[The effect of an alpha-glucosidase inhibitor on fatty liver in obesity].
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Biomedical subjects
Publications and source records attributed to Y Inui.
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Ultrastructure of the liver in ventromedial hypothalamus (VMH) lesioned rats was studied in parallel with biochemical examination. Ten weeks after the operation, VMH lesioned rats became markedly obese. Electron microscopic examination of the liver revealed lipid droplets in the cytoplasm and a high load of lipoprotein particles in the Golgi elements. Lipoprotein particles, 40-50 nm in diameter, in the Golgi elements, were scattered throughout the cytoplasm. Concentrations of triglyceride and esterified cholesterol markedly increased in the liver, while those of free cholesterol and phospholipids did not increase. Serum concentrations of triglyceride, total cholesterol and HDL-cholesterol in VMH lesioned rats were higher than control ones. These data suggest that lipoprotein synthesis was markedly increased in the livers of VMH lesioned rats.
Hybridomas secreting monoclonal antibodies that reacted with the B6 radiation leukemia virus (RadLV)-induced leukemia B6RV2 were produced by fusion of BALB/c NS-1 myeloma cells with spleen cells from (BALB/c X B6)F1 mice immunized with B6RV2. By direct and absorption analyses with 28 B6 and BALB/c leukemias, the monoclonal antibodies NU7-4 and NU7-99 were shown to react only with B6RV2, indicating that they recognized an individually distinct antigen on B6RV2 that was identified previously with conventional (BALB/c X B6)F1 anti-B6RV2 serum. Another monoclonal antibody, NU1-132, showed relatively restricted reactivity with B6 RadLV leukemias. These three monoclonal antibodies all precipitated material of approximately 80,000 daltons, which is the same size as that precipitated by anti-xenotropic MuLV gp70 serum. Sequential immunoprecipitation analysis revealed that the molecules precipitated by NU7-4 were not removed by pretreatment of NU7-99 or NU1-132 and that the molecules precipitated by NU7-99 were not removed by NU7-4 or NU1-132. The molecules precipitated by NU1-132 were partially removed by pretreatment with NU7-4, but not with NU7-99. The molecules precipitated by these three monoclonal antibodies were removed by pretreatment with anti-xenotropic gp70. These results suggested heterogeneity of the xenotropic MuLV gp70-related molecules expressed on B6RV2 and a possible relation between serologically defined unique tumor antigens and gp70-related molecules.
The effect of intravenous magnesium sulfate infusion on corrected serum calcium level and parathyroid function assessed by determination of nephrogenous cAMP (NcAMP) excretion were studied in normal human subjects. Significant hypermagnesemia induced by the magnesium sulfate infusion for 120 minutes was accompanied by a gradual and progressive decrease in the corrected serum calcium level. NcAMP excretion fell rapidly, reaching a nadir between 60 and 120 minutes after the infusion began, and after that rose above the baseline excretion. Urinary calcium excretion gradually increased, reaching a peak between 120 and 180 minutes after the infusion began and then gradually decreased. Since magnesium was given as the sulfate, it is not clear whether these changes were attributable to magnesium or sulfate or both. As a control study, we performed intravenous sodium sulfate infusion. The sodium sulfate infusion caused slight hypocalcemia, slight hypercalciuria, and a significant increase in NcAMP excretion. These findings indicate that the hypocalcemia and the hypercalciuria caused by the magnesium sulfate infusion is mainly due to the effect of magnesium, and that the decrease in NcAMP excretion during the infusion is due to the effect of magnesium alone. We conclude that the hypocalcemia caused by the magnesium sulfate infusion is mainly due to the renal calcium loss, and that the inhibition of parathyroid function caused by hypermagnesemia may be only partially involved in the early phase of this hypocalcemia.
The role of thyroid hormone in flounder metamorphosis was studied by use of thyroxine and the antithyroidal agent, thiourea (TU). T4 stimulated metamorphosis of pelagic larvae, producing miniatures of naturally metamorphosed benthic juveniles. In contrast, TU induced metamorphic stasis, resulting in giant pelagic larvae. These results indicate that the thyroid plays a role in flounder metamorphosis comparable to its well-known developmental role in amphibian metamorphosis.
In a study of the hormonal control of salmon smoltification, L-thyroxine (T4; 200 ppm in diet), ovine growth hormone (oGH; 2 micrograms/g intramuscular injection weekly), or a combination of these hormones was administered to underyearling amago salmon parr for 72 days. Administration of both T4 + oGH remarkably stimulated growth of the fish. All hormone treatments caused body silvering of the fish. The body silvering was the greatest in the group treated with T4 + oGH. Both T4 + oGH and oGH increased survival rate of the fish in 32% seawater, and kept plasma osmolarity and plasma sodium concentration lower than those of T4-treated and control groups in 27% seawater. Significant elevation of gill Na+, K+-ATPase activity was found in T4 + oGH-treated fish. On the other hand, T4 by itself did not affect the seawater tolerance of the fish. These findings suggest that GH or synergistic action of GH and T4 plays an important role in seawater adaptation during smoltification of amago salmon.
Hypophysectomy decreased plasma amino nitrogen (PAN) levels of Japanese eels. In contrast, administration of bovine or ovine growth hormone (GH; 2 micrograms/g) produced a delayed increase in PAN levels of both intact and hypophysectomized eels 48 hr after GH injection. The minimum dose of GH required to elevate PAN levels was found to be 0.1-1 micrograms/g body wt. The fact that GH treatment also increased PAN of hepatectomized eels indicates that the increased PAN was at least partly caused by the increased mobilization of amino nitrogen from body protein. GH also increased plasma free fatty acid content of intact and hypophysectomized eels 48 hr after GH injection in one experiment of the present study, but this effect was not reproducible in other experiments. No effect of GH administration was observed either in plasma glucose and lipid of intact and hypophysectomized eels 48 hr after the injection.
