Biomedical subjects

K Kawanaka

Publications and source records attributed to K Kawanaka.

18 recordsLinked to original sources

PubMed2006

Usefulness of measurement of the temporal stem on magnetic resonance imaging in the diagnosis of frontotemporal dementia.

PURPOSE: To investigate whether measurements of brain structures on routine magnetic resonance (MR) images can be used to distinguish between normal subjects and patients with frontotemporal dementia (FTD) or Alzheimer's disease (AD). MATERIAL AND METHODS: MRI studies were performed on 30 patients with dementia (FTD, n = 15; AD, n = 15) and 15 age-matched controls. Width measurements, obtained at the corpus callosum, the cingulate gyri, the hippocampi, and the temporal stem of the anterior temporal lobes, were compared among FTD and AD patients and control subjects on oblique-coronal T2-weighted images. RESULTS: The width of the temporal stem was significantly narrower in FTD than in AD patients and control subjects (6.3 +/- 1.3 mm, 7.8 +/- 1.1 mm, and 8.2 +/- 0.9 mm, respectively) (P < 0.05), although there was some overlapping between AD and FTD patients. All patients whose temporal stem width was < 6 mm had FTD. While the width of the corpus callosum, cingulate gyri, and hippocampi was significantly narrower in patients with AD and FTD than in the controls, there was no significant difference between the AD and FTD patients. CONCLUSION: The width of the temporal stem was significantly narrower in patients with FTD than in those with AD and controls. The described measurements can easily be obtained and may be useful for the diagnosis of FTD.

Aged↗

PubMed2005

Effects of high-intensity intermittent swimming on PGC-1alpha protein expression in rat skeletal muscle.

AIM: The aim of the present investigation was to elucidate the effects of exercise intensity on exercise-induced expression of peroxisome proliferator-activated receptor gamma coactivator-1alpha (PGC-1alpha) protein in rat skeletal muscle. METHODS: We measured PGC-1alpha content in the skeletal muscles of male Sprague-Dawley rats (age: 5-6 weeks old; body weight: 150-170 g) after a single session of high-intensity intermittent exercise (HIE) or low-intensity prolonged swimming exercise (LIE). During HIE, the rats swam for fourteen 20-s periods carrying a weight (14% of body weight), and the periods of swimming were separated by a 10-s pause. LIE rats swam with no load for 6 h in two 3-h sessions, separated by 45 min of rest. RESULTS: After HIE, the PGC-1alpha protein content in rat epitrochlearis muscle had increased by 126, 140 and 126% at 2, 6 and 18 h, respectively, compared with that of the age-matched sedentary control rats' muscle. Immediately, 6 and 18-h after LIE, the PGC-1alpha protein content in the muscle was significantly elevated by 84, 95 and 67% respectively. The PGC-1alpha protein content observed 6 h after HIE tended to be higher than that observed after LIE. However, there was no statistically significant difference between the two values (P = 0.12). CONCLUSION: The present investigation suggests that irrespective of the intensity of the exercise, PGC-1alpha protein content in rat skeletal muscle increases to a comparable level when stimuli induced by different protocols are saturated. Further, HIE is a potent stimulus for enhancing the expression of PGC-1alpha protein, which may induce mitochondrial biogenesis in exercise-activated skeletal muscle.

Adenylate Kinase↗

PubMed2001

Development of glucose-induced insulin resistance in muscle requires protein synthesis.

