This investigation was undertaken to clarify the in vitro effect of the various stimulations, such as exercise (E), insulin (I) direct electrical stimulation (EST) and the combinations of the above, on the glucose incorporation intro glycogen molecules (glycogen synthesis) of the normal slow (soleus) and fast twitch (plantaris) muscles, and the different responses of slow and fast twitch muscles to persistent overloads causing compensatory muscle hypertrophy. In resting state, slow twitch muscle has greater capacity for glycogen synthesis than fast twitch muscle, and responses of different muscle to various stimuli were differ as follows: In slow twitch muscle, the glycogen synthesis was increased by insulin, and electrical stimulation but not increased by exercise; exercise increased insulin sensitivity and the effect of electrical stimulation. Whereas the glycogen synthesis in fast twitch muscle was increased only by the stimuli combined with E and EST, and E, I, and EST. As the result of removal of synergistic muscle, both muscles were hypertrophied, and the degree of hypertrophy in response to persistent overload was higher in fast twitch muscle (182%) than slow twitch muscle (151%). In hypertrophied muscles, glycogen synthesis of soleus in any groups was lower than that of the control, but similar in plantaris. In conclusions, there were marked heterogeneity in different muscle fiber in the effects of exercise and insulin addition and electrical stimulation on muscle glycogen synthesis, and fast twitch muscle may be adapted more easily to that kind of persistent overload than slow twitch muscle.
Electric Stimulation ; Glucose* ; Glycogen* ; Hypertrophy ; In Vitro Techniques* ; Insulin ; Insulin Resistance ; Muscles* ; Population Characteristics

No abstract available.
Congenital Hypothyroidism*

No abstract available.
Animals ; Insulin Resistance ; Insulin ; Rats

The effect of exercise on plasma insulin, free fatty acid, and glucose uptake and glycogen concentration in soleus, and intravenous glucose tolerance of streptozotocin treated, diabetic Sprague-Dawley rats were studied. Diabetic-trained animals were subjected to a regular program of treadmill running for 4 weeks. Seventy-two hours after the last training session, basal and insulin-stimulated glucose uptake was studied in incubated strips (about 20 mg) of soleus muscle in vitro. Glucose tolerance was measured with intravenous infusion of 0.5 g glucose/kg body weight. In diabetic rats, training was associated with increase glucose uptake in basal and maximal insulin concentrations, decreased fasting glucose concentrations, and increased muscle glycogen levels, but there were no changes in glucose tolerance curve and plasma insulin concentrations. These results suggest that regular running program for 4 weeks improve responsiveness of insulin on soleus muscle, but fails to cause improvement of impaired intravenous glucose tolerance in mild degree streptozotocin induced diabetic rats.
Animals ; Body Weight ; Exercise* ; Fasting ; Glucose Tolerance Test* ; Glucose* ; Glycogen ; In Vitro Techniques ; Infusions, Intravenous ; Insulin ; Muscle, Skeletal ; Plasma ; Rats* ; Rats, Sprague-Dawley ; Running ; Streptozocin*

No abstract available.
Female ; Pregnancy ; Pregnancy, Ectopic*

No abstract available.
Aspirin* ; Epithelial Cells*

No abstract available.
Hyperthyroidism*

The effects of insulin and exercise on glucose uptake of skeletal muscle were investigated in soleus muscle isolated from low dose streptozotocin induced diabetic rat in vitro. Glucose uptake was assessed by measuring ³H-methylglucose uptake in vitro. Basal glucose uptake in diabetes was reduced by approximately one-third of the control value (5.6±0.73µMol/g/20min. in diabetes versus 8.4±0.77 in control, P<0.01). There was also a significant decrease (P<0.01) in glucose uptake of diabetes at physiologic insulin concentration (200 µIU/ml) by 40% (6.1±1.20 versus 10.0±0.81). Furthermore, maximal insulin (20000 µIU/ml)-stimulated glucose uptake was 36% lower in diabetes as compared with control (7.3±1.29 versus 11.4±1.29, P<0.01). In contrast, exercise (1.0 km/hr, treadmill running for 45 min.) effect on glucose uptake was so dramatic in diabetes that glucose uptake at basal state was 8.+1.09 and insulin stimulated-glucose uptake were 10.2±1.47 and 11.9±1.64, in 200 and 20000 µIU/ml added insulin, respectively. These results suggest that insulin insensitivity develops in skeletal muscle after 2 weeks of streptozotocin-induced diabetes, but these insensitivity was recovered significantly by single session of running exercise.
Animals ; Glucose* ; In Vitro Techniques ; Insulin* ; Muscle, Skeletal* ; Rats* ; Running ; Streptozocin

