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PubMed1999

Plasma and interstitial glucose dynamics after intravenous glucose injection: evaluation of the single-compartment glucose distribution assumption in the minimal models.

Recent experimental evidence suggests that estimates of glucose effectiveness (S(G)) from the minimal model of unlabeled glucose disappearance (Cold-MM) are in error. The single-compartment glucose distribution assumption embedded in the model has been indicated as a possible source of error. In this study, to directly examine the single-compartment assumption, we measured plasma and interstitial glucose concentrations after intravenous glucose injection. Additionally, we compared the accuracy of the estimates of glucose effectiveness from the Cold-MM and the single-compartment tracer minimal model (Hot-MM). Paired labeled intravenous glucose tolerance tests (IVGTTs) were performed in each of six C-peptide-negative type 1 diabetic subjects. Two different insulin infusion protocols were used: an infusion at constant basal rates and an infusion at variable rates to mimic a normal insulin response. During the labeled IVGTT with basal insulin infusion, the microperfusion technique was employed to sample adipose tissue interstitial fluid. Marked differences between the plasma and interstitial dynamics of (cold) glucose were observed during the first 22 min after glucose injection. These results suggest that the requirements for a single-compartment representation of glucose kinetics are not satisfied during at least the first 22 min of an IVGTT. Data from the labeled IVGTT with normal insulin response were used to identify the minimal-model parameters. The measure of S(G) derived using the Cold-MM was 3.44-fold higher than the direct measure obtained from the labeled IVGTT with basal insulin infusion (0.0179+/-0.0027 vs. 0.0052+/-0.0010 min(-1), P<0.01). The measure of glucose effectiveness (S(G)*) derived by the Hot-MM was 1.36-fold higher than the direct measure available from the labeled IVGTT with basal insulin infusion (0.0079+/-0.0013 vs. 0.0058+/-0.0004 min(-1), P>0.26). These results suggest that the Hot-MM is more appropriate for the evaluation of glucose effectiveness than the Cold-MM.

Adult↗
PubMed1989

Effects of porcine growth hormone on glucose metabolism of pigs: II. Glucose tolerance, peripheral tissue insulin sensitivity and glucose kinetics.

This study was conducted to determine whether the increase in serum glucose observed in pigs treated chronically with pGH is due to an increase in hepatic glucose output or to an impairment in glucose clearance. Barrows (n = 4 per treatment) were treated with pituitary derived pGH (ppGH), recombinant pGH analog (rpGH) or vehicle. Pigs were treated for 28 d by daily i.m. injections. Insulin tolerance and glucose tolerance tests (GTT) were performed on d 19 and 21, respectively, following treatment with pGH. Glucose turnover was quantified on d 28 using [6-3H]glucose. Chronically treating pigs with pGH resulted in a significant decrease (26%; P less than .05) in glucose clearance, as determined by the GTT. Glucose clearance was affected similarly by ppGH and rpGH. Intra-arterial glucose infusion markedly increased plasma insulin concentration in pGH-treated pigs. Peak plasma insulin response was 87% and 58%, respectively, higher (P less than .05) in ppGH- and rpGH-treated than in control pigs. Insulin infusion elicited a marked hypoglycemia in pigs; however, the extent and duration of hypoglycemia were significantly less in pGH-treated pigs (ppGH or rpGH). Glucose production rates were 23% higher (P = .085) in ppGH-treated than in control pigs. These results establish that the hyperglycemia induced by pGH is the result of an increase in hepatic glucose output and a concurrent impairment in glucose clearance.

Animals↗
PubMed2006

Sergliflozin, a novel selective inhibitor of low-affinity sodium glucose cotransporter (SGLT2), validates the critical role of SGLT2 in renal glucose reabsorption and modulates plasma glucose level.