Muscles and fat cells develop insulin resistance when exposed to high concentrations of glucose and insulin. We used an isolated muscle preparation incubated with high levels of glucose and insulin to further evaluate how glucose-induced insulin resistance (GIIR) is mediated. Incubation with 2 milliunits/ml insulin and 36 mm glucose for 5 h resulted in an approximately 50% decrease in insulin-stimulated muscle glucose transport. The decrease in insulin responsiveness of glucose transport induced by glucose was not due to impaired insulin signaling, as insulin-stimulated phosphatidylinositol 3-kinase activity and protein kinase B phosphorylation were not reduced. It has been hypothesized that entry of glucose into the hexosamine biosynthetic pathway with accumulation of UDP-N-acetylhexosamines (UDP-HexNAcs) mediates GIIR. However, inhibition of the rate-limiting enzyme GFAT (glutamine:fructose-6-phosphate amidotransferase) did not protect against GIIR despite a marked reduction of UDP-HexNAcs. The mRNA synthesis inhibitor actinomycin D and the protein synthesis inhibitor cycloheximide both completely protected against GIIR despite the massive increases in UDP-HexNAcs and glycogen that resulted from increased glucose entry. Activation of AMP-activated protein kinase also protected against GIIR. These results provide evidence that GIIR can occur in muscle without increased accumulation of hexosamine pathway end products, that neither high glycogen concentration nor impaired insulin signaling is responsible for GIIR, and that synthesis of a protein with a short half-life mediates GIIR. They also suggest that dephosphorylation of a transcription factor may be involved in the induction of GIIR.

Animals↗

PubMed2001

Effects of high-intensity swimming training on GLUT-4 and glucose transport activity in rat skeletal muscle.

This study was performed to assess the effects of short-term, extremely high-intensity intermittent exercise training on the GLUT-4 content of rat skeletal muscle. Three- to four-week-old male Sprague-Dawley rats with an initial body weight ranging from 45 to 55 g were used for this study. These rats were randomly assigned to an 8-day period of high-intensity intermittent exercise training (HIT), relatively high-intensity intermittent prolonged exercise training (RHT), or low-intensity prolonged exercise training (LIT). Age-matched sedentary rats were used as a control. In the HIT group, the rats repeated fourteen 20-s swimming bouts with a weight equivalent to 14, 15, and 16% of body weight for the first 2, the next 4, and the last 2 days, respectively. Between exercise bouts, a 10-s pause was allowed. RHT consisted of five 17-min swimming bouts with a 3-min rest between bouts. During the first bout, the rat swam without weight, whereas during the following four bouts, the rat was attached to a weight equivalent to 4 and 5% of its body weight for the first 5 days and the following 3 days, respectively. Rats in the LIT group swam 6 h/day for 8 days in two 3-h bouts separated by 45 min of rest. In the first experiment, the HIT, LIT, and control rats were compared. GLUT-4 content in the epitrochlearis muscle in the HIT and LIT groups after training was significantly higher than that in the control rats by 83 and 91%, respectively. Furthermore, glucose transport activity, stimulated maximally by both insulin (2 mU/ml) (HIT: 48%, LIT: 75%) and contractions (25 10-s tetani) (HIT: 55%, LIT: 69%), was higher in the training groups than in the control rats. However, no significant differences in GLUT-4 content or in maximal glucose transport activity in response to both insulin and contractions were observed between the two training groups. The second experiment demonstrated that GLUT-4 content after HIT did not differ from that after RHT (66% higher in trained rats than in control). In conclusion, the present investigation demonstrated that 8 days of HIT lasting only 280 s elevated both GLUT-4 content and maximal glucose transport activity in rat skeletal muscle to a level similar to that attained after LIT, which has been considered a tool to increase GLUT-4 content maximally.

Animals↗

PubMed2001

The HIV protease inhibitor indinavir decreases insulin- and contraction-stimulated glucose transport in skeletal muscle.

