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S Kristiansen

Publications and source records attributed to S Kristiansen.

34 records · Page 2Linked to original sources
PubMed1997

Progressive increase in glucose transport and GLUT-4 in human sarcolemmal vesicles during moderate exercise.

Muscle glucose uptake increases progressively during moderate-intensity exercise. To elucidate whether this is due to a progressive increase in sarcolemmal glucose transport capacity, nine men exercised for 40 min at 75% maximal oxygen uptake on a bicycle ergometer. Muscle biopsies were obtained from the vastus lateralis at rest (0 min) and after 5 and 40 min of exercise and used for production of sarcolemmal giant (SG) vesicles. SG vesicle glucose transport at 5 mM increased (P < 0.05) by 38 and 93% after 5 and 40 min of exercise, respectively, compared with glucose transport at rest. The SG vesicle GLUT-4 protein content increased (P < 0.05) by 36 and 91% after 5 and 40 min of exercise, respectively, compared with rest. Thus the increase in vesicle glucose transport was accompanied by a similar increase in SG vesicle GLUT-4 protein content. Muscle glucose and glucose 6-phosphate were low at rest, increased (P < 0.05) 2.2- and 2.3-fold, respectively, after 5 min of exercise, and returned to resting values after 40 min of exercise. It is concluded that the progressive increase in muscle glucose uptake during moderate-intensity exercise may be due at least in part to a progressive increase in sarcolemmal glucose transport and GLUT-4 protein content.

Adult↗
PubMed1997

Fructose transport and GLUT-5 protein in human sarcolemmal vesicles.

Sarcolemmal vesicles were produced from human skeletal muscle biopsy material obtained at rest and immediately after maximal dynamic exercise (100% maximal O2 uptake) for analysis of fructose transport and hexose transporter (GLUT-5) protein concentration. Human sarcolemmal vesicles displayed a time-dependent uptake of D-fructose that displayed saturable Michaelis-Menten type kinetics (maximal transport 477 +/- 37 pmol.min-1.mg protein-1; half-maximal concentration constant 8.3 +/- 1.2 mM). At a hexose concentration of 5 mM, vesicle transport rate was eight times faster for glucose than for fructose. Preincubation of human muscle vesicles with 35 microM cytochalasin B before the uptake assay resulted in > 95% inhibition in D-glucose uptake, whereas transport of D-fructose was unaffected. Sarcolemmal vesicles prepared from exercised human muscle showed a significant increase (49%) in vesicle GLUT-4 content (P < 0.03, n = 10), which accounts for the increase in vesicle glucose transport that we have recently reported [S. Kristiansen, M. Hargreaves, and E.A. Richter. Am. J. Physiol. 270 (Endocrinol. Metab. 33): E197-E201, 1996]. In contrast, exercise did not increase the vesicle GLUT-5 protein content or induce changes in vesicle fructose transport activity. In conclusion, we propose that fructose transport into human skeletal muscle occurs via a mechanism distinct from that utilized by glucose on the basis of differences in sensitivity to cytochalasin B and responsiveness to exercise. Furthermore, our findings signify that uptake of fructose in human skeletal muscle is mediated by the GLUT-5 transporter.

Adult↗
PubMed1996

Eccentric exercise decreases maximal insulin action in humans: muscle and systemic effects.

1. Unaccustomed eccentric exercise decreases whole-body insulin action in humans. To study the effects of one-legged eccentric exercise on insulin action in muscle and systemically, the euglycaemic clamp technique combined with arterial and bilateral femoral venous catheterization was used. Seven subjects participated in two euglycaemic clamps, performed in random order. One clamp was preceded 2 days earlier by one-legged eccentric exercise (post-eccentric exercise clamp (PEC)) and one was without the prior exercise (control clamp (CC)). 2. During PEC the maximal insulin-stimulated glucose uptake over the eccentric thigh was marginally lower when compared with the control thigh, (11.9%, 64.6 +/- 10.3 vs. 73.3 +/- 10.2 mumol kg-1 min-1, P = 0.08), whereas no inter-thigh difference was observed at a submaximal insulin concentration. The glycogen concentration was lower in the eccentric thigh for all three clamp steps used (P < 0.05). The glucose transporter GLUT4 protein content was on average 39% lower (P < 0.05) in the eccentric thigh in the basal state, whereas the maximal activity of glycogen synthase was identical in the two thighs for all clamp steps. 3. The glucose infusion rate (GIR) necessary to maintain euglycaemia during maximal insulin stimulation was lower during PEC compared with CC (15.7%, 81.3 +/- 3.2 vs. 96.4 +/- 8.8 mumol kg-1 min-1, P < 0.05). 4. Our data show that 2 days after unaccustomed eccentric exercise, muscle and whole-body insulin action is impaired at maximal but not submaximal concentrations. The local effect cannot account for the whole-body effect, suggesting the release of a factor which decreases insulin responsiveness systemically.