The low-affinity sodium glucose cotransporter (SGLT2), which is expressed specifically in the kidney, plays a major role in renal glucose reabsorption in the proximal tubule. We have discovered sergliflozin, a prodrug of a novel selective SGLT2 inhibitor, based on benzylphenol glucoside. In structure, it belongs to a new category of SGLT2 inhibitors and its skeleton differs from that of phlorizin, a nonselective SGLT inhibitor. We investigated its pharmacological properties and potencies in vitro and in vivo. By examining a Chinese hamster ovary-K1 cell line stably expressing either human SGLT2 or human high-affinity sodium glucose cotransporter (SGLT1), we found sergliflozin-A (active form) to be a highly selective and potent inhibitor of human SGLT2. At pharmacological doses, sergliflozin, sergliflozin-A, and its aglycon had no effects on facilitative glucose transporter 1 activity, which was inhibited by phloretin (the aglycon of phlorizin). The transport maximum for glucose in the kidney was reduced by sergliflozin-A in normal rats. As a result of this effect, orally administered sergliflozin increased urinary glucose excretion in mice, rats, and dogs in a dose-dependent manner. In an oral glucose tolerance test in diabetic rats, sergliflozin exhibited glucose-lowering effects independently of insulin secretion. Any glucose excretion induced by sergliflozin did not affect normoglycemia or electrolyte balance. These data indicate that selective inhibition of SGLT2 increases urinary glucose excretion by inhibiting renal glucose reabsorption. As a representative of a new category of antidiabetic drugs, sergliflozin may provide a new and unique approach to the treatment of diabetes mellitus.

Absorption↗
PubMed2005

Comparison of [3,4-13C2]glucose to [6,6-2H2]glucose as a tracer for glucose turnover by nuclear magnetic resonance.

A recently introduced tracer, [3,4-(13)C(2)]glucose, was compared to the widely used tracer, [6,6-(2)H(2)]glucose, for measurement of whole-body glucose turnover. The rate of glucose production (GP) was measured in rats after primed infusions of [3,4-(13)C(2)]glucose, [6,6-(2)H(2)]glucose, or both tracers simultaneously followed by a constant infusion of tracer(s) over 90 min. Blood glucose was purified and converted into monoacetone glucose for analysis by (13)C NMR (for [3,4-(13)C(2)]glucose) or (1)H and (2)H NMR (for [6,6-(2)H(2)]glucose). The values of GP measured during infusion of each single tracer were not significantly different. In rats infused with both tracers simultaneously, GP was identical as reported by each tracer, 42 +/- 4 micromol/kg/min. Since (2)H and (13)C enrichment in glucose is typically much less than 2% for in vivo studies, [3,4-(13)C(2)]glucose does not interfere with measurements of (13)C or (2)H enrichment patterns and therefore is valuable when multiple metabolic pathways are being evaluated simultaneously.

Animals↗
PubMed1999

Estimation of the initial distribution volume of glucose by an incremental plasma glucose level at 3 min after i.v. glucose in humans.

AIMS: The initial distribution volume of glucose (IDVG) could be a clinically useful indicator of the central extracellular fluid (ECF) space volume, namely the interstitial fluid volume status of highly perfused organs. In this study, we determined the formula of IDVG using incremental plasma glucose levels after i.v. glucose. METHODS: One hundred and fifty patients admitted to the general intensive care unit of the University of Hirosaki hospital were entered into this prospective study which was conducted in two stages. In the first stage 300 data points from 100 patients were used to measure the IDVG (3 determinations for each patients). This utilized a one compartment model to describe the incremental plasma glucose decay curve following an intravenous bolus injection of glucose which, in turn, was used to derive the parameters of an equation for IDVG prediction following a single plasma sample. The second stage was a validation of the equation using a separate data set (150 points) from a further 50 patients. RESULTS: A one phase exponential decay model was well-fitted for the IDVG-postadministration glucose level curve, and indicated that the incremental glucose level at 3 min after i.v. glucose was best-correlated to the IDVG compared with those at 1, 2, 4, 5 and 7 min postadministration. The formula of the IDVG was obtained from the curve: IDVG=24.44xe-0.0298xDeltaGL+2.70, where DeltaGL=incremental glucose level at 3 min after i.v. glucose. Another 150 samples showed that the measured-IDVG from a one compartment model and predicted-IDVG from the formula were 7.24+/-1. 63 and 7.27+/-1.52 l, respectively, and that there was a significant correlation between the two IDVGs (r=0.966, P<0.0001). CONCLUSIONS: Using an incremental glucose level at 3 min after i.v. glucose, we have established the reliable formula for determination of the IDVG which could be a clinically useful indicator of the central ECF volume.

