Biomedical subjects
Publications and source records attributed to S Miyabo.
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Plasma concentrations of total ketone bodies, acetoacetate (AcAc) and 3-hydroxybutyrate (3-OHBA) in monosodium glutamate (MSG)-induced obese rats were measured. MSG-treated rats showed higher Lee's indices, shorter naso-anal and tail length, and a more marked intraperitoneal fat deposition than control rats. Plasma concentrations of glucose, free fatty acid, triglyceride and phospholipids were significantly increased in the MSG-treated rats as compared to the control rats (24 weeks-old). Plasma levels of total ketone bodies, AcAc and 3-OHBA were all decreased in the MSG-treated rats as compared to control rats. The ratio, 3-OHBA/AcAc in the MSG-treated rats were not different from those in the control rats.
Characteristics of lipoprotein receptors of the isolated liver parenchymal cells prepared from the streptozotocin-induced diabetic rats were investigated. Streptozotocin-induced diabetic rats fed 1.0% cholesterol showed the exaggerated hypercholesterolemia as compared to control rats fed 1.0% cholesterol. The present study was designed to elucidate the role of lipoprotein receptor mechanisms of liver parenchymal cells in the diabetic dyslipoproteinemia. 125I-labeled lipoproteins (rat beta-VLDL, human LDL2 or rat HDL3) were incubated with liver parenchymal cells isolated by liver perfusion using collagenase. According to the Scatchard analysis, the apparent dissociation constant (kd) and maximum beta-VLDL binding (Bmax) for the higher affinity binding site in the diabetic rats (n = 6) were (11.9 +/- 5.1) X 10(2) ng/ml and 307.5 +/- 145.2 ng/10(6) cells, respectively. These binding characteristics of the diabetic rats were not significantly different from the control rats. Furthermore, there were no significant differences in the binding characteristics of human LDL2 and rat HDL3 between the diabetic rats and the control rats. The data presented suggest that significant role of alteration of lipoprotein receptor characteristics in liver parenchymal cells is not played in the diabetic dyslipoproteinemia.
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In order to study the effects of treatment with monosodium glutamate (MSG) during the neonatal period on the intrinsic circadian timekeeping system in rats, the locomotor activity of blinded MSG-treated and control (saline-treated) rats was analyzed with power spectral analysis and cross-correlation. In contrast to a robust free-running circadian rhythm in the control rats, a significant shortening of the circadian period and rapid decomposition into ultradian components were noted in the MSG-treated rats. Computer-assisted stereometry of the hypothalamic nuclei revealed that, in addition to the well-known severe damage in the arcuate nuclei (ARC), the volumes of the suprachiasmatic nuclei (SCN) and ventromedial hypothalamic nuclei (VMH) were also reduced significantly in the MSG-treated rats. Although no gross histological damage was apparent in either the SCN and VMH, neonatal MSG treatment appears to impair the function of SCN to integrate many minor oscillations in the brain into a single, definite and precise circadian period.
Slow reacting substance of anaphylaxis (SRS-A) is an important chemical mediator of bronchial asthma. Leukotriene C4 is a component of SRS-A and is synthesized from arachidonic acid. Its synthesizing and releasing processes are found to be Ca2+-dependent. We developed an in vivo inhalation asthma model, mainly mediated by SRS-A, and elucidated the relationship between a Ca2+-antagonist, nicardipine, and SRS-A. In the asthmatic model, mediated by endogenous SRS-A induced by antigen inhalation, continuous intravenous infusion of nicardipine 7 micrograms/kg/min depressed the open airway pressure by about 60% compared with the saline-treated group. Inhibition of mean pulmonary resistance (RL) was about 50% and that of the inverted value of dynamic compliance (1/Cdyn) about 36%. However, the same concentration of nicardipine did not significantly effect the airway response in the asthmatic model induced by the inhalation of leukotriene C4. These results suggest that nicardipine, at the concentration used in the present study. did not block the direct effect of SRS-A on the smooth muscle, but blocked the Ca2+ influx required for the synthesis of SRS-A and its release.
