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  • 1
    ISSN: 1432-0428
    Keywords: Hyperglycaemia ; embryogenesis ; rat embryo culture ; malformation ; sorbitol ; myo-inositol
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To demonstrate the myo-inositol depletion hypothesis in hyperglycaemia-induced embryopathy, rat conceptuses of 9.5 days of gestation in the early head-fold stage were grown in vitro during neural tube formation for 48 h with increasing amounts of glucose. The effects of an aldose reductase inhibitor and the myo-inositol supplementation were also investigated. Sorbitol and myo-inositol contents were measured in separated embryos and extra-embryonic membranes including yolk sac and amnion at the end of culture. After addition of 33.3 mmol/l and 66.7 mmol/l glucose to the culture media, the myo-inositol content of the embryos was significantly decreased by 43.1% (p〈0.05) and 64.6% (p 〈 0.01) of the control group, while a marked accumulation of sorbitol was observed (25 and 41 times that of the control). Although the addition of an aldose reductase inhibitor (0.7 mmol/l) to the hyperglycaemic culture media containing an additional 66.7 mmol/l glucose significantly reduced the sorbitol content of embryos to approximately one-eighth, the myo-inositol content of embryos remained decreased and the frequency of neural lesions was unchanged (23.1% vs 23.9%, NS). Supplementation of the myo-inositol (0.28 mmol/l) completely restored the myo-inositol content of the embryos and resulted in a significant decrease in the frequency of neural lesions (7.1% vs 23.9%, p 〈 0.01) and a significant increase in crown-rump length and somite numbers. Much less significantly, sorbitol accumulation was also observed in the extra-embryonic membrane in response to hyperglycaemia, neither hyperglycaemia nor the myo-inositol supplementation modified the myo-inositol contents of the extra-embryonic membrane. We conclude that the mechanism of hyperglycaemia-induced teratogenicity was mediated by the myo-inositol depletion of the embryo at a critical stage of organogenesis.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0428
    Keywords: C-peptide ; diabetes mellitus ; insulin secretion ; MELAS ; mitochondrial gene mutation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Recent evidence suggests possible linkage between diabetes mellitus and mitochondrial gene mutation. We surveyed mitochondrial tRNALEU(UUR) (3243) mutation in 7 mitochondrial encephalomyopathy, lactic acidosis and stroke-like episode (MELAS) families and identified 24 mutated subjects (7 MELAS probands and 17 non-MELAS relatives) as well as 11 non-mutant family members. An OGTT in the 24 mutant relatives revealed 14 diabetic subjects, 3 with impaired glucose tolerance and 7 with normal glucose tolerance and all non-mutant family members as having normal glucose tolerance. Insulinogenic index was significantly reduced in the mutant diabetic subjects and those with impaired and normal glucose tolerance in comparison with the normal control subjects and the non-mutant members. Urinary 24-h C-peptide immunoreactivity excretion was markedly reduced in the mutant diabetic subjects and those with normal and impaired glucose tolerance, compared with the control subjects and the non-mutant family members. Plasma C-peptide immunoreactivity 6 min after glucagon injection was markedly reduced in the mutant diabetic subjects and those with normal and impaired glucose tolerance compared with the control subjects and the non-mutant family members. Si, an index of insulin sensitivity of the four mutant subjects was within normal range. Islet cell antibodies were negative in sera of eight mutated diabetic subjects, 2 and 6 with impaired and normal glucose tolerance, respectively. Diabetic retinopathy and nephropathy were demonstrated in 7 (50%) and 12 (85.7%) of 14 mutant diabetic subjects, respectively. Neurosensory deafness was demonstrated in 12 (85.7%) of 14 mutated diabetic subjects, (66.7%) of 3 mutated impaired glucose tolerant subjects, but not detected in 6 mutated normal glucose tolerant subjects and 11 non-mutant family members. These findings suggest that the tRNALEU(UUR) mutation is associated with pancreatic beta-cell secretory defect of insulin.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-0428
