Biomedical subjects

I Tkác

Publications and source records attributed to I Tkác.

At least 19 recordsLinked to original sources

PubMed2005

Effect of gene polymorphisms on lipoprotein levels in patients with dyslipidemia of metabolic syndrome.

Dyslipidemia in the metabolic syndrome (MS) is considered to be one of the most important risk factors for atherosclerosis. It is characterized by hypertriglyceridemia, low concentration of plasma HDL-cholesterol, predominance of small dense LDL particles and an increased concentration of plasma apolipoprotein B (apoB). The pathogenesis of this type of dyslipidemia is partially explained, but its genetic background is still unknown. To evaluate the influence of cholesterol ester transfer protein (CETP) TaqIB polymorphism, lipoprotein lipase (LPL) PvuII and HindIII polymorphisms, hepatic lipase (LIPC) G-250A polymorphism and apolipoprotein C-III (APOC3) SstI gene polymorphism on lipid levels in dyslipidemia of the metabolic syndrome, 150 patients with dyslipidemia of metabolic syndrome were included. 96 % of patients had type 2 diabetes. The patients did not take any lipid lowering treatment. The exclusion criterion was the presence of any disease that could affect lipid levels, such as thyroid disorder, liver disease, proteinuria or renal failure. Gene polymorphisms were determined using the polymerase chain reaction and restriction fragment length polymorphisms. The genotype subgroups of patients divided according to examined polymorphisms did not differ in plasma lipid levels with the exception of apoB. The apoB level was significantly higher in patients with S1S1 genotype of APOC3 SstI polymorphism when compared with S1S2 group (1.10+/-0.26 vs. 0.98+/-0.21 g/l, p=0.02). Similarly, patients with H-H- genotype of LPL HindIII polymorphism had significantly higher mean apoB, compared with H+H- and H+H+ group (1.35+/-0.30 vs. 1.10+/-0.26 g/l, p=0.02). In the multiple stepwise linear regression analysis, apoB level seemed to be influenced by APOC3 SstI genotype, which explained 6 % of its variance. The present study has shown that the S1 allele of APOC3 SstI polymorphism and the H- allele of LPL HindIII polymorphism might have a small effect on apoB levels in the Central European Caucasian population with dyslipidemia of metabolic syndrome.

Aged↗

PubMed2005

Assessment of adrenoleukodystrophy lesions by high field MRS in non-sedated pediatric patients.

BACKGROUND: Early detection of white matter lesions in childhood-onset cerebral adrenoleukodystrophy (ALD) is important as hematopoietic cell transplantation (HCT), currently the only effective treatment, is beneficial only if performed early in the disease course. OBJECTIVE: To establish reliable biochemical markers of cerebral disease progression in patients with ALD to aid in treatment planning. METHODS: The authors used proton magnetic resonance spectroscopy (MRS) in combination with LCModel analysis to quantify brain metabolites in small volumes (3 to 16 mL) in the occipital and frontal white matter and the splenium of the corpus callosum of 17 unsedated patients and 26 healthy volunteers (adult n = 21, age-matched n = 5) at 4 tesla. RESULTS: Absolute concentrations of 12 metabolites were reliably determined, seven of which were established as markers of lesion development. Among these, creatine and choline containing compounds were the weakest markers while N-acetylaspartate, glutamine, and lipids + lactate were the strongest. The large extent of changes in the markers enabled detection of early neurochemical changes in lesion formation prior to detection of abnormalities by conventional MRI. Concentrations of a number of metabolites were also significantly different between normal appearing white matter of patients and controls indicating biochemical alterations in the absence of cerebral disease. Neurochemical improvements following HCT were measured in six patients. CONCLUSIONS: The progression of adrenoleukodystrophy, as well as effectiveness of its treatment, can be assessed with high precision using high field 1H magnetic resonance spectroscopy in individual patients without the need for sedation.

Adolescent↗

PubMed2002

[Relation of polymorphism of genes controlling endothelial function and blood pressure and the occurrence of vascular complications in type 2 diabetes].

