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Biomedical subjects

H Wallberg-Henriksson

Publications and source records attributed to H Wallberg-Henriksson.

At least 73 records · Page 4Linked to original sources
PubMed1991

Effect of human C-peptide on glucose transport in in vitro incubated human skeletal muscle.

Muscle specimens from the quadriceps femoris muscle were obtained from eight healthy subjects by means of an open muscle biopsy and prepared for in vitro incubation. C-peptide at 0.5, 1.0 and 2.5 nmol/l increased 3-0-methylglucose transport by 38% (NS), 64% (p less than 0.05), and 64% (p less than 0.05) respectively. Glucose transport increased 1.8-fold in the presence of 0.3 nmol/l of insulin (p less than 0.05). Glycogen content in muscle strips exposed to C-peptide at a concentration of 1 nmol/l increased significantly by 22% (p less than 0.05). In conclusion, C-peptide stimulates the rate of 3-0-methylglucose transport in in vitro incubated human skeletal muscle strips in a dose-response manner. These observations suggest that C-peptide may contribute to the regulation of carbohydrate metabolism in human skeletal muscle.

3-O-Methylglucose↗
PubMed1991

Decreased insulin-stimulated 3-0-methylglucose transport in in vitro incubated muscle strips from type II diabetic subjects.

Peripheral insulin resistance in type II diabetes mellitus has been attributed to alterations in skeletal muscle glucose metabolism. However the direct dose-response relationship between insulin and glucose transport has not yet been studied in human skeletal muscle. We investigated 3-0-methylglucose transport in in vitro incubated skeletal muscle strips from eight healthy controls (age 61 +/- 6 yrs) and six lean type II diabetic patients treated with oral antidiabetic medication (age 73 +/- 3 yrs). Rectus abdominis muscle samples (approximately 1 g), obtained during elective abdominal surgery, were clamped at their resting length in vivo, whereupon strips (20-50 mg) were prepared for in vitro incubation. Measurements of high-energy phosphates and glycogen levels revealed that the muscle strips maintained energy levels during the incubation period. Glucose transport responded to insulin in a dose-response manner in the control group, with a 2-fold increase following maximal stimulation. Muscle strips from the diabetic group demonstrated a marked decrease in the insulin dose-response curve (P less than 0.01), when compared to healthy muscle strips. At a maximal insulin concentration (10,000 microU x ml-1), the response of the diabetic muscle tissue was 50% less than that of the healthy control tissue (P less than 0.05). This report demonstrates a dose-response curve for insulin stimulated 3-0-methylglucose transport in in vitro incubated human skeletal muscle strips. Furthermore, in type II diabetic muscle, our results provide evidence for one or several defects at a postreceptor level.

3-O-Methylglucose↗
PubMed1991

Metformin increases insulin-stimulated glucose transport in insulin-resistant human skeletal muscle.

The effect of metformin (0.1 mM) on glucose transport was investigated in healthy control and in insulin-resistant human skeletal muscle. Muscle samples (200-400 mg) were obtained from the rectus abdominis muscle (abdominal surgery) or from the vastus lateralis portion of the quadriceps femoris muscle (open biopsy technique) from 8 healthy controls (age 38 +/- 4 yrs, BMI 23 +/- 1) and from 6 insulin-resistant subjects (age 53 +/- 5 yrs, BMI 30 +/- 2). Metformin had no effect on basal or insulin-stimulated (100 microU/ml) 3-0-methylglucose transport in incubated muscle strips from healthy subjects. Muscle tissue from the insulin resistant group did not respond to 100 microU/ml of insulin (0.73 +/- 0.17 for basal and 0.81 +/- 0.22 mumol x ml-1 x h-1 for insulin-stimulation, NS). Basal glucose transport was unaffected by metformin, whereas insulin-stimulated (100 microU/ml) glucose transport was increased by 63% in the insulin-resistant muscles (0.73 +/- 0.17 in the absence vs 1.19 +/- 0.18 mumol x ml-1 x h-1 in the presence of metformin, p less than 0.05). In conclusion, metformin abolishes insulin-resistance in human skeletal muscle by normalizing insulin-stimulated glucose transport accross the muscle cell membrane. The mechanism for this effect remains to be elucidated.

3-O-Methylglucose↗
PubMed1989

Effects of adrenaline and prior exercise on the release of alanine, glutamine and glutamate from incubated rat skeletal muscle.