    Keywords: Islet cell antibodies ; Type 1 (insulin-dependent) diabetes ; Epstein-Barr virus ; peripheral blood lymphocytes ; transformation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Islet cell antibodies are usually detected in the sera of almost all Type 1 (insulin-dependent) diabetic patients within several months after onset of the disease. The antibodies then disappear quite early during the course of the disease. The present study was undertaken to detect islet cell antibody-producing clones in peripheral blood lymphocytes of Type 1 diabetic patients whose islet cell antibodies could not be detected in sera. Epstein-Barr virus-transformed lymphocytes were employed to enhance the production of antibodies and to detect the clones from peripheral blood lymphocytes. Peripheral blood lymphocytes were obtained from 40 islet cell antibody-negative Type 1 diabetic patients, 10 antibody-positive Type 1 diabetic patients, 30 Type 2 (non-insulin-dependent) diabetic patients and 40 normal control subjects. Epstein-Barr virus-transformed lymphocytes were cultured for 4 weeks and the culture supernatants were used for assay of islet cell antibodies. Islet cell antibody assays were performed by immunohistochemical methods using peroxidase-labelled protein A for IgG antibodies, peroxidase-labelled anti-human IgM antibodies for IgM antibodies and fresh frozen human pancreatic tissue. IgG-islet cell antibodies were detected in 26 islet cell antibody-negative patients (65%), eight antibody-positive patients (80%) and one Type 2 diabetic patient (3%) in the culture supernatants. Islet cell antibodies in the supernatants could not be detected in any of the control subjects. IgM-islet cell antibodies could not be detected in any of the patients or control subjects. These findings indicate that islet cell antibody-producing clones exist in peripheral blood lymphocytes from Type 1 diabetic patients whose islet cell antibodies cannot be detected in their sera and IgG-islet cell antibodies might be a specific characteristic of Type 1 diabetes. The detection of islet cell antibodies from Epstein-Barr virus-transformed lymphocytes may be useful in examining the role of autoimmune mechanisms in the development of disease.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-0428
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-0428
    Keywords: Type 1 (insulin-dependent) diabetes mellitus ; 64,000-Mr islet protein autoantibodies ; islet cell antibodies ; autoimmune thyroid disease ; long-term diabetes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Autoantibodies to the 64,000-Mr (64K) islet cell protein, identified as glutamic acid decarboxylase, were assayed in 46 Type 1 (insulin-dependent) diabetic patients with a disease duration of more than 5 years. Of 46 Type 1 diabetic patients, 18 (39.1 %) were found to be positive for 64K antibodies and 12 of these patients had been diagnosed with autoimmune thyroid disease. Serum C-peptide levels were not detectable in 15 of 18 patients positive for 64K antibodies. The samples were also tested for titres of islet cell antibodies. Islet cell antibodies were detected in 15 (32.6%) of the 46 patients and all the islet cell antibody positive patients were also found to be positive for 64K antibodies. Furthermore, of these 15 patients 12 had previously been diagnosed with autoimmune thyroid disease. A correlation between levels of 64K antibodies and islet cell antibody titre revealed that higher levels of 64K antibodies were observed in patients who had higher islet cell antibody titre. These results demonstrate that most long-term Type 1 diabetic patients with 64K antibodies were also positive for islet cell antibodies complicated by autoimmune thyroid disease.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-0428
    Keywords: Glucose transporter ; embryogenesis ; hyperglycaemia ; rat embryo culture
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We investigated the expression of glucose transporter genes and protein in embryo and yolk sac during organogenesis and the regulation of glucose transporters during culture in hyperglycaemic media. Erythrocyte-type glucose transporter (GLUT 1) and brain-type glucose transporter (GLUT 3) mRNA were expressed in embryo and yolk sac. The expression of GLUT-1 and GLUT-3 mRNA was abundant on day 9–11 and day 9–10 in the embryo, respectively, and day 9–14 and day 10–11 in the yolk sac, respectively. The levels of GLUT-1 protein in the embryo increased in parallel with the expression of GLUT-1 mRNA during the corresponding period. Immunohistochemical staining of GLUT-1 protein was found principally in the neuroepithelial cells surrounding the neural tube in the embryo on day 10 and appeared in the microvessels surrounding the neural tube after day 12. To test whether the expression of glucose transporter genes and protein was suppressed during hyperglycaemia, conceptuses were cultured in high glucose medium. The abundant expression of GLUT-1 protein was not decreased during culture in high glucose media for 24 h (day 9–10) and was only down-regulated by prolonged exposure to this media for 48 h (day 9–11). We have demonstrated the predominant expression of the high affinity glucose transporter (GLUT 1 and GLUT 3) genes and (GLUT 1) protein in embryo during the early period of organogenesis. The persistently abundant expression of glucose transporter during the critical period of neural tube formation (day 9–10) even in the presence of hyperglycaemia may explain one of the mechanisms of increased glucose flux into the neuroepithelium, which may lead to neural tube defects.