Blood Glucose↗
PubMed2002

Glucose desensitization in INS-1 cells: evidence of impaired function caused by glucose metabolite(s) rather than by the glucose molecule per se.

Type 2 diabetes characteristically involves disturbances of the beta-cell function including reduced insulin secretion in response to elevated glucose. In experimental diabetes, beta cells are often "blind" to glucose, and clonal beta-cell lines chronically exposed to glucose show impaired glucose sensing. The present study focuses on the effect of long-term exposure to high-glucose concentrations on insulin secretion, insulin store, and insulin mRNA content in the beta-cell line INS-1. The cellular insulin mRNA content has been shown to be reduced by approximately 90% on such exposure for 4 days. This decrement could be partly counteracted by subsequent culture for 4 days at low glucose, while daily alternate culture in high and low glucose did not prevent the insulin mRNA content from being reduced. The insulin release from cells cultured at high glucose was simultaneously reduced by 50%. This change was, however, not reversed by subsequent culture at low glucose, a pattern also found for the intracellular insulin stores. The suppression of insulin mRNA, insulin release, and intracellular insulin stores induced by high glucose was completely neutralized by the metabolic glucokinase blocker, mannoheptulose, while 2-deoxyglucose, a phosphoglucose isomerase blocker, had no impact. This suggests that glucokinase activity may have a negative regulatory effect. Addition of D-glyceraldehyde (DG) induced an increase in insulin release, while insulin mRNA remained unaltered. It would therefore seem that at least one glucose metabolite is involved in the glucose desensitization in INS-1 cells, which opens the prospect of regulatory factor(s), which possess(es) negative, as well as positive, actions.

Animals↗
PubMed1988

Autoradiographic determination of cerebral glucose content, blood flow, and glucose utilization in focal ischemia of the rat brain: influence of the plasma glucose concentration.

Focal cerebral ischemia was produced by occlusion of the middle cerebral artery in rats. Cerebral blood flow measured with [14C]iodoantipyrine was severely reduced in the lateral portion of neostriatum. This area of dense ischemia was sharply demarcated against the surroundings. The adjacent cortex was perfused at one-third of normal, whereas blood flow in the medial neostriatum was only slightly reduced. This pattern of perfusion was independent of the plasma glucose concentration of the animal. In contrast, the glucose utilization calculated from the 2-[3H]deoxyglucose accumulation depended on the plasma glucose concentration. Enhanced glucose utilization was evident in the border areas surrounding the ischemic focus in normoglycemic animals. Neither acutely nor chronically diabetic animals had such an increase of metabolism in the borderzone. Moderately hyperglycemic rats had a narrow rim of enhanced glucose utilization immediately surrounding the ischemic core, whereas animals with plasma glucose values above 22 mmol/L had no such rim. In mild hypoglycemia (2-4 mmol/L), the glucose utilization was slightly enhanced in the border areas, but during severe hypoglycemia (less than 2.5 mmol/L), the glucose utilization declined gradually toward the ischemic core. Glucose content, and thereby the lumped constant (measured by 3-0-[14C]methylglucose) showed little regional variation, except in the ischemic core. These findings indicate that blood flow alterations after occlusion of the middle cerebral artery in rats are not influenced by the plasma glucose utilizations. In contrast, glucose utilization depends on a combination of plasma glucose concentration and blood flow instead of blood flow per se.

Animals↗
PubMed2006

Metabolic activation of glucose low-responsive beta-cells by glyceraldehyde correlates with their biosynthetic activation in lower glucose concentration range but not at high glucose.

Insulin synthesis and release activities of beta-cells can be acutely regulated by glucose through its glycolytic and mitochondrial breakdown involving a glucokinase-dependent rate-limiting step. Isolated beta-cell populations are composed of cells with intercellular differences in acute glucose responsiveness that have been attributed to differences in glucokinase (GK) expression and activity. This study first shows that glyceraldehyde can be used as GK-bypassing oxidative substrate and then examines whether the triose can metabolically activate beta-cells with low glucose responsiveness. Glyceraldehyde 1 mm induced a similar cellular (14)CO(2) output and metabolic redox state as glucose 4 mM. Using flow cytometric analysis, glyceraldehyde (0.25-2 mM) was shown to concentration-dependently increase the percent metabolically activated cells at all tested glucose concentrations (2.5-20 mM). Its ability to activate beta-cells that are unresponsive to the prevailing glucose level was further illustrated in glucose low-responsive cells that were isolated by flow sorting. Metabolic activation by glyceraldehyde was associated with an activation of nutrient-driven translational control proteins and an increased protein synthetic response to glucose, however not beyond the maximal rates that are inducible by glucose alone. It is concluded that glucose low-responsive beta-cells can be metabolically activated by the GK-bypassing glyceraldehyde, increasing their acute biosynthetic response to glucose but not their maximal glucose-inducible biosynthetic capacity, which is considered subject to chronic regulation.

