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  • 1
    Electronic Resource
    Electronic Resource
    Reactive Ion Beam Etching for Microcavity Surface Emitting Laser Fabrication: Technology and Damage Characterization (1993)
    s.l. ; Stafa-Zurich, Switzerland
    Materials science forum Vol. 140-142 (Oct. 1993), p. 641-658 
    Details
    ISSN: 1662-9752
    Source: Scientific.Net: Materials Science & Technology / Trans Tech Publications Archiv 1984-2008
    Topics: Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics
    Type of Medium: Electronic Resource
    URL: http://www.tib-hannover.de/fulltexts/2011/0528/02/00/transtech_doi~10.4028%252Fwww.scientific.net%252FMSF.140-142.641.pdf
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  • 2
    Electronic Resource
    Electronic Resource
    HepG2/erythrocyte glucose transporter (GLUT1) gene in NIDDM: a population association study and molecular scanning in Japanese subjects (1995)
    Springer
    Diabetologia 38 (1995), S. 942-947 
    Details
    ISSN: 1432-0428
    Keywords: Key words Non-insulin-dependent diabetes mellitus ; genetics ; GLUT1 ; single-strand conformation polymorphism ; mutation.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To evaluate the role of mutations in the glucose transporter (GLUT1) gene in Japanese patients with non-insulin-dependent diabetes mellitus (NIDDM), we first conducted a population association study using the XbaI polymorphism of the gene. A polymerase chain reaction (PCR)-based assay was developed and used for the analysis. When analysed in 91 diabetic patients and 87 non-diabetic control subjects, the distribution of the genotype frequency was significantly different between the two groups (p = 0.0025). The (−) allele was significantly associated with NIDDM (odds ratio 2.317, 95 % confidence interval 1.425–3.768). To identify possible mutation(s) in the GLUT1 gene, which was in linkage disequilibrium with the (−) allele, all ten exons of the gene were analysed by PCR single-strand conformation polymorphism (SSCP) analysis in 53 diabetic patients with at least one (−) allele. Variant SSCP patterns were detected in exons 2, 4, 5, 7, 9 and 10. Sequence analysis revealed that all the variants represented silent mutations. One of the variants in exon 2, GCT (Ala15) → GCC(Ala), created a HaeIII restriction site. This polymorphism was common in Japanese subjects with heterozygosity of 0.36 and polymorphism information content 0.29. We conclude that the structural mutation of GLUT1 is rare and not likely to be a major genetic determinant of NIDDM in Japanese subjects. The XbaI (−) allele of the GLUT1 gene appeared to be a genetic marker of NIDDM in Japanese subjects. The possibility of the presence of mutation(s) in the regulatory region of the gene or in another locus nearby could not be excluded. [Diabetologia (1995) 38: 942–947]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400583
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Overexpression of mitochondrial FAD-linked glycerol-3-phosphate dehydrogenase does not correct glucose-stimulated insulin secretion from diabetic GK rat pancreatic islets (1998)
    Springer
    Diabetologia 41 (1998), S. 649-653 
    Details
    ISSN: 1432-0428
    Keywords: Keywords FAD-linked glycerol-3-phosphate dehydrogenase ; GK rat ; non-insulin-dependent diabetes mellitus ; insulin secretion ; adenovirus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Glucose-stimulated insulin secretion is impaired in GK (Goto-Kakizaki) rats, perhaps because of abnormalities in glucose metabolism in pancreatic islet beta cells. The glycerol phosphate shuttle plays a major role in glucose metabolism by reoxidizing cytosolic NADH generated by glycolysis. In the pancreatic islets of GK rats, the activity of mitochondrial FAD-linked glycerol-3-phosphate dehydrogenase (mGPDH), the key enzyme of the glycerol phosphate shuttle, is decreased and this abnormality may be responsible, at least in part, for impaired glucose-stimulated insulin secretion. To investigate this possibility, we overexpressed mGPDH in islets isolated from GK rats via recombinant adenovirus-mediated gene transduction, and examined glucose-stimulated insulin secretion. In islets isolated from diabetic GK rats at 8 to 10 weeks of age, glucose-stimulated insulin secretion was severely impaired, and mGPDH activity was decreased to 79 % of that in non-diabetic Wistar rats. When mGPDH was overexpressed in islets from GK rats, enzyme activity and protein content increased 2- and 6-fold, respectively. Basal (3 mmol/l