Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.3.3.1 (citrate synthase)
4,488 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The main purpose of the present study was to test the hypothesis that adrenergic stimulation of muscle fibres during exercise is a major stimulus for the training-induced enhancement of skeletal muscle respiratory capacity. Therefore, Sprague-Dawley rats either underwent bilateral surgical ablation of the adrenal medulla or were sham-operated. Furthermore, unilateral surgical extirpation of the lumbar sympathetic chain was performed. Half of the rats were then trained for 12 weeks by swimming (up to 5.5 h X day-1, 4 days X week-1) and the remaining rats were sedentary controls. In the gastrocnemius muscle, training significantly increased the mitochondrial enzymes citrate synthase, succinate dehydrogenase, cytochrome c oxidase, and 3-hydroxyacyl-CoA dehydrogenase. In sham-operated rats, the increases were 40%, 43%, 66%, and 25%, respectively, in legs with intact sympathetic innervation. The training-induced enzyme adaptation after adrenodemedullation and/or sympathectomy was not significantly lower than these control values. In sham-operated rats, training decreased resting plasma insulin and glucagon levels and increased liver glycogen content. Similar changes were induced by adrenodemedullation, but training did not augment these changes in adrenodemedullated rats. In conclusion, the data suggest that neither adrenomedullary hormones nor local sympathetic nerves are prerequisites for the training-induced increase in muscle mitochondrial enzymes. The training-induced decline in resting plasma insulin and glucagon levels in intact rats may be mediated by adrenomedullary hormones.
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PMID:Skeletal muscle and hormonal adaptation to physical training in the rat: role of the sympatho-adrenal system. 298 95

Whole-body hypokinetic-hypodynamic (H/H) suspension, unlike other models of muscle disuse, allows voluntary contractile activity. This study examined the oxidative capacity and insulin sensitivity of rat hindlimb muscles subjected to 7 days of suspension H/H conditions. Oxidative capacity was determined by measuring citrate synthase activity and cytochrome c concentration in soleus and gastrocnemius muscles. A perfused hindquarter preparation was used to measure glucose uptake rates at rest with physiological and supramaximal concentrations of insulin in the perfusate. Citrate synthase activity was 17% lower in soleus and 23% lower in gastrocnemius muscles from H/H rats. Similarly, a 29% decrease in H/H rat gastrocnemius cytochrome c concentration was observed. Rates of glucose uptake were lower in muscles from H/H rats compared with controls at physiological levels of insulin and did not increase in response to a further increase in insulin concentration. Muscles undergoing a significant loss in mass after 7 days suspension were found to have increased glycogen concentrations. In conclusion, data presented in this study suggest that hindlimb muscle disuse, brought about by whole-body suspension, results in a decreased aerobic capacity in load bearing muscles and a lowered insulin sensitivity in perfused rat hindlimb muscles.
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PMID:Effect of hypokinesia-hypodynamia on rat muscle oxidative capacity and glucose uptake. 299 97

The effect of 8-wk of treadmill training on plasma glucose, insulin, and lipid concentrations, oral glucose tolerance, and glucose uptake in the perfused hindquarter of normal and streptozocin-treated, diabetic Sprague-Dawley rats was studied. Diabetic rats with initial plasma glucose concentrations of 200-450 mg/dl and control rats were divided into trained and sedentary subgroups. Training resulted in lower plasma free fatty acid concentrations and increased triceps muscle citrate synthase activity in both the control and diabetic rats; triglyceride concentrations were lowered by training only in the diabetic animals. Oral glucose tolerance and both basal and insulin-stimulated glucose uptake in hindquarter skeletal muscle were impaired in the diabetic rats, and plasma glucose concentrations (measured weekly) gradually increased during the experiment. Training did not improve the hyperglycemia, impaired glucose tolerance, or decreased skeletal muscle glucose uptake in the diabetic rats, nor did it alter these parameters in the normal control animals. In considering our results and those of previous studies in diabetic rats, we propose that exercise training may improve glucose homeostasis in animals with milder degrees of diabetes but fails to cause improvement in the more severely insulin-deficient, diabetic rat.
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PMID:Effect of exercise training on glucose homeostasis in normal and insulin-deficient diabetic rats. 304 14

Seven middle-aged men with manifest type II diabetes mellitus underwent an endurance training programme for 10-15 weeks. The maximal aerobic capacity, as well as the endurance capacity, was improved by 10% (p less than 0.05). The intramuscular glycogen store increased by more than 80% (p less than 0.05) from 350 mumol/g dw (dry weight), and the activities of citrate synthase and 3-hydroxy-acyl-CoA dehydrogenase increased by more than 50% (p less than 0.05) and 30% (p less than 0.05). The activity of glycogen synthase was decreased by approximately 20% (p less than 0.05), whereas lactate dehydrogenase remained unchanged. Capillaries/fibre and fibre area increased by more than 50% (p less than 0.05) and 30% (p less than 0.05) leaving the area of supply constant. Training did not influence fasting blood lipids and glucose, glycosylated hemoglobin, oral glucose tolerance, and insulin response to an oral glucose load measured 72 hours post-exercise. It is concluded that patients with manifest type II diabetes, as normoglycaemic individuals, adapt to physical training. However, no persistent effect on glucohomeostasis and lipaemia is produced by short-term training in the diabetic patients.
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PMID:Skeletal muscle adaptations to physical training in type II (non-insulin-dependent) diabetes mellitus. 336 17

