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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↗
PubMed1982

Abnormal oral glucose tolerance and glucose malabsorption after vagotomy and pyloroplasty. A tracer method for measuring glucose absorption rates.

The mechanisms underlying the abnormal glucose tolerance in patients who had undergone vagotomy and pyloroplasty were investigated by measuring the rates of absorption of ingested glucose and the clearance rate of glucose using tracer methods. These methods are based on labeling a 100-g oral glucose load with [1-14C]glucose and measuring glucose clearance using plasma levels of infused [3-3H]glucose. The rate of appearance of both ingested and total glucose is then calculated continuously using a two-compartment model of glucose kinetics. It was found that about 30% of the ingested glucose (100 g) failed to appear in the systemic circulation. That this was due to malabsorption was confirmed using breath-hydrogen analysis. The absorption period is short (101 +/- 11 min) compared with normal values but the clearance of glucose is identical to that in control subjects, and it peaks 132 +/- 7 min after glucose loading. The peak plasma insulin values were more than four times higher in patients than in normal subjects, and this may afford an explanation of rates of glucose clearance that are inappropriate for the short absorption period. The combination of glucose malabsorption and this clearance pattern could yield the hypoglycemia that may be observed in patients after gastric surgery.

Blood Glucose↗
PubMedDate not supplied

Inference of blood glucose concentrations from subcutaneous glucose concentrations: applications to glucose biosensors.

An approach for inference of blood glucose concentrations in real time is considered. First, a model that predicts the subcutaneous glucose concentration from the blood glucose concentration is presented. The model includes diffusive transport from the blood to the subcutaneous tissue and reactive-like cellular uptake of glucose. Next, the Phillips-Tikhonov regularization method is considered to solve the real-time input estimation problem that determines the blood glucose concentration given the subcutaneous glucose concentration. The inverse problem is regularized by imposing a smoothing condition to obtain a stable solution. Three different penalization functionals were considered in evaluating the regularization method using a synthetic function that approximates the subcutaneous glucose response to an oral glucose tolerance test in a human subject. Various levels of either white noise or time-correlated noise were superimposed onto the synthetic response to evaluate the sensitivity of the inverse to measurement error. For inversion assuming only diffusive transport, the optimal time interval of integration of previous subcutaneous measurements was found to be about 1.5/alpha, where alpha(-1) is the dominant time constant for the exchange of glucose between the blood and subcutaneous tissue. The optimal sampling rate was found to be 54alpha. Linear regularizations based on minimization of first or second derivatives of the blood glucose concentration were found to be satisfactory, each yielding a minimum error that was about 50% greater than the measurement error. Including nonlinear, reactive-like uptake of glucose was found to decrease the error magnification factor slightly. Both the model and the inverse method relating blood and subcutaneous glucose concentrations are successfully applied to experimental measurements using glucose biosensors reported by Schmidtke et al. (Proc. Natl. Acad. Sci. USA 95:294-299, 1998).

Algorithms↗
PubMed2006

Reduction of renal transport maximum for glucose by inhibition of NA(+)-glucose cotransporter suppresses blood glucose elevation in dogs.

T-1095, an orally active inhibitor of Na(+)-glucose cotransporter (SGLT), excretes excess plasma glucose into urine, lowers blood glucose levels, and thus has therapeutic potential for treatment of diabetes mellitus. To elucidate the correlation between threshold for renal glucose reabsorption and blood glucose levels, we evaluated the effects of T-1095 on transport maximum for glucose (TmG) in dogs. Intravenous infusion of T-1095A (0.25-2.0 microg/kg/min), an active metabolite of T-1095, dose-dependently increased fractional glucose excretion induced by a hyper-amount of glucose infusion in anesthetized dogs. Calculated TmG was decreased by T-1095A in a dose dependent manner, and plasma concentration of T-1095A correlated well with the reduction of TmG (R2=0.704). Then, oral glucose tolerance tests (OGTT) were carried out in dogs. T-1095 at a dose of 3 mg/kg (p.o.) slightly increased urinary glucose excretion without affecting blood glucose levels. Ten mg/kg (p.o.) of T-1095 suppressed the elevation of blood glucose levels by excreting a large quantity urinary glucose. The estimated TmG reduction by 3 and 10 mg/kg of T-1095 was about 50% and more than 80%, respectively. In conclusion, this study clarified that more than 80% reduction of TmG by inhibition of SGLT was necessary for suppressing postprandial hyperglycemia in normoglycemic dogs.