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-0428
    Keywords: Key words C-peptide, diabetes mellitus, insulin secretion, MELAS, mitochondrial gene mutation.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Recent evidence suggests possible linkage between diabetes mellitus and mitochondrial gene mutation. We surveyed mitochondrial tRNALEU(UUR) (3243) mutation in 7 mitochondrial encephalomyopathy, lactic acidosis and stroke-like episode (MELAS) families and identified 24 mutated subjects (7 MELAS probands and 17 non-MELAS relatives) as well as 11 non-mutant family members. An OGTT in the 24 mutant relatives revealed 14 diabetic subjects, 3 with impaired glucose tolerance and 7 with normal glucose tolerance and all non-mutant family members as having normal glucose tolerance. Insulinogenic index was significantly reduced in the mutant diabetic subjects and those with impaired and normal glucose tolerance in comparison with the normal control subjects and the non-mutant members. Urinary 24-h C-peptide immunoreactivity excretion was markedly reduced in the mutant diabetic subjects and those with normal and impaired glucose tolerance, compared with the control subjects and the non-mutant family members. Plasma C-peptide immunoreactivity 6 min after glucagon injection was markedly reduced in the mutant diabetic subjects and those with normal and impaired glucose tolerance compared with the control subjects and the non-mutant family members. Si, an index of insulin sensitivity of the four mutant subjects was within normal range. Islet cell antibodies were negative in sera of eight mutated diabetic subjects, 2 and 6 with impaired and normal glucose tolerance, respectively. Diabetic retinopathy and nephropathy were demonstrated in 7 (50 %) and 12 (85.7 %) of 14 mutant diabetic subjects, respectively. Neurosensory deafness was demonstrated in 12 (85.7 %) of 14 mutated diabetic subjects, (66.7 %) of 3 mutated impaired glucose tolerant subjects, but not detected in 6 mutated normal glucose tolerant subjects and 11 non-mutant family members. These findings suggest that the tRNALEU(UUR) mutation is associated with pancreatic beta-cell secretory defect of insulin. [Diabetologia (1994) 37: 818–825]
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1432-0533
    Keywords: Calcium ionophore ; Plasma membrane ; Freeze fracture ; Skeletal muscle ; Muscular dystrophy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The present study was undertaken to investigate changes in the muscle fiber when treated with calcium ionophore. Muscles treated with ionophore showed disruption of the plasma membrane of the muscle fiber, delta lesions, marked contraction of the myofibrills, and dissolution of Z lines and I bands. Black granules of calcium pyroantimonate were observed inside the plasma membrane in ionophoretreated muscle fibers without alteration of the other muscle organelles. The density of the intramembranous particles was less in muscle treated with calcium ionophore than in the control muscle. These results support the previous hypothesis that the increased concentration of intracellular calcium activates calcium-activated neutral protease and induces necrosis of the myofiber. The mechanism for the decrease in the density of intramembranous particles is unsolved. However, the disruption of the plasma membrane may not be a direct effect of calcium ionophore on it, but a secondary phenomenon which occurs after the calcium-induced necrosis of the muscle fibers.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 0006-291X
    Keywords: [abr] FBS; fetal bovine serum ; [abr] H-KCCM; hepatocyte/Kupffer cellconditioned media ; [abr] HCCM; hepatocyte-conditioned media ; [abr] KCCM; Kupffer cellconditioned media ; [abr] TNF-α; tumor necrosis factor-α
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 0006-291X
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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