In many patients with human immunodeficiency virus (HIV) treated with HIV protease inhibitors, a complication develops that resembles abdominal obesity syndrome, with insulin resistance and glucose intolerance that, in some cases, progresses to diabetes. In this study, we tested the hypothesis that indinavir, an HIV-protease inhibitor, directly induces insulin resistance of glucose transport in skeletal muscle. Rat epitrochlearis muscles were incubated with a maximally effective insulin concentration (12 nmol/l) and 0, 1, 5, 20, or 40 micromol/l indinavir for 4 h. In control muscles, insulin increased 3-O-[(3)H]methyl-D-glucose (3MG) transport from 0.15 +/- 0.03 to 1.10 +/- 0.05 micromol. ml(-)(1). 10 min(-)(1). Incubation of muscles with 5 micromol/l indinavir reduced the insulin-stimulated increase in 3MG transport by 40%, whereas 20 micromol/l indinavir reduced the insulin-stimulated increase in 3MG transport by 58%. Indinavir induced a similar reduction in maximally insulin-stimulated 3MG transport in the soleus muscle. The increase in glucose transport activity induced by stimulating epitrochlearis muscles to contract was also markedly reduced by indinavir. The insulin-stimulated increase in cell-surface GLUT4, assessed using the 2-N-4-(1-azi-2,2,2-trifluoroethyl)benzoyl-1,3-bis-[2-(3)H] (D-mannose-4-yloxy)-2-propylamine exofacial photolabeling technique, was reduced by approximately 70% in the presence of 20 micromol/l indinavir. Insulin stimulation of phosphatidylinositol 3-kinase activity and phosphorylation of protein kinase B were not decreased by indinavir. These results provide evidence that indinavir inhibits the translocation or intrinsic activity of GLUT4 rather than insulin signaling.

Animals↗

PubMed2000

Mechanisms underlying impaired GLUT-4 translocation in glycogen-supercompensated muscles of exercised rats.

Exercise training induces an increase in GLUT-4 in muscle. We previously found that feeding rats a high-carbohydrate diet after exercise, with muscle glycogen supercompensation, results in a decrease in insulin responsiveness so severe that it masks the effect of a training-induced twofold increase in GLUT-4 on insulin-stimulated muscle glucose transport. One purpose of this study was to determine whether insulin signaling is impaired. Maximally insulin-stimulated phosphatidylinositol (PI) 3-kinase activity was not significantly reduced, whereas protein kinase B (PKB) phosphorylation was approximately 50% lower (P < 0.01) in muscles of chow-fed, than in those of fasted, exercise-trained rats. Our second purpose was to determine whether contraction-stimulated glucose transport is also impaired. The stimulation of glucose transport and the increase in cell surface GLUT-4 induced by contractions were both decreased by approximately 65% in glycogen-supercompensated muscles of trained rats. The contraction-stimulated increase in AMP kinase activity, which has been implicated in the activation of glucose transport by contractions, was approximately 80% lower in the muscles of the fed compared with the fasted rats 18 h after exercise. These results show that both the insulin- and contraction-stimulated pathways for muscle glucose transport activation are impaired in glycogen-supercompensated muscles and provide insight regarding possible mechanisms.

3-O-Methylglucose↗

PubMed2000

Superselective embolisation for intractable idiopathic epistaxis.

37 patients with intractable idiopathic epistaxis were treated with superselective embolisation between 1995 and 1999. A total of 40 embolisations was performed, including three procedures for recurrence. The embolic material was gelatin sponge in 27 procedures, microcoils in 9 and both gelatin sponge and microcoils in 4. Immediate cessation of nasal bleeding was obtained in all patients after embolisation. Recurrent epistaxis occurred in 2 (5.4%) of the 37 patients within 7 days after initial embolisation, giving a short-term success rate of 94.6%. The long-term follow-up ranged from 1-51 months (mean 21.6 months). Late re-bleeding occurred in two patients, giving a long-term success rate of 94.6%. Two patients underwent re-embolisation; it was necessary to embolise the ipsilateral facial artery and/or the contralateral internal maxillary as well as the ipsilateral maxillary artery. Although the overall complication rate was 45.0%, no major complications occurred. Superselective embolisation with gelatin sponge is an effective and safe treatment technique for intractable idiopathic epistaxis.

Adult↗

PubMed1999

Decreased insulin-stimulated GLUT-4 translocation in glycogen-supercompensated muscles of exercised rats.