Animals↗
PubMed1998

Intracellular glucose concentration in derepressed yeast cells consuming glucose is high enough to reduce the glucose transport rate by 50%.

In Saccharomyces cerevisiae cells exhibiting high-affinity glucose transport, the glucose consumption rate at extracellular concentrations above 10 mM was only half of the zero trans-influx rate. To determine if this regulation of glucose transport might be a consequence of intracellular free glucose we developed a new method to measure intracellular glucose concentrations in cells metabolizing glucose, which compares glucose stereoisomers to correct for adhering glucose. The intracellular glucose concentration was 1.5 mM, much higher than in most earlier reports. We show that for the simplest model of a glucose carrier, this concentration is sufficient to reduce the glucose influx by 50%. We conclude that intracellular glucose is the most likely candidate for the observed regulation of glucose import and hence glycolysis. We discuss the possibility that intracellular glucose functions as a primary signal molecule in these cells.

Biological Transport↗
PubMed1989

Isotopic estimation of plasma glucose conversion to plasma lactate using [6-3H]glucose and [6-14C]glucose.

To determine whether [6-3H]glucose could be used to quantitatively estimate the rate of plasma glucose conversion to plasma lactate, we compared the relative transfer of [3H] and [14C]plasma glucose to plasma lactate in nine postabsorptive anesthetized rats infused to isotopic steady state with [6-3H]glucose and [6-14C]glucose. Glucose turnover (mumol/kg/min) measured with [6-3H]glucose (29.4 +/- 1.7) and [6-14C]glucose (25.0 +/- 1.5), Cori cycle activity (4.35 +/- 0.79), and the percentage of plasma lactate derived from plasma glucose calculated from 14C-specific activities (59.8 +/- 5.8) were all comparable to previously reported values for the overnight fasted rat. Although the percentage of plasma lactate derived from plasma glucose calculated from 3H-specific activities (30.0 +/- 3.3) was only half that calculated from 14C-specific activities (P less than 0.001), the 3H:14C ratios were constant over a wide range of percentage of lactate derived from glucose (r = 0.95, P less than 0.001). We conclude that 3H-specific activity ratios of plasma lactate to plasma glucose cannot be directly used as a quantitative estimate of the percentage of plasma lactate derived from plasma glucose; however, correction for the apparent constant proportionality of detritiation of lactate relative to 14C loss could permit use of [6-3H]glucose for this purpose.

Animals↗
PubMed1997

Glucose metabolism in severe malaria: minimal model analysis of the intravenous glucose tolerance test incorporating a stable glucose label.

Basal plasma glucose is usually increased in uncomplicated malaria, implying insulin resistance. If the infection progresses, the risk of hypoglycemia will increase as host glucose production becomes insufficient for host/parasite demand. To assess the relative contribution of insulin-mediated and non-insulin-mediated glucose disposal to plasma glucose levels in severe malaria, we studied six healthy controls (two males and four females; mean age, 38 years) and eight patients with complicated falciparum malaria (five males and three females; mean age, 31 years) who had a frequently sampled intravenous glucose tolerance test (FSIVGTT) in which 10% of the dextrose bolus was 6,6-D2-glucose. The minimal model was applied to native and labeled plasma glucose and serum insulin profiles over 4 hours postinjection. Basal plasma glucose concentrations in the patients were significantly greater than in the controls (median [range], 6.1 [2.1 to 8.5] v 4.3 [3.9 to 4.7] mmol/L, P = .03). Malaria-associated insulin resistance was confirmed by a lower insulin sensitivity index (SI) in patients (5.6 [2.4 to 17.4] v 16.0 [2.5 to 22.3] x 10(-4).min-1 per microU/mL in controls, P = .026). Glucose effectiveness ([SG] the ability of glucose to reduce its own plasma concentration) was higher in the patients (0.015 [0.006 to 0.024] v 0.008 [0.007 to 0.010] min-1 in controls, p = .019). Glucose disappearance at basal concentration was increased by a median of 42% in severe malaria patients, with the insulin-independent component comprising 81%, versus 67% in controls. Indices of beta-cell function were normal in malaria patients. These data demonstrate that basal plasma glucose utilization is increased approximately 50% in severe malaria, consistent with previously published isotope-turnover studies. Altered SG plays a major role. Prevention and treatment of early hypoglycemia should be based on adequate glucose replacement. Strategies that reduce insulin secretion or effects appear to be of minor importance.