Catecholamines have been proposed as important regulators of the rate of amino acid release from skeletal muscle. In the present study, we have investigated the influence of adrenergic action and its possible interaction with exercise on muscle release and tissue content of alanine, glutamine and glutamate. For this purpose epitrochlearis muscles were dissected from resting and exercised (1 and 2 h) rats and incubated for 1 h in the presence or absence of adrenaline. In addition, muscles from water-immersed resting rats were included to separate the influence of the stress involved in the swimming exercise from that of muscle contractile activity per se. In muscles from untreated resting rats, the release, tissue content and total amount (released amount + tissue content) of the three amino acids were not influenced by 10(-7) M adrenaline; when the adrenaline concentration was raised to 10(-5) M only the tissue content of glutamate was significantly changed (-50%, P less than 0.001). However, in muscles of rats subjected to 2 h prior exercise or water immersion, 10(-7) M adrenaline significantly increased the release of glutamine (+ 48% and +34%, P less than 0.05) and glutamate (+38% and +27%, P less than 0.05). Moreover, 1 h of water immersion resulted in a significant increase in muscle glutamine and glutamate compared to values from the exercised and control rats. The data suggest that adrenergic action is involved in the regulation of muscle amino acid transport during exercise and that the stress involved in exercise may mask the influence of contractile activity per se on formation of amino acids in skeletal muscle.

Alanine↗
PubMed1989

Prolonged increase in insulin-stimulated glucose transport in muscle after exercise.

Exercise can induce short-term increases in the sensitivity and responsiveness of skeletal muscle glucose transport to insulin. The purpose of this study was to determine the effect of carbohydrate deprivation on the persistence of increased insulin sensitivity and responsiveness after a bout of exercise. Three hours after a bout of exercise, epitrochlearis muscles from carbohydrate-deprived (fat fed) rats showed a 25% greater increase in 3-O-methylglucose (3-MG) transport in response to a maximal insulin stimulus compared with muscles of nonexercised rats; this increase in insulin responsiveness had reversed 18 h postexercise. Muscles of rats fed carbohydrate showed no increase in insulin responsiveness 3 h after exercise. The effect of 60 microU/ml of insulin on 3-MG transport was approximately twofold greater in muscles studied 3 h after exercise than in nonexercised controls regardless of dietary carbohydrate intake. This increase in insulin sensitivity was lost within 18 h in carbohydrate-fed rats but persisted for at least 48 h in carbohydrate-deprived rats. Muscle glycogen increased approximately 41 mumol/g in the rats fed carbohydrate for 18 h, and only approximately 14.5 mumol/g in the rats fed fat for 48 h, after exercise. The persistent increase in insulin sensitivity after exercise in carbohydrate-deprived rats was unrelated to caloric intake, as muscles of fasted and fat-fed rats behaved similarly.

3-O-Methylglucose↗
PubMed1989

Indirect effect of catecholamines on development of insulin resistance in skeletal muscle from diabetic rats.

The role of an increased sympathetic activation in the development of insulin resistance in diabetic skeletal muscle was investigated. Epitrochlearis muscles from rats with streptozocin-induced diabetes and from controls were incubated in vitro for 0.5-12.0 h. Diabetes decreased maximal insulin-stimulated (20 mU/ml) glucose transport capacity by 60% (P less than .001), but this decreased insulin responsiveness returned to normal on in vitro incubation (3.79 +/- 0.59 before vs. 8.92 +/- 0.64 mumol.ml-1.h-1 after 12 h of incubation). The reversal of decreased insulin responsiveness in diabetic muscles did not require the presence of insulin and was not affected by the presence of 5.0 x 10(-8) M of epinephrine. However, it was possible to partially prevent the development of insulin resistance with regard to glucose transport by treating the rats with the beta-adrenergic antagonist propranolol (0.5 mg/kg) every 12 h during the entire 72-h period in which the animals were kept diabetic (insulin responsiveness was 3.16 +/- 0.40 mumol.ml-1.h-1 for saline-injected group vs. 5.55 +/- 0.46 mumol.ml-1.h-1 for propranolol-treated group). This effect was not present after a single injection of the drug 2 h before the experiment or when propranolol treatment was withdrawn 12 h before the experiment. The beta-adrenergic blockade markedly reduced the plasma concentration of free fatty acids (0.5 +/- 0.01 mumol/ml for propranolol-treated rats vs. 1.1 +/- 0.1 mumol/ml for saline-treated rats; P less than .001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1989

Acute exercise: fuel homeostasis and glucose transport in insulin-dependent diabetes mellitus.

Fuel homeostasis and blood glucose levels are remarkably well maintained during exercise in healthy individuals. However, in insulin-dependent diabetics, the very basis for fuel homeostasis adjustments, i.e., a normal endogenous insulin production, is absent. The metabolic alterations characterizing diabetes may, therefore, under certain circumstances lead to pertubations of fuel homeostasis. Thus, exercise in the hyperinsulinemic patients may result in hypoglycemic reactions and, in hypoinsulinemic patients, in increased blood glucose levels. In addition, diabetes mellitus is associated with peripheral insulin resistance, which may result in a deterioration of the overall glucose homeostasis and consequently make the treatment more difficult to manage. Regular physical activity has been shown to normalize the peripheral insulin resistance in insulin-dependent diabetics. Knowledge about these responses is important in order to enable this patient group to participate in physical activities on the same conditions as non-diabetics. However, advice on how insulin-dependent diabetics should adjust insulin or diet before exercise is difficult to give due to high interindividual variability in response to exercise. Thus, individualized recommendations for exact treatment modification in association with exercise are necessary.