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↗
PubMed1994

Understanding oral glucose tolerance: comparison of glucose or insulin measurements during the oral glucose tolerance test with specific measurements of insulin resistance and insulin secretion.

The extent to which the oral glucose tolerance test can be used to estimate insulin secretion and insulin resistance has been evaluated by comparing glucose and insulin concentrations during an oral glucose tolerance test with specific measurements of insulin secretion and insulin resistance in 85 normoglycaemic subjects and 23 subjects with impaired glucose tolerance (IGT). Insulin secretion was measured by the first phase insulin response to intravenous glucose and insulin resistance by the insulin tolerance test which measures the decline of plasma glucose after the injection of a bolus of insulin. The best measure of insulin secretion was the ratio of the 30 min increment in insulin concentration to the 30 min increment in glucose concentration following oral glucose loading. This correlated with the first phase insulin release following intravenous glucose (r = 0.61, p < 0.001) but not insulin resistance (r = -0.05, p > 0.05). Insulin resistance could be estimated by the fasting insulin, proinsulin, or split proinsulin concentrations. However, fasting split proinsulin appeared to discriminate best between insulin resistance (r = -0.53, p < 0.001) and insulin secretion (r = 0.07, p > 0.05). Relative insulin resistance estimated by homeostasis model assessment (HOMA) also correlated well with insulin resistance (r = -0.57, p < 0.001) but not insulin secretion (r = 0.01, p > 0.05). We conclude that the oral glucose tolerance test can be used to derive estimates of the relative roles of insulin secretion and insulin resistance in population studies of glucose tolerance.

Blood Glucose↗
PubMed1998

Insulin secretion in normal glucose-tolerant relatives of type 2 diabetic subjects. Assessments using hyperglycemic glucose clamps and oral glucose tolerance tests.

OBJECTIVE: To assess insulin secretion in normal glucose-tolerant Caucasian first-degree relatives of type 2 diabetes subjects and in matched normal glucose-tolerant control subjects and to compare insulin secretion as assessed using a hyperglycemic glucose clamp with insulin secretion as assessed using an oral glucose tolerance test (OGTT). RESEARCH DESIGN AND METHODS: Twenty-one first-degree relatives of type 2 diabetic subjects and 21 control subjects without a family history of type 2 diabetes, who were matched for sex, age, BMI, waist-to-hip ratio, and aerobic capacity, underwent a hyperglycemic glucose clamp (10 mmol/l, 180 min). An OGTT (75 g glucose in 300 ml water) was also performed. RESULTS: First-phase insulin release (plasma insulin, 0-10 min) was not different (multiple analysis of variance [MANOVA]: F = 2.63, P = 0.11). Second-phase insulin release was lower (MANOVA: F = 4.18, P = 0.047). Separate analyses of variance showed decreased plasma insulin levels from 120 min onward (all P < 0.05), decreasing to geometric mean (95% CI) levels of 330 (270-402) and 462 (366-582) pmol/l at 180 min in relatives and control subjects, respectively. The insulin sensitivity index (ISI) as assessed using a hyperglycemic clamp was not different between the two groups. Mean +/- SE ISI during the 3rd hour was 27.5 +/- 2.2 and 30.5 +/- 3.0 micrograms.kg-1.min-1.pmol-1.l-1 in relatives and control subjects, respectively (P > 0.20). At 90 min after the OGTT, log plasma insulin levels correlated significantly with second-phase insulin release as assessed using the hyperglycemic glucose clamp. CONCLUSIONS: Normal glucose-tolerant first-degree relatives of type 2 diabetic subjects have a decreased second-phase insulin release, compared with matched control subjects. After an OGTT, 90-min values of log plasma insulin and 90-min values of the ratio of log plasma insulin to blood glucose may be good indicators of insulin secretory properties in normal glucose-tolerant family members of type 2 diabetic subjects.