Adolescent↗
PubMed2006

Assessing 1-h plasma glucose and shape of the glucose curve during oral glucose tolerance test.

OBJECTIVE: To assess the cutoff values at different time points for impaired glucose regulation (IGR) and diabetes, the glucose curve and isolated 1-h hyperglycemia were monitored during an oral glucose tolerance test (OGTT). METHODS: Two thousand eight hundred and eighty-six subjects (1300 men and 1586 women) were recruited to have an OGTT. Plasma was collected at 0, 30, 60, 120, and 180 min to analyze glucose and insulin. The diagnosis of impaired fasting glucose, impaired glucose tolerance, and diabetes was based on World Health Organization and American Diabetes Association's criteria. Those with fasting plasma glucose (FPG) < 5.6 and 2-h plasma glucose (PG) < 7.8, but 1-h PG > or = 7.8 and < 11.1 mmol/l were defined as 1h-High7.8, and those with FPG < 7.0 and 2-h PG < 11.1, but 1-h PG > or =11.1 mmol/l as 1h-High11.1. The cutoff values were calculated by receiver operating characteristic (ROC) curve. The correlation between beta-cell function and the area under the curve of glucose (AUCg) and the shape index was analyzed with linear regression. RESULTS: The cutoff values for IGR were 5.6, 9.7, 10.1, 7.8 and 6.1 mmol/l for blood glucose at 0, 30, 60, 120 and 180 min, 24 for AUCg and 1.3 mmol/l for the shape index. The cutoff values for diabetes were 6.8, 11.2, 13, 11.1 and 7 mmol/l for 0, 30, 60, 120 and 180 min, 30.9 for AUCg and 2 mmol/l for the shape index. Both AUCg and the shape index were inversely related to beta-cell function. The profiles of glucose and insulin in the subgroup with isolated 1-h hyperglycemia were very different from those seen in subjects with normal glucose tolerance or IGR. CONCLUSIONS: The present study provides new information on measures other than the fasting and 2-h PG to evaluate glucose metabolism in vivo and stimulates further research aimed at assessing the value of the OGTT 1-h PG concentration prospectively.

Adult↗
PubMed1980

Metabolism of Specifically Labeled Glucose, Glucose 1-Phosphate, and Glucose 6-Phosphate via the Oxidative Pentose Phosphate Cycle in a Reconstituted Spinach Chloroplast System in Darkness and in the Light.

