Changes in zeta potential of the red cell membrane in humans during acute exposure to cold.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to T Yahata.
Explore the source record for details and available documents.
Three-hour immobilization stress was imposed on male adult rats of Wistar strain by restraining them on a board 6 days a week for 1-8 weeks. The stressed rats showed less body weight gain during the experiment compared to the controls. These stressed animals manifested an improved cold tolerance as shown by no significant fall in colonic temperature in the cold at -5 degrees C for 300 min during the experimental period, while the colonic temperature of the controls fell progressively. Nonshivering thermogenesis as assessed by noradrenaline-induced increase in oxygen consumption was significantly potentiated in the stressed rats. The weight and protein content of the intercapsular brown adipose tissue (BAT) increased and BAT mitochondria were more packed in the stressed rats. Plasma insulin, insulin/glucagon molar ratio and thyroxine levels were lowered in the stressed rats, while the plasma triiodothyronine level remained unchanged. Removal of interscapular BAT led to a loss of improved cold tolerance and a significant reduction of nonshivering thermogenesis in the stressed rats. These results indicate that repetitive stress may induce cross adaptation between stress and cold through an enhanced capacity of nonshivering thermogenesis mediated, at least in part, via stimulation of BAT function.
Electroacupuncture (1.5 volts, 0.13 msec duration, 5 Hz for 10 min) was applied to the ten sites of lumbodorsal region in women aged 20 to 47. Immediately after the acupuncture plasma noradrenalin concentration significantly increased 9 out of 20 subjects, while it decreased in 11. Plasma noradrenaline returned to the intitial level in both groups 30 min after the acupuncture. In the noradrenaline elevated group plasma insulin concentration and plasma insulin/glucagon molar ratio significantly decreased until 30 min after the acupuncture. Such changes were not observed in the noradrenaline decreased group. Plasma glucagon, dopamine-beta-hydroxylase, free fatty acids, glycerol, creatine kinase and blood glucose were not changed in both groups.
Explore the source record for details and available documents.
Adrenal demedullation combined with chemical sympathectomy with 6-hydroxydopamine (ACS) lowered plasma glucagon and insulin levels in rats. Acute cold exposure increased plasma glucagon in both ACS and control rats, while it increased plasma insulin only in ACS rats. ACS rats responded to cold with a smaller increase in plasma glycerol and a more pronounced elevation of plasma free fatty acids.
After 30 min infusion of glucagon or noradrenaline, blood flow through brown adipose tissue (BAT) from various sites was investigated with the aid of 113Sn-labeled microspheres under hexobarbital anesthesia in cold-acclimated (CA), heat-acclimated (HA), and warm control (WC) rats. Glucagon increased cardiac output in both CA and HA, while noradrenaline increased it in HA but not in CA. Blood flow through BAT as well as the fractional distribution of cardiac output to BAT increased by glucagon dose-dependently and reached a maximum level in a dose of 2 micrograms/min. These glucagon-induced responses were significantly higher in CA and smaller in HA as compared with WC. Noradrenaline in a dose of 2 microgram/min caused larger responses than glucagon in all groups. Glucagon- or noradrenaline-induced blood flow per unit weight of BAT increased or tended to increase by cold acclimation. These results suggest that an in vivo enhanced glucagon-induced thermogenesis in cold-acclimated BAT is partly due to an increased blood flow through this tissue.
Explore the source record for details and available documents.
Some endocrine and metabolic responses to acute cold and heat exposures were observed in rats acclimated to cold, heat, or both cold and heat. Rats exposed to both cold (12 hr, 5 degrees C) and heat (12 hr, 34 degrees C) for 4 to 5 weeks (CHA) showed less fall of colonic temperature (Tc) in the cold (-5 degrees C) than heat-acclimated rats (34 degrees C, 4 to 5 weeks) (HA) and warm controls (WC), but a greater fall than cold-acclimated rats (5 degrees C, 4 to 5 weeks) (CA). CHA possessed a larger quantity of interscapular brown adipose tissue and showed greater cold-induced oxygen consumption (VO2) than WC and HA but less than CA. Blood glycerol levels rose similarly in all groups in the cold, while the increase in blood free fatty acids (FFA) levels was significantly greater in HA and smaller in CA than in WC and CHA. Acute cold exposure caused the elevation of plasma glucagon level in WC and HA, but not in CA and CHA. It lowered plasma insulin levels in HA, and the insulin/glucagon molar ratio (I/G) in WC, HA, and CHA. All groups showed the same increases in Tc during acute heat exposure (34 degrees C). However, the heat-induced increase in VO2 was greater in WC than in HA, CA, and CHA. Blood metabolite levels were not affected by acute heat exposure in all groups. Plasma glucagon levels decreased in CHA, while plasma insulin levels increased in WC and CA. I/G increased in WC and CHA. These results indicate that thermal and metabolic responses would be modified by previous exposures to cold, heat, and cold-heat.
