglucose uptake was lower in cells pre-exposed to glucose 16.7 mmol/l for 48 h compared to cells pre-exposed to 5.5 (12.0 +/- 1.6 vs 19.1 +/- 1.2 nmol/0.1 mg after 5 min, and 22.2 +/- 2.6 vs 39.0 +/- 2.9 after 10 min respectively, mean +/- SEM, n = 5, p less than 0.01). In order to investigate the mechanism(s) for glucose impairment of glucose transport, we studied the glucose carrier gene expression in the same cells by Northern and slot-blot analysis. When total RNA was extracted from HIT cells cultured at either 5.5 or 16.7 mmol/l glucose and then hybridized to 32P-labelled cDNA probes for the glucose transporter 1, the glucose transporter 2 and beta-actin, a significant reduction of both glucose transporter 1 (-63.9 +/- 4.1%, mean +/- SEM, n = 3) and glucose transporter 2 (-48.9 +/- 3.2%) mRNA was observed in HIT cells cultured with high glucose. In the same experiments no change of beta-actin mRNA was observed, suggesting that the effect of high glucose was specific on the glucose-transporter mRNAs.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1979

Metabolism of glucose in hyper- and hypo-thyroid rats in vivo. Glucose-turnover values and futile-cycle activities obtained with 14C- and 3H-labelled glucose.

1. A trace amount of glucose labelled with 14C uniformly and with 3H at position 2, 3 or 6 was injected intravenously into starved rats to measure the turnover rate of blood glucose. 2. Reliable estimates were made based on the semilogarithmic plot of specific radioactivity of the glucose contained in whole blood samples taken from the tail vein. 3. Glucose turned over more rapidly in hyperthyroid and more slowly in hypothyroid than in euthyroid rats. The percentage contribution of glucose recycling (determined from the difference in replacement rates between [U-14C]glucose and [6-3H]glucose) to the glucose utilization increased on induction of hyperthyroidism. 4. Futile cycles between glucose and glucose 6-phosphate (determined from the difference between replacement rates of [2-3H]glucose and [6-3H]glucose) were activated and inactivated by induction of hyperthyroid and hypothyroid states respectively. 5. The hepatic content of glycogen was much lower in hyper- and hypo-thyroid than in euthyroid rats. The enhanced glucose production in hyperthyroid rats resulted from not only activationof hepatic gluconeogenesis but also diversion of the final product of gluconeogenesis from liver glycogen to blood glucose. In hypothyroidism, the inhibition of gluconeogensis led to suppression of both glucose production and glycogenesis in the liver.

Animals↗

PubMed1992

Dissociated effects of 2-deoxy-D-glucose on D-[2-3H]glucose and D-[5-3H]glucose conversion into 3HOH in rat erythrocytes.

When rat erythrocytes were preincubated with 2-deoxy-D-glucose, the generation of both 3H-labelled acidic metabolites and 3HOH from D-[5-3H]glucose, the total production of L-lactate, and the generation of 14CO2, 14C-labelled acidic metabolites and 14C-labelled lactate from D-[1-14C]glucose or D-[U-14C]glucose were all lower than in erythrocytes preincubated in the absence of a hexose or in the presence of 3-O-methyl-D-glucose. However, preincubation with 2-deoxy-D-glucose failed to decrease the generation of 3H-labelled acidic metabolites and L-[3-3H]lactate from D-[2-3H]glucose, while decreasing the production of 3HOH more severely from D-[2-3H]glucose than from D-[5-3H]glucose. This may be attributable not solely to inhibition of D-glucose phosphorylation by 2-deoxy-D-glucose and 2-deoxy-D-glucose 6-phosphate, but also to inhibition by 2-deoxy-D-glucose 6-phosphate of hexose 6-phosphate interconversion in the reaction catalysed by phosphoglucoisomerase, as also observed with the purified enzyme. The generation of 3HOH from D-[2-3H]glucose should therefore be considered as a tool to assess the efficiency of interconversion of hexose 6-phosphates in the reaction catalysed by phosphoglucoisomerase, rather than to estimate D-glucose phosphorylation rate.

Animals↗

PubMed1990

Association of fasting glucose levels with a delayed secretion of insulin after oral glucose in subjects with glucose intolerance.

Two hundred and nineteen second generation Japanese-American men were classified with a 75-g oral glucose tolerance test: 77 with normal glucose tolerance, 74 with impaired glucose tolerance (IGT), and 68 with noninsulin-dependent diabetes mellitus (NIDDM). The peak insulin response to the oral glucose load was progressively delayed with each of the 3 glucose tolerance categories. A similar finding was observed with the peak C-peptide response to oral glucose, except for the absence of distinction between IGT and NIDDM. Variables measuring the initial rate of insulin or C-peptide secretion (0-30 min) after oral glucose also demonstrated a progressive diminution with increasing glucose intolerance. The relative incremental insulin response at 30 min and the relative incremental C-peptide response at 30 min were highly correlated with the fasting glucose levels (r = -0.61 and r = -0.62; P less than 0.0001, respectively). Variables measuring the 0-30 min secretory response had high variances, whereas the variance for fasting glucose was low. Twelve men who were initially classified as IGT subsequently developed NIDDM. These 12 men had significantly higher fasting glucose levels at baseline than the remaining men who did not develop diabetes, but the 30 min secretory parameters after oral glucose, although lower in those who subsequently developed diabetes, were not significantly different at baseline. However, if fasting glucose is used as a surrogate measure of secretory response, these 12 men appear to have had an impairment of oral glucose-stimulated insulin secretion antedating the development of NIDDM. The inability of the secretory parameters to detect the abnormality may be due to a type II statistical error, which may be resolved by a larger sample size.