Adult↗
PubMed1996

Effect of vanadate on glucose transporter (GLUT4) intrinsic activity in skeletal muscle plasma membrane giant vesicles.

Maximally effective concentrations of vanadate (a phosphotyrosine phosphatase inhibitor) increase glucose transport in muscle less than maximal insulin stimulation. This might be due to vanadate-induced decreased intrinsic activity of GLUT4 accompanying GLUT4 translocation. Thus, the effect of vanadate (NaVO3) on glucose transporter (GLUT4) intrinsic activity (V(max) = intrinsic activity x [GLUT4 protein]) was studied in muscle plasma membrane giant vesicles. Giant vesicles (average diameter 7.6 microns) were produced by collagenase treatment of rat skeletal muscle. The vesicles were incubated for 1.5 h with concentrations of vanadate ranging from 3 to 40 mmol l-1 at 34 degrees C before being used for determination of glucose transport. The dose-response curve showed that vanadate decreased the specific D-glucose uptake by a maximum of 70% compared with a control preparation. The vanadate-induced decrease in glucose uptake was not due to a decrease in number of vesicles. To further verify the apparent vanadate-induced decrease in GLUT4 intrinsic activity, the kinetics of glucose transport were also examined. In the presence of 10 mmol l-1 vanadate the V(max) and K(m) were decreased (P < 0.05, n = 6) 55% and 60%, respectively, compared with control. The plasma membrane GLUT4 protein content was not changed in response to vanadate. It is concluded that vanadate decreased glucose transport per GLUT4 (intrinsic activity). This finding suggests that regulation of glucose transport in skeletal muscle can involve changes in GLUT4 intrinsic activity.

Animals↗
PubMed1996

Exercise-induced increase in glucose transport, GLUT-4, and VAMP-2 in plasma membrane from human muscle.

A major effect of muscle contractions is an increase in sarcolemmal glucose transport. We have used a recently developed technique to produce sarcolemmal giant vesicles from human muscle biopsy samples obtained before and after exercise. Six men exercised for 10 min at 50% maximal O2 uptake (Vo2max) and then to fatigue at 100% Vo2max (5.7 +/- 0.2 min). Vesicle glucose transport at 5 mM increased from 3.3 +/- 0.6 pmol.microgram-1.min-1 at rest to 6.6 +/- 1.0 pmol.microgram-1.min-1 at fatigue (mean +/- SE, n = 6, P < 0.05). This increase in glucose transport was associated with a 1.6-fold increase in vesicle GLUT-4 protein content. Glucose transport normalized to GLUT-4 protein content also increased with exercise, suggesting increased intrinsic activity of GLUT-4. Furthermore, exercise resulted in a 1.4-fold increase in sarcolemmal vesicle-associated membrane protein (VAMP-2) content, suggesting that muscle contractions may induce trafficking of GLUT-4-containing vesicles via a mechanism similar to neurotransmitter release. Our results demonstrate for the first time exercise-induced translocation of GLUT-4 and VAMP-2 to the plasma membrane of human muscle and increased sarcolemmal glucose transport.

Adult↗
PubMed1996

Decreased muscle GLUT-4 and contraction-induced glucose transport after eccentric contractions.

Eccentric exercise causes muscle damage and decreased muscle glycogen and glucose transporter isoform (GLUT-4) protein content. We investigated whether the contraction-induced increase in skeletal muscle glucose transport and muscle performance is affected by prior eccentric contractions. The calf muscles from rats were stimulated for eccentric (EC) or concentric (CC) contractions or were passively stretched (ST). Muscles from unstimulated control (CT) rats were also studied. Two days later, all rats had their isolated hindlimbs perfused either at rest or during 15 min of isometric muscle contractions. EC rats had a significantly lower total GLUT-4 protein content in the white gastrocnemius (GW) muscle (55%) and red gastrocnemius (GR) muscle (34%) compared with muscle from the CT, ST, and CC rats. In contrast, GLUT-1 protein content was approximately twofold higher in the GW muscle in EC rats than in CT rats. In the GW and GR muscle, prior eccentric exercise decreased contraction-induced stimulation of glucose transport compared with CT, ST, and CC rats despite no difference in tension development and oxygen uptake among the groups. There was no change in total GLUT-4 content and glucose transport in the soleus (S) muscle among the four group. It is concluded that the GLUT-4 and GLUT-1 protein contents in fast-twitch muscle are decreased and increased, respectively, 2 days after eccentric contractions. The functional consequence of these changes appears to be decreased contraction-induced increase in skeletal muscle glucose transport.