Explore the source record for details and available documents.
Effects of temperature stimuli on plasma glucagon levels were studied in fasted (18 hr) and shorn rats. Plasma glucagon levels rose significantly on exposures to both cold (-5 degrees C, 60 min) (p less than 0.001) and heat (36 degrees C, 60 min) (p less than 0.001) from that in control rats at 25 degrees C. Cold stimulus increased blood FFA level (p less than 0.001) and both cold and heat stimuli increased blood glycerol levels (p less than 0.05-0.001). FFA/glycerol molar ratio decreased to a similar extent on both cold and heat exposures (p less than 0.02-0.01). It was noted that plasma glucagon, blood FFA and glycerol levels increased significantly more in cold-exposed rats (p less than 0.001) than in heat-exposed ones. There were positive relations of plasma glucagon levels to blood FFA and glycerol levels (p less than 0.001), while an inverse relation of plasma glucagon level to FFA/glycerol molar ratio was observed in all experimental rats (p less than 0.05). Cold exposure reduced blood glucose level (p less than 0.001), while heat exposure did not affect it. Cold-induced increases of plasma glucagon and blood FFA levels were diminished significantly in cold-acclimated rats as compared with those in controls (p less than 0.05-0.001). Blood glycerol increased and FFA/glycerol molar ratio decreased to a similar extent on cold exposure in both control and cold-acclimated rats. Correlation between plasma glucagon and FFA/glycerol molar ratio was inversely significant in controls, but not significant in cold-acclimated rats. Blood glucose level was not altered on cold exposure in cold-acclimated rats. It was concluded that acute exposures to temperature stimuli, especially to cold, stimulate glucagon release, accompanied by increased utilization and mobilization of FFA and glucose, and plasma glucagon response to cold is diminished due to cold acclimation.
In order to ascertain possible involvement of polyamines in the physiological regulation of brown fat function, effect of temperature acclimation on the polyamine contents of this tissue and effects of polyamines on the noradrenaline-induced thermogenesis is isolated brown adipocytes were investigated in rats. Daily urinary excretion of polyamines measured collectively for spermidine and spermidine per body weight was decreased in heat acclimation and increased in cold acclimation. Polyamine concentrations per fresh weight of brown fat showed extremely low values compared with those of other tissues previously reported. Putrescine and spermidine contents per fat-free dry matter of brown fat were decreased in cold acclimation, but were not affected in heat acclimation. Spermidine and spermine inhibited the noradrenaline-induced thermogenesis of brown adipocytes dose-dependently. These results suggest that polyamines regulate the heat production of brown adipose tissue in an inhibitory way and cold acclimation potentiates heat production of this tissue by reducing polyamine levels.
Calorigenic actions of noradrenaline and glucagon on isolated epididymal fat cells from warm-acclimated controls, cold-acclimated and heat-acclimated rats were measured by the use of a twin-type conduction microcalorimeter. Both noradrenaline and glucagon stimulated heat production in isolated adipocytes maximally in doses of 1 microgram/ml and 10 microgram/ml, respectively. Maximal responsiveness of adipocytes per unit cell to noradrenaline was not influenced by cold acclimation, while it was reduced by heat and acclimation. Maximal response in total epididymal fat cells to noradrenaline was increased in cold acclimation and not changed in heat acclimation at increased numbers of adipocytes in both cold-acclimated and heat-acclimated animals. Maximal response per unit cell as well as per total epididymal fat cells to glucagon was increased in cold acclimation and reduced in heat acclimation. The present results indicate that the modified responses of target adipocytes to noradrenaline and glucagon are involved in the development of temperature acclimation.