With aging, several functions related to the locomotor system will deteriorate. Still, there is a rather well-maintained adaptability for increasing physical activity and for training in the elderly with respect to strength as well as endurance. Part of the observed reduction in muscle function with age could therefore be caused by inactivity. Evidently, however, there is a reduction in muscle mass with age due to loss of motor units. Muscle strength and aerobic power will fall fairly proportionally to the reduction in muscle mass. The muscle changes are, at least up to around the age of 70, more quantitative than qualitative. There is a reduction in the size of the fast-twitch (type II) fibers in the quadriceps, but not in other muscles such as the biceps brachii, presumably due to differences in activity pattern and motor unit recruitment. Aging per se may not reduce oxidative enzymatic capacity in the skeletal muscle. There is maintained potential for increase with endurance training. Thus, as an extreme example in very well trained elderly endurance athletes, high activity of citrate synthase is found and, in connection with that, also low plasma insulin values at baseline as well as after glucose intake. Limitations to aerobic capacity besides the reduced muscle mass are mainly located in the central circulatory and respiratory systems. Comparing the oxygen cost of activities in daily living, such as walking, and the aerobic power of the elderly, suggestions will be given on the choice of training activities.
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PMID:Physical activity and effects of muscle training in the elderly. 340 16

1. The effect of dexamethasone (30 micrograms day-1 100 g-1 body wt.) on the metabolism of glucose and glutamine was studied in the small intestine of rats after 9 days of treatment. 2. Dexamethasone treatment resulted in negative nitrogen balance (P less than 0.001), and produced increases in the concentrations of plasma glucose (22%, P less than 0.05), alanine (32%, P less than 0.001) and insulin (127%, P less than 0.001), but a decrease in the plasma concentration of glutamine (20%, P less than 0.05). 3. Portal-drained visceral blood flow increased by approximately 22% (P less than 0.001) in dexamethasone-treated rats, and was accompanied by a decrease in the arterio-venous concentration difference of glucose (43%, P less than 0.001) and an increase in that of lactate (22%, P less than 0.05), glutamine (35%, P less than 0.01), glutamate (33%, P less than 0.01) and alanine (21%, P less than 0.05). 4. Enterocytes isolated from dexamethasone-treated rats showed decreased and increased rates of glucose and glutamine utilization, respectively. 5. The maximal activities of hexokinase, 6-phosphofructokinase, citrate synthase and oxoglutarate dehydrogenase were decreased (30-64%, P less than 0.001) in intestinal mucosal scrapings of dexamethasone-treated rats, whereas the activity of glutaminase was increased (35%, P less than 0.001). 6. It is concluded that glucocorticoid administration decreases the rate of glucose utilization but increases that of glutamine (both in vivo and in vitro) by the epithelial cells of the small intestine. This may be caused by changes in the maximal activities of key enzymes in the pathways of glucose and glutamine metabolism in these cells.
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PMID:Effect of glucocorticoid treatment on glucose and glutamine metabolism by the small intestine of the rat. 340 28

Female obese and lean Zucker rats were adrenalectomized (ADX) or sham-operated at 4 wk of age. ADX animals were given daily injections of 0.01, 0.05, 0.50, 1.0, or 2.0 mg hydrocortisone/100 g body wt for 30 days. ADX rats gained less weight than sham-operated controls. Obese ADX rats at the lowest dose (0.01) had a net positive energy gain but lost body fat. As steroid dose increased, obese rats deposited more fat and less protein. Doses of 0.01 and 0.05 mg produced rats that were less fat than sham-operated controls, whereas doses of 0.50, 1.0, and 2.0 mg produced rats of comparable body fat composition. Obese rats were consistently fatter and had a significantly smaller percentage body protein than lean rats at each dose. Body fat elevation was reflected by heavier parametrial and retroperitoneal fat depots and larger fat cells at all doses except the lowest. Compared with sham-operated controls, lean and obese rats at the two lowest replacement doses (0.01, 0.05) exhibited significantly decreased plasma insulin and triglyceride levels and significantly elevated brown adipose tissue protein content and citrate synthase (CS) activity. Obese rats at these doses had significantly reduced adipose tissue lipoprotein lipase (LPL) activity in the retroperitoneal depot and lower food intake. Furthermore, these obese rats had adipose depot weights, cell sizes, LPL activity, and plasma insulin, glucose, and triglyceride comparable to that of lean sham-operated controls. As steroid dose increased (0.5, 1.0, 2.0), plasma insulin and triglyceride and food intake markedly increased only in obese rats. Adipose tissue LPL activity appeared unaffected by dose. Brown adipose tissue protein content and CS activity significantly decreased as dose increased in both lean and obese rats. At all doses of replacement obese rats were more responsive to steroid than were lean rats. Obese rats receiving 0.01 mg had comparable fat depot weights, cell sizes, and plasma insulin and triglyceride as lean rats receiving 50 times as much steroid per day (0.50 mg). These results suggest glucocorticoids play an important role in the early development of obesity in the Zucker rat and support the hypothesis that obese rats are more responsive to glucocorticoids than are lean rats.
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PMID:Effect of adrenalectomy and glucocorticoid replacement on development of obesity. 351 71