Genetic polymorphisms of factors regulating the function of endothelium and blood pressure are recently intensively studied also in type 2 diabetes because endothelial dysfunction and arterial hypertension are risk factors of atherosclerosis. The following review deals with relations of polymorphisms in the renin-angiotensin-aldosterone (RAAS) system, polymorphisms of NO-synthase (NOS) as well as the gene for atrial natriuretic peptide (hANP). So far most information was assembled on the influence of polymorphisms of RAAS genes, in particular the gene coding the angiotensin converting enzyme (ACE), on complications of type 2 diabetes. A relationship with the development of coronary disease was described in ACE genes, the receptor for angiotensin II--type 1 (AT1R), angiotensinogen and in several NOS polymorphisms. Also the relationship of polymorphisms of genes ACE, AT1R, NOS and hANP was described in relation to the development of hypertension which is an important risk factor for macrovascular and microvascular complications of diabetes. In some investigations the relationship of polymorphisms of ACE and AT1R genes and the development of diabetic nephropathy was described where a significant acceleration of the process of atherogenesis occurs. As type 2 diabetes mellitus and atherosclerosis are polygenically determinal diseases, it will be in particular necessary to investigate in future the concurrent influence of several gene polymorphisms and their interactions with the diabetic milieu intérieur on the development of macrovascular and microvascular complications of diabetes.

Angiotensinogen↗

PubMed2001

Metabolic changes in quinolinic acid-lesioned rat striatum detected non-invasively by in vivo (1)H NMR spectroscopy.

Intrastriatal injection of quinolinic acid (QA) provides an animal model of Huntington disease. In vivo (1)H NMR spectroscopy was used to measure the neurochemical profile non-invasively in seven animals 5 days after unilateral injection of 150 nmol of QA. Concentration changes of 16 metabolites were measured from 22 microl volume at 9.4 T. The increase of glutamine ((+25 +/- 14)%, mean +/- SD, n = 7) and decrease of glutamate (-12 +/- 5)%, N-acetylaspartate (-17 +/- 6)%, taurine (-14 +/- 6)% and total creatine (-9 +/- 3%) were discernible in each individual animal (P < 0.005, paired t-test). Metabolite concentrations in control striata were in excellent agreement with biochemical literature. The change in glutamate plus glutamine was not significant, implying a shift in the glutamate-glutamine interconversion, consistent with a metabolic defect at the level of neuronal-glial metabolic trafficking. The most significant indicator of the lesion, however, were the changes in glutathione ((-19 +/- 9)%, P < 0.002)), consistent with oxidative stress. From a comparison with biochemical literature we conclude that high-resolution in vivo (1)H NMR spectroscopy accurately reflects the neurochemical changes induced by a relatively modest dose of QA, which permits one to longitudinally follow mitochondrial function, oxidative stress and glial-neuronal metabolic trafficking as well as the effects of treatment in this model of Huntington disease.

Amino Acids↗

PubMed2001

Increased intracranial arterial resistance in patients with type 2 diabetes mellitus.

BACKGROUND: The majority of the studies investigating risk factors for stroke have focused on the atherosclerosis of extracranial carotid arteries. Risk factors for the involvement of intracranial arteries in patients with stroke have not been widely investigated so far. The pulsatility index reflects the vascular resistance of intracranial arteries and could therefore be used as an estimate of the severity of vascular damage. MAIN PURPOSE: The present study aimed to examine the influence of type 2 diabetes mellitus and some other atherosclerosis risk factors on intracranial vascular resistance in patients with a previous stroke or transient ischemic attack. METHODS: Transcranial doppler investigations were performed in 103 patients with previous stroke (31 with diagnosis of type 2 diabetes, 72 without diabetes), at least 3 months after stroke occurred. Blood flow velocities of anterior cerebral arteries, middle cerebral arteries, the intracranial part of vertebral arteries and the basilar artery, as well as of the extracranial part of the internal carotid artery were measured, and Gosling's pulsatility index was calculated. The maximal pulsatility index of intracranial arteries was defined to express the most pronounced damage. RESULTS: Diabetic patients had a significantly higher pulsatility index than non-diabetic patients in all examined intracranial arteries. The maximal pulsatility index was also significantly higher in diabetic patients than in non-diabetic patients (1.24 +/- 0.25 vs. 1.00 +/- 0.23; p < 0.0001). There was no significant difference in the pulsatility index between men and women and between groups of patients with or without hypertension. In the multivariate analysis, the presence of diabetes (p < 0.0001) and the age of patients (p < 0.0001) were the only factors significantly predicting maximal pulsatility index, and this relationship was independent on the presence of hypertension. CONCLUSIONS: Diabetic patients with previous stroke have a higher pulsatility index than non-diabetic patients with previous strokes, which indicates a higher increase in intracranial arterial resistance and more severe damage to cerebral blood flow in diabetes mellitus.