Heat production of isolated brown-fat cells by addition of noradrenaline and glucagon was measured in warm-acclimated control, cold-acclimated and heat-acclimated rats by use of a twin-type conduction microcalorimeter. Noradrenaline and glucagon induced maximum heat production per 10(6) cells in dose of 1 microgram/ml. Heat produced by maximum thermogenic response to glucagon was twice as much as that to noradrenaline. Thermogenic response to noradrenaline was markedly increased in cold-acclimated brown adipocytes, while it was reduced in heat-acclimated ones. Thermogenic response to glucagon was significantly reduced in heat-acclimated brown adipocytes, while it was not affected in cold-acclimated brown adipocytes.
Cold tolerance and metabolic responses to cold were studied in cold-acclimated rats on high fat diet (CAHF). Cold tolerance at-5 degrees C was assessed by fall of colonic temperature of clipped rats after 18 h of fasting. Rate of fall in colonic temperature was greatest in warm-acclimated control rats (WAST), slowest in cold-acclimated rats on standard diet (CAST), and remained unchanged in CAHF during cold exposure for 240 min. Increment in blood free fatty acid (FFA) concentration 80 min after cold exposure was greatest in WAST, less in CAST, and least in CAHF. Blood glucose decreased similarly in WAST and CAST after cold exposure, while it remained unchanged in CAHF. Blood beta-hydroxybutyrate also increased similarly in WAST and CAST, while it did not change in CAHF. Nonshivering thermogenesis tested by noradrenaline was greatest in CAHF, followed by CAST and WAST. Shivering induced by cold exposure was less pronounced in CAST than in WAST and did not develop in CAHF; changes in colonic temperature were inversely related to the extent of shivering during cold exposure for 90 min. These results suggest that an integrating effect of cold and high fat diet could improve cold tolerance much more than cold acclimation itself, possibly through enhanced nonshivering thermogenesis caused by metabolic modifications such as increased lipid use and gluconeogenesis.
Explore the source record for details and available documents.
Mitochondria became larger and some numerous in the internal red fibers of M. quadriceps femoris and neck muscle in cold-acclimated rats than in warm-acclimated ones, while they became less in number in spite of remarkable increase of size in the external white fibers of the former muscle. Mitochondrial cristae and sarcoplasmic reticuli developed better in the muscles of cold-acclimated rats.
We report a case of a stage IV uterine papillary serous carcinoma (UPSC) with multiple organ metastases. The patient was treated with docetaxel and carboplatin combination chemotherapy. After five courses, uterine tumor, Douglas tumor, lymphadenopathy, and distant metastases on magnetic resonance imaging or computed tomography scan were completely resoluted. Moreover, endometrial biopsy showed no carcinoma tissues after six courses. We suggest that this regimen may be effective for treatment of advanced-stage UPSC.
Cases of metastatic placental site trophoblastic tumor (PSTT) have a very poor prognosis because these tumors tend to be less sensitive to chemotherapy than other types of gestational trophoblastic disease. We describe the case of a 25-year-old woman who presented with occipital tumor and abnormal vaginal bleeding. Hysterectomy, bilateral salpingo-oophorectomy, and occipital tumor removal revealed a primary PSTT in the uterus, with ovarian and occipital subaponeurotic metastases. She received etoposide, methotrexate, actinomycin-D/cyclophosphamide, vincristine chemotherapy and had a complete clinical remission. Fifteen months later, she had a recurrent subaponeurotic occipital tumor invading the cranium and underwent tumor removal along with cranial bone followed by local irradiation. She was then treated with etoposide, cis-platinum/etoposide, methotrexate, actinomycin-D chemotherapy and again had a remission for 5 months. The patient, however, had a left parietal subaponeurotic tumor, invading the dura mater, and received local irradiation. Soon after, she developed left orbital bone metastasis, treated by local irradiation. These bone metastases responded to the radiation completely. However, multiple organ metastases were found, and she died of the disease. This represents the first case of PSTT with initial subaponeurotic metastasis in a living patient. New modalities of treatment for high-risk or metastatic PSTT need to be developed.