Animals↗
PubMed1995

Eccentric muscle damage transiently decreases rat skeletal muscle GLUT-4 protein.

The effects of concentric and muscle-damaging eccentric contractions on muscle glucose transporter GLUT-4 content were studied in rat muscles. Rats were anesthetized, the calf muscles on one side were stimulated electrically for concentric or eccentric contractions, and bilateral calf muscles were obtained in the postexercise period. Inflammatory and phagocytic cells accumulated in the eccentric white and red gastrocnemius muscles, whereas there were only discrete changes in the eccentric soleus. Glycogen was depleted to the same extent in the white and red gastrocnemius muscles after both types of stimulation, and it remained decreased > 2 days in eccentric muscles. The total GLUT-4 protein content was decreased in the eccentric white and red gastrocnemius muscles 1 and 2 days after the eccentric stimulation, whereas the maximal activity of glycogen synthase was unaffected at these time points. In conclusion, our one-legged stimulation model caused eccentric muscle damage in the white and red gastrocnemius, whereas only minor damage was observed in the soleus muscle. In damaged muscle, muscle glycogen and GLUT-4 protein content were decreased for > 2 days. These findings may suggest (but do not prove) that decreased muscle GLUT-4 protein is involved in the delayed glycogen resynthesis after eccentric exercise.

Animals↗
PubMed1994

Effect of glucose-6-phosphate and pH on glucose transport in skeletal muscle plasma membrane giant vesicles.

The effect of glucose-6-phosphate (G-6-P) and pH on glucose transport was studied in skeletal muscle plasma membrane giant vesicles containing GLUT4 but not GLUT1. Vesicles (average diameter 7.6 microns) were obtained by collagenase treatment of muscle. The vesicles were incubated with 10 mmol l-1 G-6-P and, after 0.5 and 2 h of incubation, the intravesicular G-6-P concentration was 0.93 +/- 0.4 mmol l-1 and 1.18 +/- 0.5 mmol l-1 (mean +/- SE, n = 4), respectively. In order to increase the intravesicular G-6-P concentration, 0.001% saponin was added during incubation, which increased the 2-h intravesicular G-6-P concentration to 4.57 +/- 1.0 mmol l-1 (n = 4). Initially, vesicles were used for glucose transport studies after 30 min of incubation with 10 mmol l-1 of G-6-P. There was no effect of G-6-P on either the affinity constant (Km) or maximal velocity (Vmax) of the glucose transport. Subsequently, vesicles were incubated for 2 h with 10 mmol l-1 of G-6-P and 0.001% saponin. Still no effect of G-6-P on glucose transport could be detected. In contrast, the rate of D-glucose transport was affected, when extravesicular pH was varied from 6.0 to 7.8. The maximum glucose transport rate was found at pH 7.2 and was decreased at both higher and lower pH. It is concluded that G-6-P has no effect on GLUT4 intrinsic activity in rat skeletal muscle plasma membrane. In contrast, GLUT4 intrinsic activity is sensitive to changes in pH.

Animals↗
PubMed1994

Kinetics of lactate transport in sarcolemmal giant vesicles obtained from human skeletal muscle.

We developed a method that allows the measurement of muscle lactate transport in humans. The transport studies were carried out with giant (1.8- to 36-microns-diam) sarcolemmal vesicles obtained by collagenase treatment of needle biopsy material. Marker enzyme analyses demonstrated that the vesicular membrane is predominantly of sarcolemmal origin, contamination with sarcoplasmic reticulum membranes is very low, and mitochondrial membranes are not a major contaminant. The vesicles were loaded with labeled lactate, and the efflux was measured. The system displayed saturation kinetics and inhibitor sensitivity. In equilibrium exchange experiments (pH 7.4, 21 degrees C), the Michaelis-Menten constant (Km) for the carrier-mediated flux was 30 +/- 8 (SD) mM and maximal transport rate (Vmax) was 184 +/- 24 pmol.cm-2.s-1 (142 nmol.mg protein-1.min-1). In zero-trans efflux experiments, Km was 24 +/- 8 mM and Vmax was 81 +/- 11 pmol.cm-2.s-1 (63 nmol.mg protein-1.min-1). In infinite-cis experiments with a variable lactate concentration on the outside of the vesicles, Km was 8 +/- 4 mM and Vmax was 136 +/- 9 pmol.cm-2.s-1 (105 nmol.mg protein-1.min-1). Thus, the system displayed transacceleration. Low pH (6.4) had no significant effect on equilibrium exchange experiments, whereas in zero-trans experiments low pH at the trans side inhibited the flux by 50%. We concluded that lactate transport can be studied in giant vesicles obtained from a single human muscle biopsy. Our data provide evidence for the existence of a lactate carrier in human sarcolemma. This transport system must be taken into account in models of human lactate kinetics.