Aged↗

PubMed2001

Carotid intima-media thickness in type 2 diabetes is more strongly related to serum apoprotein A-I in females.

BACKGROUND: Dyslipidemia in type 2 diabetes has been shown to be related to the incidence of macrovascular events. Increased carotid intima-media thickness is considered to be a marker of macrovascular disease. MAIN PURPOSE: To investigate a possible relationship between lipoprotein levels and carotid intima-media thickness as a marker of early atherosclerosis in patients with type 2 diabetes. METHODS: Seventy-one consecutively selected eligible patients (31 males, 40 females) with type 2 diabetes were studied. Common carotid intima-media thickness was measured bilaterally by high-resolution ultrasound and the mean value from both sides was used for further analysis. Fasting blood samples were taken from each individual and their serum was analyzed for lipoprotein levels. RESULTS: In the entire group of patients, intima-media thickness was inversely related to apoprotein A-I (r = -0.33, p = 0.008) and HDL cholesterol (r = -0.23, p = 0.059) in univariate correlation analysis, and a positive correlation between intima-media thickness and apoprotein B/apoprotein A-I ratio was found (r = 0.33, p = 0.007). When genders were analyzed separately, intima-media thickness was significantly correlated with apoprotein A-I and apoprotein B/apoprotein A-I ratio in females, while no significant correlation of any lipid variable with intima-media thickness was observed in males. In multiple linear regression analysis, age (p = 0.005), male gender (p = 0.002) and apoprotein A-I (p = 0.035) were the only risk factors in the entire group of diabetic patients, which significantly predicted carotid intima-media thickness in models adjusted for demographic and other known risk factors. As was the case in the univariate analysis, no risk factor significantly predicted carotid intima-media thickness in males while age, apoprotein A-I and B significantly predicted intima-media thickness in females. CONCLUSIONS: In the present study, low serum apoprotein A-I, a major protein component of HDL, was found to be related to increased carotid intima-media thickness. This relationship was stronger in females than in males, which suggests possible gender differences in the relationship between apoprotein A-1 and early atherosclerotic lesions in subjects with type 2 diabetes mellitus.

Adult↗

PubMed2001

In vivo 1H NMR spectroscopy of the human brain at 7 T.

In vivo 1H NMR spectra from the human brain were measured at 7 T. Ultrashort echo-time STEAM was used to minimize J-modulation and signal attenuation caused by the shorter T2 of metabolites. Precise adjustment of higher-order shims, which was achieved with FASTMAP, was crucial to benefit from this high magnetic field. Sensitivity improvements were evident from single-shot spectra and from the direct detection of glucose at 5.23 ppm in 8-ml volumes. The linewidth of the creatine methyl resonance was at best 9 Hz. In spite of the increased linewidth of singlet resonances at 7 T, the ability to resolve overlapping multiplets of J-coupled spin systems, such as glutamine and glutamate, was substantially increased. Characteristic spectral patterns of metabolites, e.g., myo-inositol and taurine, were discernible in the in vivo spectra, which facilitated an unambiguous signal assignment.

Adult↗

PubMed2000

Carotid intima-media thickness in relation to macrovascular disease in patients with type 2 diabetes mellitus.

BACKGROUND: Increased carotid intima-media thickness is regarded as a marker of atherosclerosis. Type 2 diabetes mellitus is associated with a high prevalence of macrovascular disease. MAIN PURPOSE: The present study aimed to examine the relationship between carotid intima-media thickness and the presence of macrovascular disease in patients with type 2 diabetes. METHODS: 71 patients with type 2 diabetes mellitus were studied. The distal common carotid artery and carotid bifurcation intima-media thickness were measured bilaterally with high-resolution ultrasonography. The relationship between the presence of coronary artery disease, cerebrovascular disease and peripheral arterial disease and carotid intima-media thickness was evaluated. RESULTS: Patients with coronary artery disease had significantly (p = 0.048) increased intima-media thickness of the distal common carotid artery. This difference ceased to be significant after adjustment for cardiovascular risk factors. Patients with peripheral arterial disease had a significantly higher bifurcation (p < 0.0001), distal common carotid (p = 0.03) and mean intima-media thickness (p = 0.0008) than did those without peripheral arterial disease. This difference remained significant even after adjustment for other cardiovascular risk factors. In the multiple linear regression analysis, the presence of peripheral arterial disease, age and male gender significantly predicted bifurcation intima-media thickness, while age and the presence of peripheral arterial disease significantly predicted mean intima-medial thickness. CONCLUSIONS: In the present study, the increased carotid intima-media thickness in patients with type 2 diabetes mellitus was related to the presence of peripheral arterial disease. This finding probably reflects morphologic and hemodynamic similarities between the two vascular beds and indicates that increased carotid intima-media thickness in patients with type 2 diabetes may be a marker of atherosclerosis in different locations.

