PubMed HealthSearch

Biomedical subjects

J Nagasawa

Publications and source records attributed to J Nagasawa.

At least 19 recordsLinked to original sources

Interaction between heat acclimation and exogenous insulin in brown adipose tissue of rats.

Seventy-one male Wistar strain rats (7 weeks old) were kept at 5, 25, or 34 degrees C, respectively, for 2 weeks with or without insulin administration. Insulin (Novo Lente MC) was given subcutaneously in a dose of 3.62 nmol/125 microliters saline per 100 g body weight. An apparent effect of insulin treatment was noted only in heat-exposed rats, resulting in a remarkable gain in interscapular brown adipose tissue (BAT) mass of heat-acclimated, insulin-treated rats in terms of weight or weight per unit body weight. The BAT from heat-acclimated, insulin-treated rats had significantly higher levels of protein, DNA, RNA, and triglyceride than BAT from heat-acclimated, saline-treated rats. Therefore, it seems likely that the growth of BAT in heat-acclimated, insulin-treated rats was mostly due to the anabolic effects of insulin. The uncoupling protein mRNA was, however, present in BAT of heat-acclimated, insulin-treated rats at rather a depressed level, explaining a corresponding decrease in cold tolerance. On the other hand, the expression of insulin receptor mRNA was attenuated in BAT of rats from all the insulin-treated groups, possibly due to the down-regulation of insulin. Thus, there appeared to be some linkage among BAT, heat acclimation, and insulin.

Acclimatization

Time course of in vivo insulin sensitivity after a single bout of exercise in rats.

After a single bout of treadmill running (20 m.min-1, 1 hour), the time course of the in vivo insulin sensitivity was determined in previously untrained rats. The glucose infusion rate (GIR, mg.kg-1.min-1) as an index of insulin sensitivity was assessed by the euglycemic insulin clamp technique 1 (1h-post-Ex group), 3 (3h-post-Ex), 6 (6h-post-Ex) and 24 hours after exercise (24h-post-Ex), n = 8 in each group. GIRs increased with time from 5.72 +/- 1.02 (1h-post-Ex), to 7.58 +/- 1.07 (3h-post-Ex), 10.31 +/- 1.52 (6h-post-Ex) and 10.23 +/- 1.62 (24h-post-Ex) vs control (5.51 +/- 0.63); the GIR in the 6h-post-Ex and the 24h-post-Ex were significantly higher than those in the control and the 1h-post-Ex groups (p less than 0.05). The rate of increase was equivalent to that observed after long-term training in our previous study. GIR of alpha-adrenergic blockade infused 1 hour after exercise (1h-post-Ex alpha) significantly increased (8.32 +/- 0.96) compared to the control and no exercise alpha-blocker-infused control (C alpha) (p less than 0.05). But no significant difference was shown between 1h-post-Ex and 1h-post-Ex alpha groups. In the beta-blocker-infused group, GIR did not show a significant increase. These results indicate that an increase in the in vivo insulin sensitivity after a single bout of exercise is not evident until 6 hours post-exercise. The delay in the sensitivity might partly be explained by the suppression caused by catecholamines via the alpha-mechanism.

Adrenergic alpha-Antagonists

Effects of training and training cessation on insulin action.

Physical training has been shown to improve glucose tolerance and insulin action. In the present study, insulin action was determined using the euglycemic clamp technique in six trained male athletes compared with six untrained controls matched by age, sex, and weight at 14, 38, and 86 hours and at 6 days after cessation of exercise. The rate of insulin-mediated glucose uptake (glucose disposal) was 9.40 +/- 0.46 mg.kg-1.min-1 (mean +/- SEM) for the athletes at 14 h after the last exercise bout, compared with 6.80 +/- 0.86 mg.kg-1.min-1 obtained for the untrained controls (p less than 0.01). Glucose disposal was gradually decreased to 7.78 +/- 0.87 mg.kg-1.min-1 at 38 h, 6.82 +/- 0.49 mg.kg-1.min-1 at 86 h and to 7.11 +/- 1.00 mg.kg-1.min-1 at 6 days after cessation of physical training. At 38 h, 86 h, and 6 days of detraining, glucose disposal exhibited by training athletes did not differ significantly from untrained controls. These results suggest that physical training increases insulin action, and that this effect could be reversed to the control levels within 38 h after detraining.

Adolescent

Immobilization of biocatalysts with poly(vinyl alcohol) supports.

Two polymer materials, poly(vinyl alcohol) (PVA) superfine fibers and photocrosslinkable PVA bearing styrylpyridinium groups, have been developed to immobilize biocatalysts. The former has a large surface consisting of relatively large-size pores and the fibers can immobilize a large amount of biocatalyst on their surface by ionic interaction. The latter entraps many kinds of biocatalysts by cyclodimerization caused by visible light irradiation. The biocatalysts on/in these supports maintain high activity and thermal stability. These materials can easily be formed into various shapes suitable for various applications. A new bioreactor system was constructed for evaluating a variety of biocatalysts and supports.