Diabetes Mellitus, Type 1↗
PubMed1988

Acute exercise increases the number of plasma membrane glucose transporters in rat skeletal muscle.

To determine whether increased glucose transport following exercise is associated with an increased number of glucose transporters in muscle plasma membranes, the D-glucose inhibitable cytochalasin B binding technique was used to measure glucose transporters in red gastrocnemius muscle from exercised (1 h treadmill) or sedentary rats. Immediately following exercise there was a 2-fold increase in cytochalasin B binding sites, measured in purified plasma membranes enriched 30-fold in 5'-nucleotidase activity. This increase in glucose transporters in the plasma membrane may explain in part, the increase in glucose transport rate which persists in skeletal muscle following exercise. Where these transporters originate, remains to be elucidated.

5'-Nucleotidase↗
PubMed1988

Glucose transport into rat skeletal muscle: interaction between exercise and insulin.

This study was done to evaluate the effect of insulin on sugar transport into skeletal muscle after exercise. The permeability of rat epitrochlearis muscle to 3-O-methylglucose (3-MG) was measured after exposure to a range of insulin concentrations 30, 60, and 180 min after a bout of exercise. Thirty and 60 min after exercise, the effects of exercise and insulin on 3-MG transport were additive over a wide range of insulin concentrations, with no increase in sensitivity or responsiveness to insulin. After 180 min, when approximately 66% of the exercise-induced increase in sugar transport had worn off, both the responsiveness and sensitivity of the glucose transport process to insulin were increased. These findings appear compatible with the hypothesis that the actions of exercise and insulin result in activation and/or translocation into the plasma membrane of two separate pools of glucose transporters in mammalian skeletal muscle.

3-O-Methylglucose↗
PubMed1987

Reversibility of decreased insulin-stimulated glucose transport capacity in diabetic muscle with in vitro incubation. Insulin is not required.

The mechanisms by which insulin deficiency affects muscle glucose transport were investigated. Epitrochlearis muscles from rats with streptozotocin-induced diabetes and from controls were incubated in vitro for 0.5-14 h. The incubation was shown not to impair muscle energy stores or tissue oxygenation. Diabetes decreased basal 3-O-methylglucose transport by 40% (p less than 0.01), and insulin-stimulated (20 milli-units/ml) glucose transport capacity by 70% (p less than 0.001). In vitro incubation gradually normalized insulin responsiveness (3.77 +/- 0.38 before versus 8.97 +/- 0.65 mumol X ml-1 X h-1 after 12 h of incubation). Basal glucose transport remained significantly reduced. The reversal of the insulin responsiveness did not require the presence of rat serum and, furthermore, took place even in the absence of insulin. In fact, insulin responsiveness was higher after incubation (14 h) with no insulin than with 100 microunits/ml insulin (9.85 +/- 0.59 versus 8.06 +/- 0.59 mumol X ml-1 X h-1, p less than 0.05). Glucose at 30 mM did not affect the normalization of the insulin-stimulated glucose transport capacity, whereas incubation in serum from diabetic rats resulted in a slightly (26%) blunted reversal (7.60 +/- 0.39 versus 8.89 +/- 0.45 mumol X ml-1 X h-1 with diabetic versus control serum for 14 h, p less than 0.05; before incubation the value was 3.87 +/- 0.40). Inhibition of protein synthesis by cycloheximide blocked the normalization by 80%. These results suggest the presence in diabetic serum of some labile factor that might inhibit the glucose transport system. The results indicate that the decreased insulin-stimulated glucose transport capacity, in the insulin-deficient diabetic muscle, is not a direct consequence of the lack of insulin or of high glucose concentrations.

3-O-Methylglucose↗
PubMed1987

Reversal of the exercise-induced increase in muscle permeability to glucose.

Exercise is associated with an increase in permeability of muscle to glucose that reverses slowly (h) in fasting rats during recovery. Previous studies showed that carbohydrate feeding speeds and carbohydrate restriction slows reversal of the exercise-induced increase in glucose uptake. This study was designed to evaluate the roles of glucose transport, glycogen synthesis, and protein synthesis in the reversal process in rat epitrochlearis muscle. In contrast to recovery in vivo, when muscles were incubated without insulin in vitro, the exercise-induced increase in muscle permeability to sugar reversed rapidly regardless of whether glucose transport or glycogen synthesis occurred. Inhibition of protein synthesis did not prevent the reversal. Addition of 33% rat serum or a low concentration of insulin to the incubation medium markedly slowed reversal in vitro. We conclude that 1) prolonged persistence of the increased permeability of mammalian muscle to glucose after exercise requires a low concentration of insulin, and 2) reversal of the increase in permeability does not require glucose transport, glycogen synthesis, or protein synthesis.