Using isolated spinach (hybrid 424) chloroplasts deprived of their envelopes (reconstituted chloroplast system), the metabolism of glucose, glucose 1-phosphate, and glucose 6-phosphate via the oxidative pentose phosphate cycle was analyzed. The activity of oxidative pentose phosphate cycle was monitored by continuous sampling of the CO(2) released during the decarboxylation process of 6-phosphogluconate.The rate of CO(2) released in the dark from [C-1-(14)C]glucose 6-phosphate was 4 to 6 micromoles per milligram chlorophyll per hour. A CO(2) release from the C-6 position of [C-6-(14)C]glucose 6-phosphate was hardly measurable within 60 minutes of incubation. Glucose 1-phosphate was readily converted to glucose 6-phosphate without externally added glucose bisphosphate and was metabolized via the oxidative pentose phosphate cycle. The phosphorylation of glucose to glucose 6-phosphate was mediated by hexokinase present in the reconstituted system. This step was rate-limiting for the over-all reaction of the oxidative pentose phosphate cycle with glucose being the substrate (0.5 micromoles per milligram chlorophyll per hour). Addition of hexokinase increased the rate of CO(2) release to 5 micromoles per milligram chlorophyll per hour.The flow of carbon through the oxidative pentose phosphate cycle was greatly reduced upon the addition of NADPH and ATP. Whereas NADPH inhibited the metabolism of [C-1-(14)C]glucose 6-phosphate via the oxidative pentose phosphate cycle, ATP stimulated carbon flow into the 3-phosphoglycerate, dihydroxyacetone phosphate, and bisphosphates pools via the glycolytic pathway mediated by phosphofructokinase. This regulatory phenomenon could also be demonstrated with the reconstituted system undergoing a dark-light-dark transition. Data are presented indicating the conditions under which glucose 6-phosphate or glucose 1-phosphate are metabolized via the oxidative pentose phosphate cycle and the glycolytic pathway.

Journal Article↗
PubMed2000

Portal glucose infusion in the mouse induces hypoglycemia: evidence that the hepatoportal glucose sensor stimulates glucose utilization.

To analyze the role of the murine hepatoportal glucose sensor in the control of whole-body glucose metabolism, we infused glucose at a rate corresponding to the endogenous glucose production rate through the portal vein of conscious mice (Po-mice) that were fasted for 6 h. Mice infused with glucose at the same rate through the femoral vein (Fe-mice) and mice infused with a saline solution (Sal-mice) were used as controls. In Po-mice, hypoglycemia progressively developed until glucose levels dropped to a nadir of 2.3 +/- 0.1 mmol/l, whereas in Fe-mice, glycemia rapidly and transiently developed, and glucose levels increased to 7.7 +/- 0.6 mmol/l before progressively returning to fasting glycemic levels. Plasma insulin levels were similar in both Po- and Fe-mice during and at the end of the infusion periods (21.2 +/- 2.2 vs. 25.7 +/- 0.9 microU/ml, respectively, at 180 min of infusion). The whole-body glucose turnover rate was significantly higher in Po-mice than in Fe-mice (45.9 +/- 3.8 vs. 37.7 +/- 2.0 mg x kg(-1) x min)-1), respectively) and in Sal-mice (24.4 +/- 1.8 mg x kg(-1) x min(-1)). Somatostatin co-infusion with glucose in Po-mice prevented hypoglycemia without modifying the plasma insulin profile. Finally, tissue glucose clearance, which was determined after injecting 14C-2-deoxyglucose, increased to a higher level in Po-mice versus Fe-mice in the heart, brown adipose tissue, and the soleus muscle. Our data show that stimulation of the hepatoportal glucose sensor induced hypoglycemia and increased glucose utilization by a combination of insulin-dependent and insulin-independent or -sensitizing mechanisms. Furthermore, activation of the glucose sensor and/or transmission of its signal to target tissues can be blocked by somatostatin.

Animals↗
PubMed1995

Interleukin-3 facilitates glucose transport in a myeloid cell line by regulating the affinity of the glucose transporter for glucose: involvement of protein phosphorylation in transporter activation.