Adult↗

PubMed2000

Field mapping without reference scan using asymmetric echo-planar techniques.

Improvements in Bo mapping and shimming were achieved by measuring the static field information in multiple subsequent echoes generated by an asymmetric echo-planar readout gradient train. With careful compensation, eddy current effects were shown to affect the adjustment of the shim coils minimally. In addition to reducing the time required for field mapping by two-fold, the sensitivity was simultaneously optimized irrespective of the prevalent T2* present, thereby minimizing the error of the static field measurement to below 0.1 Hz. With adiabatic low flip-angle excitation, the time required for field mapping was below 1 second.

Echo-Planar Imaging↗

PubMed2000

Single-shot, three-dimensional "non-echo" localization method for in vivo NMR spectroscopy.

Metabolite signals with short T(1) or T(2) are difficult to localize with full sensitivity. This limitation was overcome with the development and implementation of a single-shot, complete three-dimensional "non-echo" localization method with reduced sensitivity to spatial B(1) variation, which is suitable for measuring signals with very short T(1) or T(2), e.g., the (13)C NMR signals of glycogen. The proposed method is based on a T(1)-optimized outer volume suppression scheme using pulses of the hyperbolic secant type applied at different power levels, which is robust over a fivefold range of T(1). Strong lipid, muscle glycogen, and glucose signals originating outside the rat brain were suppressed. Signals of glycogen, aspartate, glutathione, GABA C4, N-acetyl aspartate as well as the C3 and C4 signals of glutamate and glutamine with resolved homonuclear (13)C-(13)C coupling were fully resolved in vivo at 9.4 Tesla using higher-order shimming. The method can be extended to other nuclei and to localized MRS of humans.

Acetates↗

PubMed2000

Metabolic changes in rat brain after prolonged ethanol consumption measured by 1H and 31P MRS experiments.

1. In vivo 1H and 31P magnetic resonance spectroscopy techniques were applied to reveal biochemical changes in the rat brain caused by prolonged ethanol consumption. 2. Three models of ethanol intoxication were used. 3. 1H MRS showed a significant decrease in the concentration of myo-inositol in the brain of rats fed with 20% ethanol for 8 weeks. This change is consistent with perturbances in astrocytes. On the other hand, N-acetyl aspartate and choline content did not differ from controls. 4. 31P MRS did not reveal any significant changes in the high-energy phosphates or intracellular free Mg2+ content in the brain of rats after 14 weeks of 20% ethanol drinking. The intracellular pH was diminished. 5. By means of a 31P saturation transfer technique, a significant decrease was observed for the pseudo first-order rate constant k(for) of the creatine kinase reaction in the brain of rats administered 30% ethanol for 3 weeks using a gastric tube. 6. The 1H MRS results may indicate that myo-inositol loss, reflecting a disorder in astrocytes, might be one of the first changes associated with alcoholism, which could be detected in the brain by means of in vivo 1H MRS. 7. The results from 31p MRS experiments suggest that alcoholism is associated with decreased brain energy metabolism. 8. 31P saturation transfer, which provides insight into the turnover of high-energy phosphates, could be a more suitable technique for studying the brain energetics in chronic pathological states than conventional 31P MRS.

Adenosine Triphosphate↗

PubMed2000

Extracellular-intracellular distribution of glucose and lactate in the rat brain assessed noninvasively by diffusion-weighted 1H nuclear magnetic resonance spectroscopy in vivo.

To determine the distribution of cerebral glucose and lactate between the intracellular and the extracellular space of the rat brain in vivo, the diffusion characteristic of glucose and lactate was compared with that of metabolites known to be mainly intracellular (N-acetylaspartate, choline, creatine, glutamate, myo-inositol, and taurine) using a pulsed-field-gradient 1H nuclear magnetic resonance technique. The detection of a glucose signal at large diffusion weighting provided direct experimental evidence of intracellular glucose in the rat brain. At large diffusion weighting, the apparent diffusion coefficient (ADC) of glucose and lactate was similar to that of the intracellular metabolites such as N-acetylaspartate, creatine, and glutamate. At small diffusion weighting, the ADC of glucose and lactate was increased, which was explained by a decreased relative contribution of intracellular glucose to the total signal. The calculated extracellular volume fraction of glucose (0.19 +/- 0.05) and lactate (0.17 +/- 0.06) was consistent with a substantial fraction of glucose and lactate signals being intracellular. The findings were direct in vivo evidence that the largest concentration gradient of glucose is at the blood-brain barrier and that glucose is evenly distributed in the brain in vivo between the intracellular and extracellular space.