Adult↗
PubMed1993

Glucose transport and transporters in muscle giant vesicles: differential effects of insulin and contractions.

Collagenase treatment of skeletal muscle results in the formation of large spheres of membranes (3-30 microns diam). A procedure is described for purification and concentration of these giant membrane vesicles prepared from rat muscle. Morphological observations, marker enzyme analysis, and immunoblotting demonstrate that the vesicles are of plasma membrane origin and that sarcoplasmic reticulum, T-tubules, and mitochondrial inner membranes are absent from the preparation. Western blots demonstrate that the vesicles contain GLUT-4 glucose transporters, whereas GLUT-1 could not be detected. Vesicles prepared from control muscle display specific transport of D-glucose with a maximum velocity (Vmax) for glucose influx of approximately 2,500 pmol.mg plasma membrane protein-1.s-1 and an apparent Michaelis constant (Km) of 16 mM measured at zero-trans conditions at room temperature. Muscle contractions in vivo doubled the Vmax of vesicle glucose transport and membrane GLUT-4 content but did not change Km. In contrast, in vivo administration of insulin did not affect vesicle glucose transport or membrane GLUT-4 content. The combination of insulin and contractions caused similar changes as did contractions alone. It is concluded that the present vesicle population contains membrane components almost exclusively derived from the plasma membrane and contains very little if any GLUT-1 but substantial amounts of GLUT-4. Thus the preparation allows the study of transport kinetics of pure GLUT-4 transporters. The procedure for preparing vesicles probably results in activation of the glucose transport system similar to the activation by insulin but not by contractions.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Fansimef for prophylaxis of malaria: a double-blind randomized placebo controlled trial.

At a time when Fansimef, the fixed combination of mefloquine, sulfadoxine and pyrimethamine was considered for prophylaxis of falciparum malaria, a randomized double-blind study comparing the efficacy and tolerability of Fansimef with that of Lariam (mefloquine), Fansidar, chloroquine and placebo in malaria prophylaxis was performed in Thailand from July 1987 to January 1988. The study population of 602 adult males was recruited in Pak Tongchai District, some 360 km North-East of Bangkok, where multiresistant P. falciparum is endemic. All active treatments and placebo were given once weekly for 24 weeks with doses as follows: Fansimef: 125 mg mefloquine + 250 mg sulfadoxine + 12.5 mg pyrimethamine (1 half-strength tablet); Lariam: 125 mg mefloquine (1 half-strength tablet); Fansidar: 500 mg sulfadoxine + 25 mg pyrimethamine; chloroquine; 300 mg. A loading dose of 2 half-strength tablets was given in the Fansimef group in weeks 1 and 2 and in the Lariam group in weeks 1 to 4. The incidence of acute episodes of P. falciparum per 100 person months of prophylaxis was 0.17 each in the Fansimef and the Lariam groups, 1.18 in the Fansidar group, 0.69 in the chloroquine group and 0.64 in the placebo group (differences statistically not significant). Clinically adverse events were reported by 170 subjects (Fansimef 28, Lariam 29, Fansidar 41, choroquine 43, placebo 29; differences statistically not significant). The most frequent adverse events in all groups were headache, sleepiness, dizziness and weakness.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1991

A statistical procedure for the estimation of accuracy parameters in interlaboratory studies.

Interlaboratory studies are conducted to estimate the accuracy of methods of laboratory measurements. The standard parameters used to describe this accuracy are the repeatability and the reproducibility. Usually variance components models are used to estimate these parameters. If the model assumptions are violated the resulting estimates for reproducibility and repeatability may, however, be biased. A new method of residual analysis in variance components models--developed by the author--may be used to detect violations of the model assumptions. If the residual analysis indicates that the model assumptions are violated, a simple robust method--which makes fewer assumptions--may be used for the estimation of accuracy parameters. The application of this residual analysis is demonstrated using data of an interlaboratory study. Graphical methods play an important role in the evaluation of the residuals. The analysis of the residuals uses methods similar to those used for the analysis of Studentized residuals in the linear model. The estimates obtained by the variance components model and the simple robust method are compared. The results of the residual analysis may be used to decide which of the two estimates can be considered more appropriate. The necessity of residual analysis in the analysis of interlaboratory studies by variance components models is pointed out. Potential hazards inherent to residual analysis in variance components models are discussed. Conclusions for the analysis of interlaboratory studies are drawn.