Growth factors promote cell survival and proliferation by activating signal transduction pathways that result in progression through the cell cycle and differential gene expression. Uptake of simple sugars needed for basal cell metabolism, and for macromolecular synthesis necessary for cell growth and proliferation, is thought to follow as a consequence of signal transduction to the nucleus. However, in the presence of inhibitors of DNA synthesis and respiration, growth factors can still promote cell survival responses in the short term, raising the possibility that they may also regulate critical membrane and cytosolic processes necessary for cell survival. We have tested this hypothesis directly by investigating the role of the haemopoietic growth factor, interleukin-3 (IL-3), in the regulation of glucose transport in the bone marrow-derived cell line, 32D. We show that IL-3 promotes glucose transport by actively maintaining the affinity of the plasma membrane, glucose transporter for glucose (Km 1.35 +/- 0.15 mM, n = 4). Withdrawal of IL-3 for 1 h resulted in reduced affinity for glucose (Km 2.96 +/- 0.28 mM, n = 4) without an associated change in Vmax. Furthermore, glucose transporter molecules as the cell surface, as determined by cytochalasin B binding to isolated plasma membranes, did not differ significantly between control and IL-3-treated cells. Inhibition of DNA synthesis with mitomycin C or with the respiratory poison, sodium azide, did not affect the ability of IL-3 to promote glucose transport. In contrast, the tyrosine kinase inhibitors genistein and erbstatin extensively inhibited control and IL-3-stimulated glucose transport, some preference of IL-3-stimulated glucose transport, some preference for IL-3-stimulated responses being observed at low inhibitor concentrations. The light-activated protein kinase C inhibitor, calphostin C, also inhibited control and IL-3-stimulated glucose transport but without preference for IL-3 responses. Additionally, the tyrosine phosphatase inhibitor, orthovanadate, stimulated control and IL-3-dependent glucose transport by 50-80% while the protein kinase A inhibitor, KT5720, inhibited glucose transport by about 20% at plateau values. These results indicate that IL-3 is involved in continuous maintenance of glucose transporter activity by a mechanism that involves tyrosine kinases and protein kinase C, and demonstrate that this activation is not dependent on respiration or signal transduction to the nucleus.

Animals↗
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↗
PubMed2003

Elevated free fatty acids impair glucose metabolism in women: decreased stimulation of muscle glucose uptake and suppression of splanchnic glucose production during combined hyperinsulinemia and hyperglycemia.

The present study sought to determine whether elevated plasma free fatty acids (FFAs) alter the splanchnic and muscle glucose metabolism in women. To do so, FFAs were increased in seven women by an 8-h Intralipid/heparin (IL/hep) infusion, and the results were compared with those observed in nine women who were infused with glycerol alone. Glucose was clamped at approximately 8.3 mmol/l and insulin was increased to approximately 300 pmol/l to stimulate both muscle and hepatic glucose uptake. Insulin secretion was inhibited with somatostatin. Leg and splanchnic glucose metabolism were assessed using a combined catheter and tracer dilution approach. The glucose infusion rates required to maintain target plasma glucose concentrations were lower (P < 0.01) during IL/hep than glycerol infusion (30.8 +/- 2.6 vs. 65.0 +/- 7.9 micro mol. kg(-1). min(-1)). Whole-body glucose disappearance (37.0 +/- 2.2 vs. 70.9 +/- 8.7 micro mol. kg(-1). min(-1); P < 0.001) and leg glucose uptake (24.3 +/- 4.2 vs. 59.6 +/- 10.0 micro mol. kg fat-free mass of the leg(-1). min(-1); P < 0.02) were also lower, whereas splanchnic glucose production (8.2 +/- 0.8 vs. 4.3 +/- 0.7 micro mol. kg(-1). min(-1); P < 0.01) was higher during IL/hep than glycerol infusion. We conclude that in the presence of combined hyperinsulinemia and hyperglycemia, elevated FFAs impair glucose metabolism in women by inhibiting whole- body glucose disposal, muscle glucose uptake, and suppression of splanchnic glucose production.

Adult↗
PubMed1994

Development of a miniaturized glucose monitoring system by combining a needle-type glucose sensor with microdialysis sampling method. Long-term subcutaneous tissue glucose monitoring in ambulatory diabetic patients.