glucose) and glucose-stimulated (20 mmol/l) insulin secretion from the Adex1CAlacZ-infected GK rat islets were, respectively, 4.4 ± 0.7 and 8.1 ± 0.7 ng · islet−1· 30 min−1, and those from mGPDH-overexpressed GK rat islets 4.7 ± 0.3 and 9.1 ± 0.8 ng · islet−1· 30 min−1, in contrast to those from the Adex1CAlacZ-infected non-diabetic Wistar rat islets (4.7 ± 1.6 and 47.6 ± 11.9 ng · islet−1· 30 min−1). Thus, glucose-stimulated insulin secretion is severely impaired in GK rats even in the stage when mGPDH activity is modestly decreased, and at this stage, overexpression of mGPDH cannot restore glucose-stimulated insulin secretion. We conclude that decreased mGPDH activity in GK rat islets is not the defect primarily responsible for impaired glucose-stimulated insulin secretion. [Diabetologia (1998) 41: 649–653]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050963
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  • 4
    Electronic Resource
    Electronic Resource
    Overexpression of dominant negative mutant hepatocyte nuclear factor (HNF)-1α inhibits arginine-induced insulin secretion in MIN6 cells (1999)
    Springer
    Diabetologia 42 (1999), S. 887-891 
    Details
    ISSN: 1432-0428
    Keywords: Keywords MODY ; hepatocyte nuclear factor-1α ; recombinant adenovirus ; MIN6 cells ; dominant negative effect ; arginine.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. To explain the mechanisms whereby mutations in the HNF-1α gene cause insulin secretory defects. Methods. A truncated mutant HNF-1α (HNF-1α288 t) was overexpressed in hepatoma cells (HepG2) and murine insulinoma cells (MIN6) using a recombinant adenovirus system and expression of the HNF-1α target genes and insulin secretion were examined. Results. Expression of phenylalanine hydroxylase and α1-antitrypsin genes, the target genes of HNF-1α, was suppressed in HepG2 cells by overexpression of HNF-1α288 t. In MIN6 cells, overexpression of HNF-1α288 t did not change insulin secretion stimulated by glucose (5 mmol/l and 25 mmol/l) or leucine (20 mmol/l). Potentiation of insulin secretion by arginine (20 mmol/l, in the presence of 5 mmol/l or 25 mmol/l glucose) was, however, reduced (p 〈 0.0001 and p = 0.027, respectively). Similarly reduced responses were observed when stimulated with homoarginine. Expression of the cationic amino acid transporter-2 was not reduced and insulin secretory response to membrane depolarization by 50 mmol/l KCl was intact. Conclusion/interpretation. The HNF-1α288 t, which is structurally similar to the mutant HNF-1α expressed from the common MODY3 allele, P291fsinsC, exerts a dominant negative effect. Suppression of HNF-1α in MIN6 cells severely impaired potentiation of insulin secretion by arginine, whereas glucose-stimulated and leucine-stimulated insulin secretion was intact. Our findings delineate the complex nature of beta-cell failure in patients with MODY3. This cell model will be useful for further investigation of the mechanism of insulin secretory defects in these patients. [Diabetologia (1999) 42: 887–891]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051242
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  • 5
    Electronic Resource
    Electronic Resource
    HepG2/erythrocyte glucose transporter (GLUT1) gene in NIDDM: a population association study and molecular scanning in Japanese subjects (1995)
    Springer
    Diabetologia 38 (1995), S. 942-947 
    Details
    ISSN: 1432-0428
    Keywords: Non-insulin-dependent diabetes mellitus ; genetics ; GLUT1 ; single-strand conformation polymorphism ; mutation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To evaluate the role of mutations in the glucose transporter (GLUT1) gene in Japanese patients with non-insulin-dependent diabetes mellitus (NIDDM), we first conducted a population association study using the XbaI polymorphism of the gene. A polymerase chain reaction (PCR)-based assay was developed and used for the analysis. When analysed in 91 diabetic patients and 87 non-diabetic control subjects, the distribution of the genotype frequency was significantly different between the two groups (p=0.0025). The (−) allele was significantly associated with NIDDM (odds ratio 2.317, 95% confidence interval 1.425−3.768). To identify possible mutation(s) in the GLUT1 gene, which was in linkage disequilibrium with the (−) allele, all ten exons of the gene were analysed by PCR single-strand conformation polymorphism (SSCP) analysis in 53 diabetic patients with at least one (−) allele. Variant SSCP patterns were detected in exons 2, 4, 5, 7, 9 and 10. Sequence analysis revealed that all the variants represented silent mutations. One of the variants in exon 2, GCT (Ala15)→GCC(Ala), created a HaeIII restriction site. This polymorphism was common in Japanese subjects with heterozygosity of 0.36 and polymorphism information content 0.29. We conclude that the structural mutation of GLUT1 is rare and not likely to be a major genetic determinant of NIDDM in Japanese subjects. The Xbal (−) allele of the GLUT1 gene appeared to be a genetic marker of NIDDM in Japanese subjects. The possibility of the presence of mutation(s) in the regulatory region of the gene or in another locus nearby could not be excluded.