Adult↗
PubMed2004

Enhanced glucose cycling and suppressed de novo synthesis of glucose-6-phosphate result in a net unchanged hepatic glucose output in ob/ob mice.

AIMS/HYPOTHESIS: Leptin-deficient ob/ob mice are hyperinsulinaemic and hyperglycaemic; however, the cause of hyperglycaemia remains largely unknown. METHODS: Glucose metabolism in vivo in 9-h fasted ob/ob mice and lean littermates was studied by infusing [U-(13)C]-glucose, [2-(13)C]-glycerol, [1-(2)H]-galactose and paracetamol for 6 h, applying mass isotopomer distribution analysis on blood glucose and urinary paracetamol-glucuronide. RESULTS: When expressed on the basis of body weight, endogenous glucose production (109+/-23 vs 152+/-27 micromol.kg(-1).min(-1), obese versus lean mice, p<0.01) and de novo synthesis of glucose-6-phosphate (122+/-13 vs 160+/-6 micromol.kg(-1).min(-1), obese versus lean mice, p<0.001) were lower in ob/ob mice than in lean littermates. In contrast, glucose cycling was greatly increased in obese mice (56+/-13 vs 26+/-4 micromol.kg(-1).min(-1), obese versus lean mice, p<0.001). As a result, total hepatic glucose output remained unaffected (165+/-31 vs 178+/-28 micromol.kg(-1).min(-1), obese vs lean mice, NS). The metabolic clearance rate of glucose was significantly lower in obese mice (8+/-2 vs 18+/-2 ml.kg(-1).min(-1), obese versus lean mice, p<0.001). Hepatic mRNA levels of genes encoding for glucokinase and pyruvate kinase were markedly increased in ob/ob mice. CONCLUSIONS/INTERPRETATION: Unaffected total hepatic glucose output in the presence of hyperinsulinaemia reflects hepatic insulin resistance in ob/ob mice, which is associated with markedly increased rates of glucose cycling. Hyperglycaemia in ob/ob mice primarily results from a decreased metabolic clearance rate of glucose.

Animals↗
PubMed2000

Glucose infusion attenuates endogenous glucose production and enhances glucose use of horses during exercise.

We examined the effects of increased glucose availability on glucose kinetics and substrate utilization in horses during exercise. Six conditioned horses ran on a treadmill for 90 min at 34 +/- 1% of maximum oxygen uptake. In one trial [glucose (Glu)], glucose was infused at a mean rate of 34.9 +/- 1.1 micromol. kg(-1). min(-1), whereas in the other trial [control (Con)] an equivalent volume of isotonic saline was infused. Plasma glucose increased during exercise in Glu (90 min: 8.3 +/- 1.7 mM) but was largely unchanged in Con (90 min: 5.1 +/- 0.4 mM). In Con, hepatic glucose production (HGP) increased during exercise, reaching a peak of 38.6 +/- 2.7 micromol. kg(-1). min(-1) after 90 min. Glucose infusion partially suppressed (P < 0.05) the rise in HGP (peak value 25.8 +/- 3.3 micromol. kg(-1). min(-1)). In Con, glucose rate of disappearance (R(d)) rose to a peak of 40.4 +/- 2.9 micromol. kg(-1). min(-1) after 90 min; in Glu, augmented glucose utilization was reflected by values for glucose R(d) that were twofold higher (P < 0.001) than in Con between 30 and 90 min. Total carbohydrate oxidation was higher (P < 0.05) in Glu (187.5 +/- 8.5 micromol. kg(-1). min(-1)) than in Con (159.2 +/- 7.3 micromol. kg(-1).min(-1)), but muscle glycogen utilization was similar between trials. We conclude that an increase in glucose availability in horses during low-intensity exercise 1) only partially suppresses HGP, 2) attenuates the decrease in carbohydrate oxidation during such exercise, but 3) does not affect muscle glycogen utilization.

Animals↗
PubMed1980

Estimation of glucose turnover and 13C recycling in the human newborn by simultaneous [1-13C]glucose and [6,6-1H2]glucose tracers.