Animals↗
PubMed1987

Glucose transport into skeletal muscle. Influence of contractile activity, insulin, catecholamines and diabetes mellitus.

The influence of contractile activity, insulin, catecholamines and diabetes mellitus on the acute as well as long-term regulation of glucose transport into skeletal muscle was investigated. In Paper I, glucose uptake was determined in the perfused hindlimb preparation; in Papers II-VI the glucose transport process was studied independently of glucose metabolism by determining the uptake of the non-metabolizable glucose analogue 3-O-methylglucose into isolated rat epitrochlearis muscles. The main findings are: Acute regulation of muscle glucose transport: 1. Muscle contraction-induced glucose uptake does not require the presence of insulin. 2. Exercise and a maximal insulin stimulus have additive effects on glucose transport. 3. Catecholamines decrease non-insulin-mediated glucose transport in the absence of albumin, whereas in the presence of albumin an enhancement occurs. 4. The effects of catecholamines are abolished during beta-adrenergic blockade, but remain unaffected during alpha-adrenergic blockade. Long-term regulation of muscle glucose transport: 5. The rat epitrochlearis muscle, a thin, predominantly fast-twitch muscle of the forearm, was shown to be a suitable preparation for the study of factors regulating glucose transport capacity on a long-term basis, since it maintains energy stores and tissue oxygenation for periods of at least 14 h. 6. Sustained insulin deficiency results in marked decreases in basal (40-45%), contraction-induced (50-60%), and insulin-stimulated (65-70%) glucose transport into rat epitrochlearis muscle. 7. The decreased contraction-induced glucose transport capacity can be prevented by frequent exercise during the period of insulin deficiency. 8. The decreased insulin responsiveness of the muscle glucose transport system can be reversed either by treating previously untreated diabetic rats with insulin or by in vitro incubation of the muscles for 12-14 hours. 9. The in vitro normalization of the insulin-stimulated glucose transport capacity (a) does not require the presence of serum or insulin, (b) occurs despite high (30 mM) concentrations of glucose, (c) is incomplete in the presence of diabetic serum and (d) is blocked to the amount of 30-80% in the presence of protein synthesis inhibition. On the basis of these findings, the following is concluded: Muscle contraction can activate the glucose transport system independently of insulin.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenergic alpha-Antagonists↗
PubMed1986

Long-term physical training in female type 1 (insulin-dependent) diabetic patients: absence of significant effect on glycaemic control and lipoprotein levels.

No objective evidence has been presented to support the beneficial effect of physical training on glycaemic control in Type 1 (insulin-dependent) diabetic patients trained two to three times a week for several months. In the present study we examined the possibility that a daily exercise programme would be more suitable for improving glycaemic control. Thirteen patients completed a 5-month study; 6 were randomized to exercise training (20 min daily bicycle exercise) and 7 served as non-exercising controls. The training resulted in an 8% increase in maximal oxygen uptake (p less than 0.05). No change in glycaemic control occurred during the study period in either group. In addition, serum lipid and lipoprotein levels were followed. Total cholesterol decreased during the study period irrespective of training. No effect was noted on the levels of LDL, VLDL, HDL and HDL2 cholesterol. A significant training effect was obtained in the HDL3 subfraction (-10%, p less than 0.05). Total triglycerides were unchanged, but a decrease in the level of LDL triglycerides was observed with training (-12%, p less than 0.01). It is concluded that, in female Type 1 diabetic patients, daily physical training for several months does not improve glycaemic control and results only in minor changes in serum lipoprotein profiles.

Adult↗
PubMed1986

Repeated exercise regulates glucose transport capacity in skeletal muscle.

The present study was undertaken to test the hypothesis that a muscle's habitual level of contractile activity might act as a long-term regulator of glucose transport capacity. Rats were rendered severely diabetic by injection of streptozotocin, 125 mg kg-1 body wt. Three days after the injection, insulin-stimulated and contraction-induced 3-methylglucose transport in the in vitro epitrochlearis muscle preparation was reduced to 25% and 52% of control capacity, respectively (P less than 0.001). However, when repeated 1-h swimming sessions (twice a day) were introduced during the 3 days of insulin deficiency, the reduction in contraction-induced glucose transport capacity was completely abolished. This indicates that the habitual level of contractile activity of a muscle regulates its capacity for exercise-stimulated glucose transport. Furthermore, one exercise session and a maximal insulin stimulus had an additive effect on 3-methylglucose transport, suggesting that there are two pools of intracellular glucose transporters or two mechanisms for mobilizing the same pool.

3-O-Methylglucose↗