It was recently found that the effect of an exercise-induced increase in muscle GLUT-4 on insulin-stimulated glucose transport is masked by a decreased responsiveness to insulin in glycogen-supercompensated muscle. We evaluated the role of hexosamines in this decrease in insulin responsiveness and found that UDP-N-acetyl hexosamine concentrations were not higher in glycogen-supercompensated muscles than in control muscles with a low glycogen content. We determined whether the smaller increase in glucose transport is due to translocation of fewer GLUT-4 to the cell surface with the 2-N-4-(1-azi-2,2,2-trifluroethyl)-benzoyl-1, 3-bis(D-mannose-4-yloxy)-2-propylamine (ATB-[2-3H]BMPA) photolabeling technique. The insulin-induced increase in GLUT-4 at the cell surface was no greater in glycogen-supercompensated exercised muscle than in muscles of sedentary controls and only 50% as great as in exercised muscles with a low glycogen content. We conclude that the decreased insulin responsiveness of glucose transport in glycogen-supercompensated muscle is not due to increased accumulation of hexosamine biosynthetic pathway end products and that the smaller increase in glucose transport is mediated by translocation of fewer GLUT-4 to the cell surface.

Animals↗

PubMed1999

Insulin resistance of muscle glucose transport in male and female rats fed a high-sucrose diet.

It has been reported that, unlike high-fat diets, high-sucrose diets cause insulin resistance in the absence of an increase in visceral fat and that the insulin resistance develops only in male rats. This study was done to 1) determine if isolated muscles of rats fed a high-sucrose diet are resistant to stimulation of glucose transport when studied in vitro and 2) obtain information regarding how the effects of high-sucrose and high-fat diets on muscle insulin resistance differ. We found that, compared with rat chow, semipurified high-sucrose and high-starch diets both caused increased visceral fat accumulation and insulin resistance of skeletal muscle glucose transport. Insulin responsiveness of 2-deoxyglucose (2-DG) transport measured in epitrochlearis and soleus muscles in vitro was decreased approximately 40% (P < 0.01) in both male and female rats fed a high-sucrose compared with a chow diet. The high-sucrose diet also caused resistance of muscle glucose transport to stimulation by contractions. There was a highly significant negative correlation between stimulated muscle 2-DG transport and visceral fat mass. In view of these results, the differences in insulin action in vivo observed by others in rats fed isocaloric high-sucrose and high-starch diets must be due to additional, specific effects of sucrose that do not carry over in muscles studied in vitro. We conclude that, compared with rat chow, semipurified high-sucrose and high-cornstarch diets, like high-fat diets, cause increased visceral fat accumulation and severe resistance of skeletal muscle glucose transport to stimulation by insulin and contractions.

Adipose Tissue↗

PubMed1998

Effects of space flight on GLUT-4 content in rat plantaris muscle.

The effects of 14 days of space flight on the glucose transporter protein (GLUT-4) were studied in the plantaris muscle of growing 9-week-old, male Sprague Dawley rats. The rats were randomly separated into five groups: pre-flight vivarium ground controls (PF-VC) sacrificed approximately 2 h after launch; flight groups sacrificed either approximately 5 h (F-R0) or 9 days (F-R9) after the return from space; and synchronous ground controls (SC-R0 and SC-R9) sacrificed at the same time as the respective flight groups. The flight groups F-R0 and F-R9 were exposed to micro-gravity for 14 days in the Spacelab module located in the cargo bay of the shuttle transport system--58 of the manned Space Shuttle for the NASA mission named "Spacelab Life Sciences 2". Body weight and plantaris weight of SC-R0 and F-R0 were significantly higher than those of PF-VC. Neither body weight nor plantaris muscle weight in either group had changed 9 days after the return from space. As a result, body weight and plantaris muscle weight did not differ between the flight and synchronous control groups at any of the time points investigated. The GLUT-4-content (cpm/microgram membrane protein) in the plantaris muscle did not show any significant change in response to 14 days of space flight or 9 days after return. Similarly, citrate synthase activity did not change during the course of the space flight or the recovery period. These results suggest that 14 days of space flight does not affect muscle mass or GLUT-4 content of the fast-twitch plantaris muscle in the rat.

Animals↗

PubMed1998

Dural carotid cavernous fistulas: role of conventional radiation therapy--long-term results with irradiation, embolization, or both.