Slow-reacting substance of anaphylaxis (SRS-A) is an important factor mediating bronchoconstriction in asthma. We developed a guinea pig model for SRS-A-mediated bronchoconstriction induced by antigen inhalation. Using this model, we investigated the effect of N-(3', 4'-dimethoxycinnamoyl) anthranilic acid (N-5'), a new anti-allergic drug, on the bronchoconstriction. FPL 55712 inhibited most of the bronchoconstriction induced by antigen inhalation. N-5' inhibited the antigen-induced bronchoconstriction in a dose-dependent fashion. Intraperitoneal administration of 200 mg/kg N-5' was effective for 40 min after antigen inhalation, while the effect of 60 mg/kg lasted only 7 min. On the other hand, 200 mg/kg N-5' showed no inhibitory effect on the bronchoconstriction caused by direct inhalation of leukotriene C4, a component of SRS-A. These findings indicate that one of the anti-allergic actions of N-5' is due to inhibition of synthesis and/or release of SRS-A.
In a patient with lymphoid interstitial pneumonia (LIP), confirmed by open lung biopsy, immunological derangement was evaluated using bronchoalveolar lavage fluid and peripheral blood. In the bronchoalveolar lavage fluid there were 20% null cells, 0% B cells, 77% alveolar macrophages and 3% T cells; in the peripheral blood these were 12% null cells, 43% B cells, 26% mononuclear phagocyte system cells, 2% double marker cells and 17% T cells. Thus there was T cell depletion and null cell increment in bronchoalveolar lavage, in contrast to T cell depletion and increment of B cells and mononuclear phagocyte system cells in the peripheral blood.
The effect of dietary cholesterol (Ch) on plasma lipoprotein and apolipoproteins (apo) in diabetic rats was investigated. Ch-fed diabetic rats were severely hypercholesterolemic and hypertriglyceridemic. They had higher concentrations of very low density lipoprotein (VLDL), intermediate density lipoprotein (IDL) and low density lipoprotein (LDL). Concentration of high density lipoprotein (HDL) was decreased. beta-VLDL increased predominantly in Ch-fed diabetic rats, whereas IDL increased in the Ch and propylthiouracil-fed control rats. According to sodium dodecyl sulfate polyacrylamide gel electrophoresis, VLDL and IDL from Ch-fed diabetic rats were unusual in that they contained more apo E, A-I and A-IV. Concentrations of plasma apo A-I and apo E were measured by radioimmunoassay. The diabetic rats fed a labo chow showed a significantly lower concentration of plasma apo E than control rats. Plasma apo E was extremely higher in the diabetic rats fed a cholesterol diet. Plasma apo A-I was significantly increased in the diabetic rats fed a labo chow and those fed a cholesterol. Insulin treatment significantly decreased the concentrations of VLDL, IDL and LDL and plasma concentration and distribution of apolipoproteins in lipoprotein subfractions changed toward normal. However, decreased HDL in the Ch-fed diabetic rats was not recovered by insulin treatment.
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In the asthmatic model mainly mediated by the endogenous slow reacting substance of anaphylaxis (SRS-A) induced by the antigen inhalation to passively sensitized guinea pigs, continuous intravenous infusion of nifedipine (Adalat) at a speed of 7 micrograms/kg/min depressed the airway open pressure by about 68% compared to the saline-treated group and produced a delay in the time to peak response. Moreover, nifedipine inhibited the response of the peripheral airway more strongly than that of the central airway. The same concentration of nifedipine inhibited the airway open pressure by about 43% compared to the saline-treated group in the asthmatic model induced by the inhalation of leukotriene C4. The effect of nifedipine on the central airway was shorter in duration than that on the peripheral airway. The inhibitory effect of nifedipine on the airway response was greater in the asthmatic model mediated mainly by the endogenous SRS-A induced by the antigen inhalation than in the asthmatic model produced by the inhalation of leukotriene C4.
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