Cross-Linking Reagents

Effect of training and detraining on in vivo insulin sensitivity.

Insulin sensitivity was determined in rats to clarify the effect of detraining at 1 (trained state), 2, 3, and 7 days (7 rats each) and 14 days (n = 8) after five weeks of voluntary training using euglycemic insulin clamp technique. The relationship between basal insulin and glucose shifted towards a decrease in metabolic insulin needs compared to untrained controls (n = 20). During the insulin clamp study, to maintain comparable plasma glucose and insulin levels in all groups, the glucose infusion rate had to be increased significantly (p less than 0.01) to 9.92 +/- 1.12 mg.kg-1.min-1 compared to control group (6.57 +/- 0.57). This improved sensitivity persisted for 2 days after training but was significantly lowered in the 7-days-after group (p less than 0.01). In summary, this study shows that training effect on insulin sensitivity can be determined after voluntary training in rat. This training effect lasted 2 days after training.

Animals

Immunosorbent consisting of DNA immobilized on oxirane-activated sepharose.

The preparation of adsorbents for DNA antibodies is described. The degree of immobilization of native DNA on Sepharoses activated with epichlorohydrin or bisoxirane was investigated as a function of pH, temperature, time, concentration of DNA, and oxirane content in the supports. The maximum amount of DNA bound was obtained after 8 h at 40-50 degrees C at pH 11-11.5. The amount bound was increased by raising either the concentration of DNA or the oxirane content of the supports, and could reach 300 mg/g dry support. The immobilized DNA was applied to the adsorption of DNA antibodies using either commercial human serum with anti-native DNA activity or the sera of patients with systemic lupus erythematosus. The amount of antibody adsorbed depended on the amount of DNA. The thermal stability of the immobilized DNA was also examined. After heating at 80 degrees C, the leakage of DNA was slight and the adsorption of antibodies was not affected.

Adsorption

Dependency of transcoronary circulatory transport function on coronary perfusion pressure and flow.

Transcoronary circulatory transport function was computed from the dye-dilution curves recorded simultaneously at the entrance (aortic root) and exit (coronary sinus) of the coronary circulation after the injection of dye bolus into the femoral vein in open-chest dog. The effect of coronary perfusion pressure and flow on the first (delta-t) and second (deltapi2) moments of the transport function was examined before and during intra-aortic angiotensin infusion. It was observed that the relative dispersion (deltapi2 1/2/delta-t) in the canine coronary circulation is the largest among the organ-circulations that have been examined by the investigators, suggesting that cardiac wall is highly heterogeneously perfused, and that the relative dispersion was variable depending on the coronary perfusion pressure and flow. It is concluded that sole measurement of the moment of transcoronary transport function such as -t cannot be a reliable indicator of the coronary circulatory disturbances. The underlying mechanisms for the dependency of the relative dispersion on the perfusion was discussed.

Animals

Determination of transcoronary circulatory transport function.

A method is described to determine the transcoronary circulatory transport function (h(t)) from input (Ci'(t)) and output (Co'(t)) dye-dilution curves obtained at the inlet and outlet of the coronary circulation. Assuming the mathematical linearity and stationarity of the coronary circulation, it is demonstrated that h(t) can be computed in terms of lagged normal density curve as a model from the sole measurement of the first to third moments of Ci'(t) and Co'(t) when recorded by a pair of our dye sampling systems that have shown to have identical response to step function. The method is useful because of its simplicity in practice. The physiological meaning of the determination of h(t) is discussed. It could be helpful to the estimation of the change in coronary path-length distribution under some conditions, although the method is still of limited value at present, because the averaged path-length through the coronary circulation cannot be evaluated correctly.

Animals

Exocytosis: the common release mechanism of secretory granules in glandular cells, neurosecretory cells, neurons and paraneurons.

Exocytotic granule release in glandular cells (exocrine and endocrine), neurosecretory cells, neurons and paraneurons was discussed. Attention was focused on the neurosecretory terminals in the mammalian posterior pituitary gland and adrenomedullary cells. The concept of "exocytosis-vesiculation sequence" proposed by Douglas and Nagasawa was introduced. This theory states that the exocytotic release of secretory granules was followed by the mechanism of granule membrane recovery; this process occurred at the bottom of the exocytotic pit in the form of coated microvesicles. Experimental results were presented which substantiated the theory for the transformation of coated microvesicles into smooth microvesicles. The origin and the nature of long enigmatic "synaptic vesicles" in the posterior pituitary gland was thus explained. The exocytotic release probably operates as the general and perhaps sole mechanism of granule release in a variety of glandular cells, neurosecretory cells, neurons and paraneurons.

Adrenal Medulla