PURPOSE: To evaluate the long-term results of irradiation alone or of embolization with or without irradiation in patients with dural carotid cavernous fistulas (DCCFs). MATERIALS AND METHODS: Between 1984 and 1996, symptomatic DCCFs in 26 patients were treated by using irradiation alone (protocol 1, n = 12) before April 1988 and by using embolization as an initial treatment (protocol 2, n = 14) during and after April 1988. When angiography showed no improvement after embolization, irradiation was added (n = 6). On the basis of drainage flow speed, DCCFs were classified as fast, medium, or slow. RESULTS: With irradiation alone, all six patients with slow- to medium-type DCCFs had cure with a mean follow-up of 62 months. Four of six patients with fast-type DCCFs had cure or improvement, but the remaining two had no change. In the embolization group, irradiation was added in six patients with fast-type DCCFs. With a mean follow-up of 24 months, four of the six patients had cures, one had improvement, and one had no clinical change. Those who underwent protocol 2 had cures significantly earlier than those who underwent protocol 1 (P < .05). CONCLUSION: Conventional radiation therapy resulted in cure of DCCFs in nine (75%) of the 12 patients and in improvement of signs and symptoms in one (8%). Fast-type DCCFs may not always be improved. Radiation therapy may be useful in DCCFs after embolization.

Adult↗

PubMed1998

Effects of high-intensity intermittent swimming on glucose transport in rat epitrochlearis muscle.

Recently (K. Kawanaka, I. Tabata, and M. Higuchi. J. Appl. Physiol. 83: 429-433, 1997), we demonstrated that glucose transport activity after repeated 10-s-long in vitro tetani in rat epitrochlearis (Epi) muscle was negatively correlated with the postcontraction muscle glycogen concentration. Therefore, we examined whether high-intensity intermittent swimming, which depletes muscle glycogen to a lower level than that observed after ten 10-s-long in vitro tetani, elicits higher glucose transport than that observed after ten 10-s-long in vitro tetani, which has been regarded as the exercise-induced maximal stimulus for glucose transport. In male rats, 2-deoxy-D-glucose transport rate in Epi muscle after eight bouts of high-intensity intermittent swimming with a weight equal to 18% of body mass (exercise duration: 20 s, rest duration between exercise bouts: 40 s) was higher than that observed after the ten 10-s-long tetani (2.25 +/- 0.08 vs. 1.02 +/- 0.16 micromol . ml intracellular water-1 . 20 min-1). Muscle glycogen concentration in Epi after eight bouts of high-intensity intermittent swimming was significantly lower than that observed after ten 10-s-long in vitro tetani (7.6 +/- 0.5 vs. 14.8 +/- 1.4 micromol glucose/g muscle). These observations show that the high-intensity intermittent swimming increases glucose transport in rat Epi to a much higher level than that induced by ten 10-s-long in vitro tetani, which has been regarded as the exercise-related maximal stimulus for glucose transport. Furthermore, this finding suggests that the lower muscle glycogen level after high-intensity intermittent swimming than after in vitro tetani may play a role, because there was a significant negative correlation between glucose transport and muscle glycogen concentration in Epi after high-intensity swimming and in vitro tetani.

Animals↗

PubMed1997

Cholate inhibits high-fat diet-induced hyperglycemia and obesity with acyl-CoA synthetase mRNA decrease.

The effects of sodium cholate on high-fat diet-induced hyperglycemia and obesity were investigated. Insulin resistance was estimated by measuring 2-deoxyglucose uptake in epitrochlearis muscles incubated in vitro. Addition of 0.5% cholate to high-safflower oil diet completely prevented high fat-induced hyperglycemia and obesity in C57BL/6J mice with a slight decrease of energy intake but with no inhibition of fat absorption. Furthermore, the addition of cholate decreased blood insulin levels and prevented high-fat diet-induced decrease of glucose uptake in epitrochlearis. However, there was no change in the unsaturation index of fatty acids in skeletal muscles and in GLUT-4 levels by cholate. In liver, cholate addition resulted in cholesterol accumulation and completely prevented high-fat diet-induced triglyceride accumulation. The changes of triglyceride level in the liver were paralleled to the changes of acyl-CoA synthetase (ACS) mRNA. ACS catalyzes the formation of acyl-CoA from fatty acid, and acyl-CoA is utilized for triglyceride formation in liver. ACS has a sterol-responsive element 1 in its promoter region. These data indicate that the favorable effects of cholate could be partly the result of downregulation of ACS mRNA.