Asian↗

PubMed1979

Glucose requirements following burn injury. Parameters of optimal glucose infusion and possible hepatic and respiratory abnormalities following excessive glucose intake.

Glucose and leucine metabolism in 18 severely burned patients were studied using the primed constant infusion of U-13C-glucose and 1-13C-leucine, respectively. The leucine data were used to calculate rates of whole-body protein synthesis. In four additional burn patients and seven normal controls, the effects of exogenously infused insulin on the metabolism of infused glucose were evaluated. Also, the effect on leucine metabolism of adding insulin to infused glucose was tested and rates of protein synthesis were calculated. The protein studies were divided into two groups depending on the rate of glucose infusion. Protein synthesis was 4.3 + 0.54 g protein/kg/day during the lower infusion rates (1.4--4.5 mg/kg/min) and 5.17 + 0.19 g protein/kg/day during the higher infusion rates (4.7--9.3 mg/kg/min) (statistically different, p less than 0.05). However, when the high infusion rate group was divided into two subgroups (high, 4.7--6.8 mg/kg/min, and very high, 7.03--9.31 mg/kg/min), there was no difference in the rate of protein synthesis. When U-13C-glucose was infused during varying rates of unlabeled glucose infusion, we found that the per cent of CO2 coming from the direct oxidation of glucose rose rapidly at the lower infusion rates but reached a plateau at approximately 55% as the infusion rates exceeded 5 mg/kg/min. Addition of insulin did not affect the rate of glucose oxidation but did seem to exert a stimulatory effect on protein synthesis. It was concluded that there appears to be a maximal rate of glucose infusion, beyond which physiologically significant increases in protein synthesis and direct oxidation of glucose cannot be expected. Furthermore, there appears to be a physiological cost of exceeding the optimal glucose infusion rate, as indicated by increased rates of CO2 production during infusion as well as large fat deposits in the liver at autopsy in patients infused with large amounts of glucose.

Adolescent↗

PubMed1991

Abnormal sensitivity to glucose of human islets cultured in a high glucose medium: partial reversibility after an additional culture in a normal glucose medium.

In the experimental animal chronic hyperglycemia alters the islet's sensitivity to glucose. In the present study the glucose sensitivity of human pancreatic islets, isolated and purified, obtained from seven human pancreases using an automated method was evaluated. After a 12-h stabilization period, islets were cultured for 48 h in normal (5.5 mmol/L) or high glucose (16.7 mmol/L) medium. Islets were then perifused to study their insulin response to glucose. Islets cultured in the high glucose medium lost glucose-induced insulin release and, when challenged with an acute fall of glucose concentration in the perifusate, showed a paradoxical insulin release. Insulin release in response to 10 mmol/L L-arginine was preserved in these islets, suggesting a selective reduction of the insulin response to glucose. An additional 48-h culture in 5.5 mmol/L glucose medium partially restored the sensitivity to glucose of the previously unresponsive islets. These findings indicate that short term exposure to high glucose concentrations induces a selective glucose insensitivity of human islets, which can be partially reversed by an additional culture in normal glucose medium.

Arginine↗

PubMed1978

The effect of urinary glucose excretion on the plasma glucose clearances and plasma insulin responses to intravenous glucose loads in unanaesthesized dogs.

The effect of urinary glucose excretion on the plasma glucose clearance and insulin response to varying sizes of glucose loads was studied in normal unanaesthesized dogs. Glucose loads ranging from 0.15 to 1.25 g/kg b.w. were infused intravenously in a standard time period of 30 seconds. Plasma glucose and plasma immunoreactive insulin (IRI) concentrations were determined during one-hour after infusion. All urine excreted during the one-hour was collected by a catheterization and bladder wash-out procedure. The urinary glucose excretion was expressed as the percent of the glucose load. The urinary glucose excretion varied directly with the size of the glucose load and ranged from minimal to 12%. This would indicate that urinary losses play a considerable role proportionate to the degree of hyperglycaemia above the renal threshold. Thus, urinary loss of glucose must be recognized as an important factor infuencing the plasma glucose clearance and hence the plasma IRI response. A glucose load of 0.5 g/kg b.w. given in 30 seconds with the k-value calculated between 15-45 min would minimize the influence of urinary loss and provide more accurate plasma clearance values.

Animals↗

PubMed1979

Effects of insulin on glucose metabolism and glucose transport in fat cells of hormone-treated hypophysectomized rats: evidence that growth hormone restricts glucose transport.

In earlier studies we have shown that insulin does not stimulate glucose incorporation in adipocytes of hypophysectomized (hypox) rats. Basal glucose incorporation is decreased, although basal 3-O-methylglycose transport is very rapid and cannot be further stimulated by insulin. In this study we treated hypox rats with human GH, ACTH, and T3, alone or in combination, and examined the effects of insulin on glucose incorporation into fat cells and on 3-O-methylglucose transport. The results show that chronic administration of T3 alone to hypox rats partially restores glucose incorporation into fat cells and, in combination with ACTH, completely restores this incorporation. The two hormones have no effect on the glucose carrier system. The transport rate under T3 and ACTH replacement therapy continues to proceed at a maximal rate, so that basal glucose incorporation is high but not further enhanced by insulin. In contrast, administration of human GH to hypox rats does not influence glucose incorporation but has a marked effect on glucose transport. The basal glucose transport rate returns toward normal and again responds to insulin. This suggests 1) that enzyme activities responsible for the lipogenetic capacity of the fat cell are decreased in hypox rats and returned toward normal by the combined T3/ACTH treatment, and 2) that the limitation of glucose transport in the fat cell is controlled by GH. GH seems to induce a change of the glucose-carrier system; it leads to a restriction of glucose transport, which is acutely modulated by insulin.

Adipose Tissue↗