To compare two methods of estimating systemic glucose production rates and to quantify carbon tracer recycling, six newborn infants, aged 2 h to 3 days, were infused simultaneously with [1-13C]glucose and [6,6-2H2]glucose tracers. The older infants were studied 6 h after a meal. [1-13C]Glucose was infused at 6 microgram/kg.min. Systemic glucose production rates were calculated from tracer dilution, assuming steady state kinetics. Although 13C was expected to randomize away from the C-1 of glucose, recycling occurred and was estimated from the difference in the rate of systemic glucose production quantified by the dilution of the two tracers. Systemic glucose production rates ranged from 4.2--5.4 mg/kg.min. Recycling on the glucose C-1 was 3--20% of the systemic glucose production rate and did not change with the age of the infant. Because recycling of glucose carbon signifies gluconeogenesis from lactate or pyruvate, it is concluded that the human newborn is able to initiate gluconeogenesis soon after birth.

Blood Glucose↗
PubMed1987

Estimation of endogenous glucose production during hyperinsulinemic-euglycemic glucose clamps. Comparison of unlabeled and labeled exogenous glucose infusates.

Tracer methodology has been applied extensively to the estimation of endogenous glucose production (Ra) during euglycemic glucose clamps. The accuracy of this approach has been questioned due to the observation of significantly negative estimates for Ra when insulin levels are high. We performed hyperinsulinemic (300 microU/ml)-euglycemic glucose clamps for 180 min in normal dogs and compared the standard approach, an unlabeled exogenous glucose infusate (cold GINF protocol, n = 12), to a new approach in which a tracer (D-[3-3H]glucose) was added to the exogenous glucose used for clamping (hot GINF protocol, n = 10). Plasma glucose, insulin and glucagon concentrations, and glucose infusion rates were similar for the two protocols. Plasma glucose specific activity was 20 +/- 1% of basal (at 120-180 min) in the cold GINF studies, and 44 +/- 3 to 187 +/- 5% of basal in the hot GINF studies. With the one-compartment, fixed pool volume model of Steele, Ra for the cold GINF studies was -2.4 +/- 0.7 mg X min-1 X kg-1 at 25 min and remained significantly negative until 110 min (P less than .05). For the hot GINF studies, Ra was never significantly less than zero (P greater than .05) and was greater than in the cold GINF studies at 20-90 min (P less than .05). There was substantially less between-(78%) and within- (40%) experiment variation for the hot GINF studies compared with the cold GINF studies. An alternate approach (regression method) to the application of the one-compartment model, which allows for a variable and estimable effective distribution volume, yielded Ra estimates that were suppressed 60-100% from basal. In conclusion, the one-compartment, fixed pool volume model of glucose kinetics is inadequate for the estimation of Ra during euglycemic glucose clamps. Two new strategies for estimating Ra from the one-compartment model, the hot GINF protocol and the regression method calculation, yielded more accurate and physiologically plausible estimates of Ra than currently used methodology.

Animals↗
PubMed2006

[Monitoring of glucose concentration in critical patients, comparing arterial blood glucose concentrations and interstitial glucose concentration measured by microdialysis technique].

INTRODUCTION: Recent studies have shown that normalization of blood glucose in critically ill patients by intensive insulin therapy significantly decreases their mortality and morbidity. The aim of our study was to compare interstitial glucose concentrations in subcutaneous adipose tissue (measured by microdialysis technique) and arterial blood glucose concentrations to test the suitability of subcutaneous adipose tissue for long-term placement of biosensors for glucose measurement in critically ill patients. PATIENTS AND METHODS: 20 patients (16 men and 4 women) after cardiac surgery hospitalized at postoperative intensive care unit were included into the study. Mean age was 68 +/- 10 years, BMI was 28.3 +/- 3.9 year. Only patients with glycemia higher than 6.7 mmol/l at a time of admission to the ICU were included. Samples for measurement of interstitial glucose concentrations were collected in 60 minutes intervals during 48 hours using microdialysis of the subcutaneous adipose tissue. Perfusion fluid was 5% mannitol, perfusion rate was 1 microl/min. Arterial blood glucose concentration was measured in 60 minutes intervals, absolute concentrations of interstitial glucose were calculated using ionic reference technique. RESULTS: Mean arterial glucose concentration during the study was 6.7 +/- 0.56 mmol/l, absolute concentration of glucose in interstitial fluid was 3.55 +/- 0.58 mmol/l. Mean correlation coefficient between arterial and interstitial concentrations was 0.77 +/- 0.15. CONCLUSION: Our study demonstrated good correlation between interstitial glucose concentrations in subcutaneous adipose tissue and arterial blood glucose concentrations in post-cardiac surgery patients. Further studies are needed to evaluate this relationship in patients with more severely disturbed perfusion of subcutaneous adipose tissue.