Insulin resistance is a prominent feature of diabetic state and has heterogeneous nature. However, the pathogenetic sequence of events leading to the emergence of the defect in insulin action remains controversial. It is well-known that prolonged hyperglycemia and hyperinsulinemia are one of the causes of development of insulin resistance, but both hyperglycemia and hyperinsulinemia stimulate glucose uptake in peripheral tissue. Therefore, it is hypothesized that insulin resistance may be generated by a kind of protective mechanism preventing cellular hypertrophy. In this study, to evaluate whether the acutely increased glucose uptake inhibits further glucose transport stimulated by insulin, insulin sensitivity was measured after preloaded glucose infusion for 2 hours at various conditions in rats. And also, to evaluate the mechanism of decreased insulin sensitivity, insulin receptor binding affinity and glucose transporter 4 (GLUT4) protein of plasma membrane of gastrocnemius muscle were assayed after hyperinsulinemic euglycemic clamp studies. Experimental animals were divided into five groups according to conditions of preloaded glucose infusion: group I, basal insulin (14+/-1.9 micronU/ml) and basal glucose (75+/-0.7 mg/dl), by normal saline infusion; group II, normal insulin (33+/-3.8 micronU/ml) and hyperglycemia (207+/-6.3 mg/dl), by somatostatin and glucose infusion; group III, hyperinsulinemia (134+/-34.8 micronU/ml) and hyperglycemia (204+/-4.6 mg/dl), by glucose infusion; IV, supramaximal insulin (100+/-2.2 mg/dl), by insulin and glucose infusion; group V, supramaximal insulin(4813+/-687.9 micronU/ml) and hyperglycemia (233+/-3.1 mg/dl), by insulin and glucose infusion. Insulin sensitivity was assessed with hyperinsulinemic euglycemic clamp technique. The amounts of preloaded glucose infusion(gm/kg) were 1.88+/-0.151 in group II, 2.69+/-0.239 in group III, 3.54+/-0.198 in groupIV, and 4.32+/-0.621 in group V. Disappearance rates of glucose (Rd, mg/kg/min) at steady state of hyperinsulinemic euglycemic clamp studies were 16.9+/-3.88 in group I, 13.5+/-1.05 in group II, 11.2+/-1.17 in group III, 13.2+/-2.05 in group IV, and 10.4+/-1.01 in group V. A negative correlation was observed between amount of preloaded glucose and Rd )r=-0.701, p<0.001) when all studies were combined. Insulin receptor binding affinity and content of GLUT4 were not significantly different in all experimental groups. These results suggest that increased glucose uptake may inhibit further glucose transport and lead to decreased insulin sensitivity.
Animals

PURPOSE: This study was performed to determine the incidence of BMM and to correlate the presence of these micrometastases with prognosis and othet clinicopathologic features. Materials AND Methods: BMM was evaluated in 220 breast cancer patients between July, 1991 and January, 1997, using mouse monoclonal antibody (AE1/AE3) against cytokeratin in an immunofluorescent assay. RESULTS: Of the 220 patients, 71 (32.3%) were positive for BMM. There were no association between bone marrow positivity and nodal status, TNM stage, known histopathologic parameters, and hormona1 receptor. Median follow-up for 220 patients was 41.6 month. The relapse rate was 16.8% (37/220). Twenty-four (33.8%) of 37 patients were positive for BMM and 13 (8.7%) were negative (p<0.05). Bone metastasis occurred in 16 cases, and was more common in BMM positive patients (14 of 24, 54.2%, versus 2 of 13, 15.4%, p < 0.05). Twenty-six patients were died of relapsed breast cancer. In overall survival, patients who was negative for BMM showed higher survival rate (p<0.05). CONCLUSION: BMM was a good predictor for distant metastasis, especially bone metastasis, and for poor prognosis. But no association was found between bone marrow positivity and tumor size, nodal status, stage, histologic parameter and hormonal receptor status.
Animals ; Bone Marrow* ; Breast Neoplasms* ; Breast* ; Fluorescent Antibody Technique ; Follow-Up Studies ; Humans ; Incidence ; Keratins ; Mice ; Neoplasm Metastasis ; Neoplasm Micrometastasis* ; Prognosis ; Recurrence ; Survival Rate