Animals↗

PubMed2000

[Effect of bisoprolol on heart rate variability in patients with hyperthyroidism].

OBJECTIVE: The objective of the submitted work was to assess by the method of spectral analysis of the heart rate how the use of bisoprolol will affect the autonomous modulation of the heart rate in hyperthyroid patients and what are the time relations of this effect. MATERIAL AND METHODS: In the investigation 10 female patients with thyreotoxicosis caused by Graves-Basedow's disease were included. Their average age was 38 years and along with a thyrostatic drug bisoprolol was administered. Spectral analysis of the heart rate was made before the onset of treatment, after a week and after six weeks with the patients in an upright and recumbent position. The activity of the sympathicus was evaluated from the ratio of low and high frequencies. RESULTS: Already during the first week a significant decline of the heart rate was observed. During the first week of treatment a decline of the activity of the sympathicus in a recumbent position occurred associated with milder palpitations or their complete disappearance. The decline in an upright position occurred after the first week of treatment. From the trend of other parameters of cardiac variability, the differences of some reached statistical significance, it may be concluded that the activity of the parasympathicus, formerly inhibited, was restored. CONCLUSION: Based on the results it may be stated that bisoprolol is a suitable supplementary drug in the early treatment of thyrotoxicosis because by reducing the hyperadrenergic state it improves the quality of life of these patients.

Adolescent↗

PubMed1999

Cardiovascular risk factors as predictors of mortality in type II diabetic patients.

BACKGROUND: Mortality among diabetic patients is high and attempts have been made to find clinical markers which would help to identify patients at risk. MAIN PURPOSE: The purpose of this study was to assess whether cardiovascular risk factors like previous myocardial infarction, left ventricular dysfunction, hypertension, renal insufficiency, and 24-hour mean or minimum heart rate, significantly contribute to the mortality in this group of patients. METHODS: 45 male patients with type II diabetes mellitus were studied by ambulatory electrocardiography to obtain the information about the 24-hour mean and minimum heart rates; records from baseline hospitalization were reviewed for clinical variables. After 55 months mortality data were retrieved. Cox's proportional hazards regression model was used to study the effect of clinical variables on mortality in multivariate analysis. RESULTS: All-cause mortality was 38%. The groups of survivors and nonsurvivors differed significantly in terms of age, the presence of left ventricular dysfunction and renal insufficiency. No significant difference in 24-hour mean or minimum heart rate was registered. In the Cox's model, the presence of left ventricular dysfunction, renal insufficiency and age significantly and independently predicted mortality. CONCLUSION: The present study, showed that left ventricular dysfunction and renal insufficiency were related to the all-cause mortality of type II diabetic patients independently of age, after 55 months of follow-up. Prognostic significance of 24-hour mean or minimum heart rate has not been proven.

Adult↗

PubMed1999

In vivo 1H NMR spectroscopy of rat brain at 1 ms echo time.

Using optimized, asymmetric radiofrequency (RF) pulses for slice selection, the authors demonstrate that stimulated echo acquisition mode (STEAM) localization with ultra-short echo time (1 ms) is possible. Water suppression was designed to minimize sensitivity to B1 inhomogeneity using a combination of 7 variable power RF pulses with optimized relaxation delays (VAPOR). Residual water signal was well below the level of most observable metabolites. Contamination by the signals arising from outside the volume of interest was minimized by outer volume saturation using a series of hyperbolic secant RF pulses, resulting in a sharp volume definition. In conjunction with FASTMAP shimming (Gruetter Magn Reson Med 1993;29: 804-811), the short echo time of 1 msec resulted in highly resolved in vivo 1H nuclear magnetic resonance spectra. In rat brain the water linewidths of 11-13 Hz and metabolite singlet linewidths of 8-10 Hz were measured in 65 microl volumes. Very broad intense signals (delta v(1/2) > 1 kHz), as expected from membranes, for example, were not observed, suggesting that their proton T2 are well below 1 msec. The entire chemical shift range of 1H spectrum was observable, including resolved resonances from alanine, aspartate, choline group, creatine, GABA, glucose, glutamate, glutamine, myo-inositol, lactate, N-acetylaspartate, N-acetylaspartylglutamate, phosphocreatine, and taurine. At 9.4 T, peaks close to the water were observed, including the H-1 of alpha-D-glucose at 5.23 ppm and a tentative H-1 resonance of glycogen at 5.35 ppm.