OBJECTIVE: To develop a reliable and practical glucose monitoring system by combining a needle-type glucose sensor with a microdialysis sampling technique for long-term subcutaneous tissue glucose measurements. RESEARCH DESIGN AND METHODS: A microdialysis Cuprophan hollow-fiber probe (inner diameter, 0.20 mm; length, 15 mm) was perfused with isotonic saline solution (120 microliters/h) and glucose concentrations in the dialysate were measured by a needle-type glucose sensor extracorporeally. This system was tested both in vitro and in vivo. Subcutaneous tissue glucose concentrations were then monitored continuously in 5 healthy and 8 diabetic volunteers for 7 to 8 days. A hollow-fiber probe was inserted into the abdominal subcutaneous tissue. RESULTS: This monitoring system achieved excellent results in vitro. Subcutaneous tissue glucose concentrations were measured in a wide range from 1.7 to > 27.8 mM glucose, with a time delay of 6.9 +/- 1.2 min associated with a rise in glucose and 8.8 +/- 1.6 min with a fall in the glucose level (means +/- SE). The overall correlation between subcutaneous tissue (Y) and blood (X) glucose concentration was Y = 1.08X + 0.19 (r = 0.99). The subcutaneous tissue glucose concentration could be monitored precisely for 4 days without any in vivo calibrations and for 7 days by introducing in vivo calibrations. CONCLUSIONS: Glycemic excursions could be monitored precisely in the subcutaneous tissue by this microdialysis sampling method with a needle-type glucose sensor in ambulatory diabetic patients.

Adult↗
PubMed1993

A glucose monitoring system for on line estimation in man of blood glucose concentration using a miniaturized glucose sensor implanted in the subcutaneous tissue and a wearable control unit.

We have developed a miniaturized glucose sensor which has been shown previously to function adequately when implanted in the subcutaneous tissue of rats and dogs. Following a glucose load, the sensor output increases, making it possible to calculate a sensitivity coefficient to glucose in vivo, and an extrapolated background current in the absence of glucose. These parameters are used for estimating at any time the apparent subcutaneous glucose concentration from the current. In the previous studies, this calibration was performed a posteriori, on the basis of the retrospective analysis of the changes in blood glucose and in the current generated by the sensor. However, for clinical application of the system, an on line estimation of glucose concentration would be necessary. Thus, this study was undertaken in order to assess the possibility of calibrating the sensor in real time, using a novel calibration procedure and a monitoring unit which was specifically designed for this purpose. This electronic device is able to measure, to filter and to store the current. During an oral glucose challenge, when a stable current is reached, it is possible to feed the unit with two different values of blood glucose and their corresponding times. The unit calculates the in vivo parameters, transforms every single value of current into an estimation of the glucose concentration, and then displays this estimation. In this study, 11 sensors were investigated of which two did not respond to glucose. In the other nine trials, the volunteers were asked to record every 30 s what appeared on the display during the secondary decrease in blood glucose.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2002

Diagnostic value of fasting capillary glucose, fructosamine and glycosylated haemoglobin in detecting diabetes and other glucose tolerance abnormalities compared to oral glucose tolerance test.

New diagnostic criteria for diabetes mellitus recommend lowering of the fasting plasma glucose to 7.0 mmol/l. In contrast to recommendations of the American Diabetes Association (ADA), WHO recommends using the oral glucose tolerance test (OGTT) in clinical practice. In this study. based on OGTT results and WHO 1998 criteria, we determined if measuring fasting capillary glycaemia (FCG) along with fructosamine and/or glycosylated haemoglobin allows the detection of glucose tolerance abnormalities better than FCG alone. OGTT was performed in 538 patients. Serum fructosamine was determined in 480 of the patients, and glycosylated haemoglobin in 234 of the patients. According to WHO 1998 criteria, the patients were divided into groups due to glucose tolerance abnormalities. Fructosamine correlated stronger with 2-h post-load glucose concentrations than with FCG. HbAlc correlated stronger with FCG than with 2-h post-load glucose. Combined use of fructosamine and FCG predicted 2-h post-load glucose better than combined use of FCG and HbA1c. Receiver operating characteristic curve analyses showed that FCG was the best criterion in discriminating diabetes. Combined use of FCG and fructosamine slightly improved the ability to discriminate glucose tolerance abnormalities from normal glucose tolerance. FCG is the most effective predictor of 2-h post-load glucose and the best criterion for discriminating diabetes and other glucose tolerance abnormalities from normal glucose tolerance. Fructosamine is a potentially useful post-load glycaemia index. OGTT is irreplaceable in identification of patients with high post-load glycaemia.

Biomarkers↗
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↗