Bias↗
PubMed1988

Effect of adaptation and wavelength on the power spectrum of human oscillatory potentials.

Oscillatory potentials were recorded from four adult subjects under dark- and light-adapted conditions with photopically balanced red and blue flashes. The responses between 80 and 200 Hz were analyzed by means of a Fast Fourier transform program. The results show a robust change in the power--but not in the frequency composition--with the different stimulus conditions. We suggest that an analysis of the total power within this frequency band may provide a quantitative way of evaluating the duplex nature of the oscillatory potentials.

Adaptation, Physiological↗
PubMed1982

Biliary excretion of bisacodyl and picosulphate in man: studies in gallstone patients after biliary tract surgery.

Bisacodyl (=BIS) and picosulphate (=PICO) have been given perorally to postoperative gallstone patients, who have undergone biliary tract surgery with the insertion of an indwelling T-tube. The doses corresponded to 7.7 mg of their common free diphenol desacetylbisacodyl (=DES). The bile was sampled in hourly fraction from the external limb of the T-tube; these fractions were analysed by a modification of the HPLC method previously used to study biliary excretion in the rat. In the BIS-patients (n=8), DES in conjugated form occurred in significant concentration already in the first fractions; peak excretion values equivalent to 4-8 microgram DES/ml bile were reached in 2-5 hours. Unchanged BIS could not be detected, and the concentration levels of unconjugated DES were insignificant. The PICO-patients (n=8) on the other hand showed low DES concentrations (conjugated + free less than or equal to 0.5 microgram DES/ml) in all fractions, or low initial concentrations followed by a more or less pronounced rise in the later fractions. These results are, qualitatively, as in the rat. However, the dose fractions excreted in bile (assuming a total hepatic output of 50ml/hours) seem smaller than those to be expected from rat experiments, at least as far as BIS is concerned.

Adult↗
PubMed1981

Enterohepatic circulation, urinary excretion and laxative action of some bisacodyl derivatives after intragastric administration in the rat.

Bisacodyl (BIS), the parent diphenol (DES) and its sulphuric acid di-ester (picosulphate = PICO) were given by stomach tube to fasted rats at a dose of 3.1 mumol/100 g rat. Bile was sampled in the periods 0-6, 6-12 and 12-18 hrs after drug administration, and assayed for total diphenol (= free + conjugated) by HPLC. Mean fractions (% of dose +/- S.E.M.) excreted in 5 rats per compound and period were: BIS 74.0 +/- 4.7, 51.9 +/- 7.9 and 30.8 +/- 2.5; DES 41.2 +/-4.3, 46.8 +/- 4.7 and 25.1 +/- 2.5; PICO 9.0 +/- 0.9, 26.0 +/- 5.4 and 19.6 +/- 3.1. Only minor amounts were excreted as free diphenol. Urine samples taken by bladder puncture and assayed as above furthermore showed that the renal excretion of total diphenol was insignificant compared to the amounts excreted in bile. Practically no diphenol was present in urine 0-6 hrs after the administration of PICO. In experiments with BIS and DES at 0.85 mumol/100 g, total diphenol excreted in bile during 0-6 hrs was: BIS 67.1 +/- 2.6 (n = 5); DES: 55.4 +/- 3.0 (5). - The latency time for laxative effect was studied in groups of 10 unfasted rats per compound. cumulative time response curves showed that PICO caused diarrhoea more promptly at 0.85 mumol/100 g than either BIS or DES. In most rats, this delayed action of BIS and DES persisted also at 1.7 mumol/100 g. At 3.1 mumol/100 g, however, the majority of the rats reacted as promptly to these two compounds as to PICO. These results are discussed in relation to the biliary excretion experiments, and interpreted in terms of the relative importance at the different dose levels of: 1. The enterohepatic recirculated fraction, and 2. The non-absorbed fraction, which passes directly to the large intestine. For PICO, the latter fraction is the single determinant of the effect, which is triggered when the di-ester is being hydrolyzed to active diphenol in this part of the GI-tract.

Animals↗