Aged↗
PubMed1989

Glucose tolerance and insulin response to glucose load before and after enzyme inducing therapy in subjects with glucose intolerance and patients with NIDDM having hyperinsulinemia or relative insulin deficiency.

We evaluated the role of insulin availability in the induction therapy of non-insulin dependent diabetes mellitus (NIDDM). Plasma glucose (BG) and insulin (IRI) response to glucose loading (OGTT) was investigated before and after placebo and phenobarbitone (PB) therapy in patients with glucose intolerance and NIDDM treated with diet only, sulphonylureas (SU) plus metformin (M) or insulin. The antipyrine test was used to reflect the liver mixed function oxidase system. Therapy with PB, but not placebo, reduced fasting IRI and BG in subjects with glucose intolerance and improved the glucose tolerance, insulin response to glucose and antipyrine metabolism. The effects of PB on patients with NIDDM were dependent on the insulin availability and duration of the disease. Best responses were seen in hyperinsulinemic patients at the early phase of the disease. They had lowered fasting BG and IRI values, improved glucose tolerance, insulin response to OGTT and antipyrine metabolism after PB therapy. The SU plus M treated patients responded beneficially if they had high fasting and postglucose IRI values and were non-responders if they had relative insulin deficiency. Antipyrine metabolism improved among the responders and non-responders. The hyperglycemic patients treated with insulin showed improved glucose metabolism, an improved C-peptide response and antipyrine metabolism. The subjects could be classified into responders and non-responders by calculating the ratio of areas above the fasting level curve of insulin and glucose (sigma delta I-OGTT/sigma delta G-OGTT). These values for the former were 0.2-0.4 and the latter 0.03-0.04, as compared to healthy volunteers (1.0) and subjects with glucose intolerance (1.4). A PB type inducer improves insulin sensitivity but does not alter its production or secretion. The outcome of glucose metabolism is therefore dependent on insulin availability.

Adult↗
PubMed1991

Correction of glucose carbon recycling for the determination of 'true' hepatic glucose production rates by (1-13C1)glucose.

Hepatic glucose production (HGP) and glucose carbon recycling are traditionally estimated by the combined use of hydrogen and carbon-labeled glucose tracers. A single-isotope method such as that of Reichard et al. for the determination of HGP and glucose carbon recycling requires the determination of activities in different glucose carbons by chemical degradation. Since the 13C content in the glucose carbon skeleton can be determined from mass fragmentography, the use of 13C-labeled glucose and mass fragmentography can provide a single-isotope method for the quantification of the recycled carbons. Correction for the recycling makes it possible to determine the true HGP. In this study, (1-13C1)glucose and mass fragmentography were used for the determination of HGP and glucose carbon recycling in six colon cancer patients. Molar enrichment of the molecular ion (m/z 328 cluster of glucose aldonitrile pentaacetate) was used to determine 'uncorrected' HGP, which was 1.93 +/- 0.11 mg kg-1 min-1 (mean +/- s.e.m.). The difference in molar enrichment of the molecular ion C1-C6 (m/z 328) and the ion corresponding to C1-C4 fragment (m/z 242) was used to determine the contribution of recycled label carbon. After this correction, the 'corrected' HGP was 2.04 +/- 0.12 mg kg-1 min-1, which is not significantly different from the 'true' HGP rate of 2.05 +/- 0.15 mg kg-1 min-1 determined by using (6-3H)glucose. HGP determined from the enrichment of the molecular ion C1-C6 underestimates true HGP, as expected. The corrected HGPs correlate well with those from 6-3H method (r = 0.86, y = 1.06x - 0.12; p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