Animals↗

PubMed1999

Localized in vivo 1H NMR detection of neurotransmitter labeling in rat brain during infusion of [1-13C] D-glucose.

Resolved localized nuclear magnetic resonance (NMR) signals of 1H bound to 13C label in the carbon positions of glutamate C4, C3 and glutamine C4, C3, as well as in aspartate C3, lactate C3, alanine C3, gamma-aminobutyric acid C3, and glucose C1 were simultaneously observed in spectra obtained from rat brain in vivo. Time-resolved label incorporation was measured with a new adiabatic carbon editing and decoupling (ACED) single-voxel stimulated echo acquisition mode (STEAM) sequence. Adiabatic carbon broadband decoupling of 12 kHz bandwidth was achieved in vivo, which decoupled the entire 13C spectrum at 9.4 T. Resonances from N-acetyl-aspartate and creatine were also detected, consistent with natural-abundance 13C levels. These results emphasize the potential of 1H NMR for following complex biochemical pathways in localized areas of resting rat brain as well as during focal activation using infusions of 13C-labeled glucose.

Animals↗

PubMed1999

Toward an in vivo neurochemical profile: quantification of 18 metabolites in short-echo-time (1)H NMR spectra of the rat brain.

Localized in vivo (1)H NMR spectroscopy was performed with 2-ms echo time in the rat brain at 9.4 T. Frequency domain analysis with LCModel showed that the in vivo spectra can be explained by 18 metabolite model solution spectra and a highly structured background, which was attributed to resonances with fivefold shorter in vivo T(1) than metabolites. The high spectral resolution (full width at half maximum approximately 0.025 ppm) and sensitivity (signal-to-noise ratio approximately 45 from a 63-microL volume, 512 scans) was used for the simultaneous measurement of the concentrations of metabolites previously difficult to quantify in (1)H spectra. The strongly represented signals of N-acetylaspartate, glutamate, taurine, myo-inositol, creatine, phosphocreatine, glutamine, and lactate were quantified with Cramér-Rao lower bounds below 4%. Choline groups, phosphorylethanolamine, glucose, glutathione, gamma-aminobutyric acid, N-acetylaspartylglutamate, and alanine were below 13%, whereas aspartate and scyllo-inositol were below 22%. Intra-assay variation was assessed from a time series of 3-min spectra, and the coefficient of variation was similar to the calculated Cramér-Rao lower bounds. Interassay variation was determined from 31 pooled spectra, and the coefficient of variation for total creatine was 7%. Tissue concentrations were found to be in very good agreement with neurochemical data from the literature.

Amino Acids↗

PubMed1999

Noninvasive measurements of [1-(13)C]glycogen concentrations and metabolism in rat brain in vivo.

Using a specific 13C NMR localization method, 13C label incorporation into the glycogen C1 resonance was measured while infusing [1-(13)C]glucose in intact rats. The maximal concentration of [1-(13)C]glycogen was 5.1 +/- 0.6 micromol g(-1) (mean +/- SE, n = 8). During the first 60 min of acute hyperglycemia, the rate of 13C label incorporation (synthase flux) was 2.3 +/- 0.7 micromol g(-1) h(-1) (mean +/- SE, n = 9 rats), which was higher (p < 0.01) than the rate of 0.49 +/- 0.14 micromol g(-1) h(-1) measured > or = 2 h later. To assess whether the incorporation of 13C label was due to turnover or net synthesis, the infusion was continued in seven rats with unlabeled glucose. The rate of 13C label decline (phosphorylase flux) was lower (0.33 +/- 0.10 micromol g(-1) h(-1)) than the initial rate of label incorporation (p < 0.01) and appeared to be independent of the duration of the preceding infusion of [1-(13)C]glucose (p > 0.05 for correlation). The results implied that net glycogen synthesis of approximately 3 micromol g(-1) had occurred, similar to previous reports. When infusing unlabeled glucose before [1-(13)C]glucose in three studies, the rate of glycogen C1 accumulation was 0.46 +/- 0.08 micromol g(-1) h(-1). The results suggest that steady-state glycogen turnover rates during hyperglycemia are approximately 1% of glucose consumption.

Animals↗