Men with regular physical training habits voluntarily increased their dietary fat intake from 43 to 54% of energy (E%) for four weeks. This was followed by a low-fat (29 E%), high-carbohydrate diet for another four weeks. During the high-fat diet period, the muscle lipoprotein lipase activity (LPLA) increased from 59 +/- 8 to 106 +/- 12 mU/g (mean +/- SE) (P less than 0.05). After the high-carbohydrate diet, LPLA was 57 +/- 16 mU/g, and unchanged relative to the pre-trial value. The triglyceride content in m. vastus lateralis increased from 30 +/- 4 to 47 +/- 9 mmol/kg d.w. (P less than 0.05; mean +/- SE) following the high-fat diet and to 41 +/- 8 following the high-carbohydrate diet. Neither of the diets affected the serum triglyceride and insulin concentrations, nor glucose, glycerol, beta-hydroxybutyrate, citrate and lactate levels in the blood. Nor did they alter enzyme activities in muscle used as markers for the oxidative (citrate synthase, beta-hydroxy-acyl CoA dehydrogenase) and glycolytic (glyceraldehyde phosphate dehydrogenase, lactate dehydrogenase) capacity. It is concluded that one month's adaptation to a high-fat diet results in increased muscle-LPL activity indicating a higher capacity for uptake of fatty acids from circulating serum triglycerides into the muscle cell in association with a greater capacity for triglyceride storage in the muscle. Under these conditions serum triglycerides were not decreased despite the increased muscle LPLA, and serum insulin variations could not explain the change in muscle LPLA.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lipoprotein lipase activity and intramuscular triglyceride stores after long-term high-fat and high-carbohydrate diets in physically trained men. 354 51

Exercise has been shown to increase insulin sensitivity, and muscle is quantitatively the most important tissue of insulin action. Since the first step in insulin action is the binding to a membrane receptor, we postulated that exercise training would change insulin receptors in muscle and in this study we have investigated this hypothesis. Female rats initially weighing approximately 100 g were trained by treadmill running for 2 h/day, 6 days/wk for 4 wk at 25 m/min (0 grade). Insulin receptors from vastus intermedius muscles were solubilized by homogenizing in a buffer containing 1% Triton X-100 and then partially purified by passing the soluble extract over a wheat germ agglutinin column. The 4 wk training regimen resulted in a 65% increase in citrate synthase activity in red vastus lateralis muscle, indicating an adaptation to exercise. Insulin binding by the partially purified receptor preparation s was approximately doubled in muscle of trained rats at all insulin concentrations, suggesting an increase in the number of receptors. Training did not alter insulin receptor structure as evidenced by electrophoretic mobility under reducing and nonreducing conditions. Basal insulin receptor protein kinase activity was higher in trained than untrained animals and this was likely due to the greater number of receptors. However, insulin stimulation of the protein kinase activity was depressed by training. These results demonstrate that endurance training does alter receptor number and function in muscle and these changes may be important in increasing insulin sensitivity after exercise training.
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PMID:Insulin receptor binding and protein kinase activity in muscles of trained rats. 354 17

Six men and three women with insulin-dependent diabetes (without complications) participated in physical training three times a week for 20 weeks. Physical training did not change the concentration of fasting blood-glucose, glucose excretion in urine or glucosylated haemoglobin (HbA1). However, the glucose disposal rate during euglycaemic clamp increased after training. In two patients a minor reduction of insulin dosage was necessary to alleviate slight hypoglycaemic episodes. The training resulted in significant increases in quadriceps isometric and dynamic strength and endurance. Maximal oxygen uptake increased by 8%, the activity of glycolytic enzymes in vastus lateralis muscle by 47% for hexokinase, and 30% for tri-osephosphate dehydrogenase and 25% for lactic dehydrogenase, the activity of oxidative enzymes by 42% for citrate synthase and 46% for 3-hydroxy-acyl-CoA-dehydrogenase. The glycogen concentration in the vastus lateralis muscle did not change significantly. Lipoprotein lipase activity did not change in muscle, nor in adipose tissue. The mean muscle fibre area increased by 25% and the area of FTa fibres by 30%. The new formation of capillaries around different muscle fibres was significant for FTb fibres (26%). The proliferation of capillaries, however, appeared to be insufficient to cope with the increased area of muscle fibres. As a result, the mean area of muscle fibre supplied by one capillary (a measure of diffusion distance) significantly increased after training for FTa fibres. It is concluded that with the exception of deficient proliferation of capillaries, patients with insulin-dependent diabetes mellitus show a normal central and peripheral adaptation to physical training. Physical training does not apparently improve blood glucose control in most cases, despite an increased insulin sensitivity.
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PMID:Muscle adaptations and glucose control after physical training in insulin-dependent diabetes mellitus. 394 85


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