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400583
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    Paper (German National Licenses)
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  • 6
    Electronic Resource
    Electronic Resource
    Detection of variants in the mitochondrial glycerophosphate dehydrogenase gene in Japanese NIDDM patients (1997)
    Springer
    Diabetologia 40 (1997), S. 339-343 
    Details
    ISSN: 1432-0428
    Keywords: Keywords mGPDH gene ; amino acid variants ; NIDDM ; PCR-SSCP ; beta cells.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Mitochondrial FAD-linked glycerophosphate dehydrogenase (mGPDH) is thought to be an important factor for glucose sensing in pancreatic beta cells. To evaluate the significance of the mGPDH gene in the development of non-insulin-dependent diabetes mellitus (NIDDM), we set up primers and conditions for polymerase chain reaction (PCR) amplification of the coding exons and flanking regions. Screening of 100 Japanese NIDDM patients for mutations using the PCR-single strand conformation polymorphism (SSCP) method revealed four variants (ACA:Thr243-ACG:Thr243, CAT:His264-CGT:Arg264, GCA:Ala305-GCC:Ala305, GCA:Ala 306-TCA:Ser306). The His264-Arg264 variant was found in 36 patients, while the other variants were found in only one patient each. Neither the genotypic (χ2 = 3.15, p = 0.21) nor the allelic (χ2 = 2.27, p = 0.13) frequency of the His264-Arg264 mutation differed between 253 Japanese NIDDM patients and 157 non-diabetic subjects. In addition, in NIDDM patients, neither the treatment modality nor body mass index differed between those with and without this mutation. These results suggest that inherited defects at this locus do not make a major contribution to genetic susceptibility to NIDDM in the Japanese population. [Diabetologia (1997) 40: 339–343]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050684
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  • 7
    Electronic Resource
    Electronic Resource
    Effect of tolbutamide on fructose-6-phosphate, 2-kinase and fructose-2, 6-bisphosphatase in rat liver
    Amsterdam : Elsevier
    Biochemical and Biophysical Research Communications 139 (1986), S. 687-692 
    Details
    ISSN: 0006-291X
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1016/S0006-291X(86)80045-6
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  • 8
    Electronic Resource
    Electronic Resource
    Mapping the human liver/islet glucose transporter (GLUT2) gene within a genetic linkage map of chromosome 3q using a (CA)"n dinucleotide repeat polymorphism and characterization of the polymorphism in three racial groups
    Amsterdam : Elsevier
    Genomics 13 (1992), S. 495-501 
    Details
    ISSN: 0888-7543
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1016/0888-7543(92)90116-A
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    Paper (German National Licenses)
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  • 9
    Electronic Resource
    Electronic Resource
    A polymorphic (CA)"n repeat element maps the human glucokinase gene (GCK) to chromosome 7p
    Amsterdam : Elsevier
    Genomics 12 (1992), S. 319-325 
    Details
    ISSN: 0888-7543
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1016/0888-7543(92)90380-B
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    Paper (German National Licenses)
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  • 10
    Electronic Resource
    Electronic Resource
    Effect of tolbutamide on fructose-6-phosphate, 2-kinase and fructose-2, 6-bisphosphatase in rat liver
    Amsterdam : Elsevier
    Biochemical and Biophysical Research Communications 139 (1986), S. 687-692 
    Details
    ISSN: 0006-291X
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1016/S0006-291X(86)80045-6
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
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