Analysis of Variance↗

PubMed1997

More tetanic contractions are required for activating glucose transport maximally in trained muscle.

Exercise training increases contraction-stimulated maximal glucose transport and muscle glycogen level in skeletal muscle. However, there is a possibility that more muscle contractions are required to maximally activate glucose transport in trained than in untrained muscle, because increased glycogen level after training may inhibit glucose transport. Therefore, the purpose of this study was to investigate the relationship between the increase in glucose transport and the number of tetanic contractions in trained and untrained muscle. Male rats swam 2 h/day for 15 days. In untrained epitrochlearis muscle, resting glycogen was 26.6 micromol glucose/g muscle. Ten, 10-s-long tetani at a rate of 1 contraction/min decreased glycogen level to 15.4 micromol glucose/g muscle and maximally increased 2-deoxy-D-glucose (2-DG) transport. Training increased contraction-stimulated maximal 2-DG transport (+71%; P < 0.01), GLUT-4 protein content (+78%; P < 0.01), and resting glycogen level (to 39.3 micromol glucose/g muscle; P < 0.01) on the next day after the training ended, although this training effect might be due, at least in part, to last bout of exercise. In trained muscle, 20 tetani were necessary to maximally activate glucose transport. Twenty tetani decreased muscle glycogen to a lower level than 10 tetani (18.9 vs. 24.0 micromol glucose/g muscle; P < 0.01). Contraction-stimulated 2-DG transport was negatively correlated with postcontraction muscle glycogen level in trained (r = -0.60; P < 0.01) and untrained muscle (r = -0.57; P < 0.01).

Animals↗

PubMed1997

Changes in insulin-stimulated glucose transport and GLUT-4 protein in rat skeletal muscle after training.

After running training, which increased GLUT-4 protein content in rat skeletal muscle by <40% compared with control rats, the training effect on insulin-stimulated maximal glucose transport (insulin responsiveness) in skeletal muscle was short lived (24 h). A recent study reported that GLUT-4 protein content in rat epitrochlearis muscle increased dramatically ( approximately 2-fold) after swimming training (J.-M. Ren, C. F. Semenkovich, E. A. Gulve, J. Gao, and J. O. Holloszy. J. Biol. Chem. 269, 14396-14401, 1994). Because GLUT-4 protein content is known to be closely related to skeletal muscle insulin responsiveness, we thought it possible that the training effect on insulin responsiveness may remain for >24 h after swimming training if GLUT-4 protein content decreases gradually from the relatively high level and still remains higher than control level for >24 h after swimming training. Therefore, we examined this possibility. Male Sprague-Dawley rats swam 2 h a day for 5 days with a weight equal to 2% of body mass. Approximately 18, 42, and 90 h after cessation of training, GLUT-4 protein concentration and 2-[1,2-3H]deoxy-D-glucose transport in the presence of a maximally stimulating concentration of insulin (2 mU/ml) were examined by using incubated epitrochlearis muscle preparation. Swimming training increased GLUT-4 protein concentration and insulin responsiveness by 87 and 85%, respectively, relative to age-matched controls when examined 18 h after training. Forty-two hours after training, GLUT-4 protein concentration and insulin responsiveness were still higher by 52 and 51%, respectively, in muscle from trained rats compared with control. GLUT-4 protein concentration and insulin responsiveness in trained muscle returned to sedentary control level within 90 h after training. We conclude that 1) the change in insulin responsiveness during detraining is directly related to muscle GLUT-4 protein content, and 2) consequently, the greater the increase in GLUT-4 protein content that is induced by training, the longer an effect on insulin responsiveness persists after the training.

Animals↗

PubMed1996

Muscle contractile activity modulates GLUT4 protein content in the absence of insulin.