In vivo administration of ovine GH (2 micrograms/g body wt) increased [14C]leucine incorporation into protein of the liver, skeletal muscle, and opercular muscle of hypophysectomized eels. Addition of ovine GH into the medium (5 micrograms/ml) slightly increased [14C]leucine incorporation into protein of liver slices during 5 hr in vitro incubation, but did not affect protein synthesis from [14C]leucine in opercular muscle. In vivo pretreatment with ovine GH (2 micrograms/g body wt) 48 hr prior to tissue preparation clearly increased [14C]leucine incorporation into protein of liver slices in vitro. However, no statistically significant change was observed for in vitro incorporation of [14C]leucine into protein of opercular muscle of hypophysectomized eels which had been previously treated with ovine GH (2 micrograms/g body wt). These results indicate that ovine GH has a protein anabolic action in the liver and muscle of the eel and that compared to mammals a rather long lag period is needed to elicit such protein anabolic actions of GH in these animals.
A case of malignant hemangioendothelioma of the stomach is reported. The patient was a 21-year-old female who developed bloody stool. Pathological studies on the stomach revealed a gastric submucosal tumor. This tumor was growing on the outside of the stomach wall and formed a large abdominal mass. Evidence of metastases was detected in the liver, omentum and parietovisceral peritoneum. Biopsies were taken of the gastric mucosa and the metastatic lesions of the liver and omentum, and histological studies on these specimens led to the diagnosis of malignant hemangioendothelioma. A laparoscopic examination yielded very interesting findings: the presence of small red tumors on the omentum and the parietovisceral peritoneum. The usefulness of laparoscopic examination in the diagnosis of malignant hemangioendothelioma of the stomach is stressed.
Effects of insulin and glucagon on the incorporation of [14C]glycine into the protein of liver slices and the opercular muscle of the eel were studied in vitro. Addition of insulin (0.1 IU/ml) to the medium increased the radioactivity both of the trichloroacetic acid (TCA)-soluble fraction and of the protein of the opercular muscle, indicating an acceleration by the hormone both of entry of the amino acid into the tissue and of protein synthesis. Insulin also increased the incorporation of [14C]glycine into the liver protein, while a decrease in the radioactivity of the TCA-soluble fraction was observed. These findings suggest that the hormone accelerated protein synthesis at the expense of an intracellular amino acid pool. In contrast, glucagon (5 micrograms/ml) did not affect the radioactivity either of the TCA-soluble fraction or of protein for either the opercular muscle or the liver. Thus, the present results highlight the importance of insulin in the regulation of protein synthesis in the eel both in muscle and in liver.
Effects of insulin and glucagon on amino acid transport in vitro into liver slices and the opercular muscle of the eel were studied using a labeled nonmetabolizable amino acid analog, alpha-[1-14C]aminoisobutyric acid (AIB). Addition of insulin (0.1 IU/ml) to the medium increased the radioactivity in the deproteinized fractions of both the liver slices and opercular muscle, indicating an accelerated movement of this amino acid analog into these tissues. Glucagon (5 micrograms/ml) also enhanced the entry of [14C]AIB into the liver slices; however, treatment of opercular muscle with glucagon did not alter the radioactivity in the deproteinized fraction. These findings clearly indicate that the entry of amino acids into eel tissues independent of protein synthesis can be altered by insulin and glucagon.
In order to evaluate relationship between circulating androgens levels and development of ovarian hyperstimulation syndrome (OHS) in anovulatory patients treated sequentially with hMG and hCG, serum concentrations of androstenedione (A), testosterone (T) as well as estradiol (Ed) were measured serially in a total of 17 anovulatory patients including 9 who did not develop OHS and 8 who developed mild or moderate OHS. Increase of Ed levels during the period of hMG treatment varied remarkably in individual patients with OHS ranging from 7.2 to 190.1 times as much the pretreatment value. On the other hand, increase of A levels during the hMG treatment was recorded in the range from 2.0 to 3.2 times as much the pretreatment value in 4 patients with mild OHS, and from 1.5 to 5.9 in 4 patients with moderate OHS. However, the ratio of A increase remained within 1.4 times in patients without OHS. A transient increase of circulating T was observed in 2 days after commencement of hCG treatment, ranging between 1.4 and 3.2 times in patients without OHS, between 1.8 and 2.4 times in patients with mild OHS and between 3.8 and 6.8 times in patients with moderate OHS. It is concluded that serial measurements of A and T during the course of hMG and hCG treatments respectively appear to be an additional index other than Ed to predict development of OHS.
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The turnover of cholesterol of red blood cells in healthy hamsters was faster than that in cardiomyopathic hamsters. The uptake of 2-deoxy-D-glucose by heart cells was more rapid in the diseased hamsters compared with that of the healthy ones. Freeze-etch study of heart cells disclosed a difference of membrane structure between the two groups. Results of lactate content in hearts with nonexercised and exercised hamsters of both the diseased and healthy groups revealed the retention of lactate in the diseased hearts, even in a nonexercised state. Electron microscopic findings confirmed that an increased hypoxic condition caused by exercise aggravates the diseaes in the cardiomyopathic hamsters. These two conditions, membrane abnormality and hypoxia, probably play a role fundamental to the genesis of the disease, because hypoxia in the cellular level may well be caused by membrane abnormality.
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