We examined whether muscle contractile activity directly modulates GLUT4 protein content in rat skeletal muscle without the participation of insulin action or via amplified insulin action. To attain this purpose, the effects of increased, by training, or eliminated, by denervation, muscle contractile activity on muscle GLUT4 protein concentration were investigated in severely insulin-deficient diabetic rats. For the first set of experiments, insulin-deficient diabetic rats (induced by injection of 80 mg/kg B.W. streptozotocin) were trained for three weeks by treadmill running (90 min/day, 19 m/min, 10%, 6 days/week). GLUT4 protein concentration in soleus muscle was increased by 48% (p < 0.01) as compared with diabetic sedentary animals. For the second set of experiments, rats were injected with streptozotocin (100 mg/kg). The muscles innervated by the sciatic nerve of one leg were denervated four days after injection of streptozotocin. Three days after denervation, soleus muscles in both legs were excised. Insulin deficiency decreased GLUT4 protein concentration in innervated soleus muscle. In insulin-deficient diabetic rats, denervation also decreased soleus GLUT4 protein concentration by 50% (p < 0.01) as compared with the contralateral innervated muscle. Furthermore, the effects of insulin-deficiency and denervation on GLUT4 protein concentration were additive. These results provide evidence that muscle contractile activity directly modulates skeletal muscle GLUT4 protein concentration independent of insulin action.

Animals↗

PubMed1992

Exercise training increases glucose transporter content in skeletal muscles more efficiently from aged obese rats than young lean rats.

Glucose uptake in rat skeletal muscles decreases with age and obesity, but increases with chronic exercise training. The purpose of our study was to determine whether the GLUT4 content in several skeletal muscles from 1-mo-old young, lean rats and 12-mo-old aged, obese rats alters with exercise training. For exercise, a treadmill run of approximately 1 km/day was made for 4 wk by both groups of rats. The concentration of GLUT4 per protein in membrane fraction from several skeletal muscles was measured by immunoblotting. The amount of GLUT4 in the gastrocnemius and white quadriceps from aged rats slightly but significantly decreased to 73% and 78% of that from young rats, respectively. However, no significant difference in GLUT4 amount in the soleus, plantaris, and red quadriceps was observed between young and aged rats. The exercise training resulted in a larger increase in the amount of GLUT4 in each muscle from aged rats than in muscles from young rats. In aged rats, GLUT4 amount increased significantly with exercise training by 30, 33, 41, and 27% in the soleus, plantaris, gastrocnemius, and red quadriceps, respectively, compared with the sedentary controls. However, in young rats, exercise-induced increase of GLUT4 amount was significant only in the plantaris, and the increase was 17%. In exercised aged, obese rats, decreases of body weight, plasma triglyceride levels, and plasma free fatty acid were also observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗

PubMed1984

Determination of complement breakdown fragments C3d and its subfragments in health and disease.

The breakdown products of the third component of complement in approximately 400 samples were measured by rocket immunoelectrophoresis and two-dimensional electrophoresis using the method of Brandslund et al [3]. It was confirmed that the measurement of the C3d level provides useful information on increased C3 consumption irrespective of the synthetic rate. Furthermore, three subfragments with C3d but without C3c antigenicity were distinguished, which were designated as C3d1, C3d2, and C3d3. The subfragment C3d3 which migrated to the most anodal side was a predominant component in the plasma from patients with autoimmune diseases. Little C3d3 subfragment was detected in normal plasma and in normal sera incubated in vitro for 24 hr. Even in the normal sera converted completely in vitro which contained little intact C3, only a limited amount of C3d3 was detected. In the plasma from postsurgical patients in whom activation of the complement system was considered to be in an acute phase, C3d3 was detected, but the C3d2 level was higher than the C3d3 level. In the plasma from patients with systemic lupus erythematosus having the normal C3d level, C3d3 was a major fragment. It is predicted that the preponderant presence of C3d3 in plasma could be the result of chronic continuous complement activation by immune complexes.

Arthritis, Rheumatoid↗