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  • Flavonoid  (1)
  • Key words Mitochondrial DNA  (1)
  • Keywords Insulin resistance  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Mitochondrial DNA, diabetes and pancreatic pathology in Kearns–Sayre syndrome (1995)
    Springer
    Diabetologia 38 (1995), S. 868-871 
    Details
    ISSN: 1432-0428
    Keywords: Key words Mitochondrial DNA ; pancreatic islets ; diabetes ; Kearns ; Sayre syndrome.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Mitochondrial DNA (mtDNA) mutations are associated with diabetes mellitus but their role in the onset of hyperglycaemia is unclear. A patient presented with diabetes requiring insulin therapy at the age of 7 years, followed by diagnosis of Kearns–Sayre syndrome (KSS). Beta-cell function was absent at age 19 years as shown by lack of glucose-stimulated C-peptide secretion. Following development of a cardiac conduction defect the patient died aged 21 years. Analysis of mtDNA in blood and several tissues revealed related re-arranged deletions, duplications and deletion dimers in addition to normal mtDNA with the highest levels of duplications in kidney and blood. Pancreatic tissue from the KSS patient was compared with tissue from an insulin-dependent diabetic patient with a similar clinical history of diabetes. Islets in KSS were small, regular in shape and contained predominantly glucagon-containing cells with no evidence of beta cells. In comparison, a small number of beta cells were present in some of the larger more irregularly-shaped islets from the insulin-dependent diabetic patient. These data together suggest that in KSS the loss of beta cells at the onset of diabetes is less disruptive to islet architecture: a small proportion of beta cells or their gradual destruction over a long period would allow retention of islet shape. Abnormal function of the re-arranged mtDNA could affect both development and function of pancreatic islet cells since glucose-stimulated insulin secretion is energy dependent. [Diabetologia (1995) 38: 868–871].
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050366
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    A common mitochondrial DNA variant is associated with insulin resistance in adult life (1998)
    Springer
    Diabetologia 41 (1998), S. 54-58 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Insulin resistance ; mitochondrial DNA ; mitochondrial diabetes.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Mitochondrial DNA is maternally inherited. Mitochondrial DNA mutations could contribute to the excess of maternal over paternal inheritance of non-insulin-dependent diabetes mellitus (NIDDM). We therefore investigated the relationship between this variant, insulin resistance and other risk factors in a cohort which had been well characterised with respect to diabetes. Blood DNA was screened from 251 men born in Hertfordshire 1920–1930 in whom an earlier cohort study had shown that glucose tolerance was inversely related to birthweight. The 16 189 variant (T- 〉 C transition) in the first hypervariable region of mitochondrial DNA was detected using the polymerase chain reaction and restriction digestion. DNA analysis showed that 28 of the 251 men (11 %) had the 16 189 variant. The prevalence of the 16 189 variant increased progressively with fasting insulin concentration (p 〈 0.01). The association was independent of age and body mass index and was present after exclusion of the patients with NIDDM or impaired glucose tolerance. We found that insulin resistance in adult life was associated with the 16 189 variant. This study provides the first evidence that a frequent mitochondrial variant may contribute to the phenotype in patients with a common multifactorial disorder. [Diabetologia (1998) 41: 54–58]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050866
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Identification of an UDP-glucose: Flavonol 3-O-glucosyl-transferase from cell suspension cultures of soybean (Glycine max L.) (1977)
    Springer
    Planta 136 (1977), S. 53-59 
    Details
    ISSN: 1432-2048
    Keywords: Cell culture ; Flavonoid ; Glycine ; O-glucosyltransferase ; UDP-glucose
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract A glucosyltransferase, which catalyses the glucosylation of flavonols, using uridine diphosphate-D-glucose as glucose donor, has been isolated and purified about 5–10 fold from cell suspension cultures of soybean (Glycine max L., var. Mandarin). The pH optimum for this reaction was ca. 8.5 in glycine-NaOH buffer, and no additional cofactors were required. The enzyme glucosylated the following flavonols predominantly at the 3-position: quercetin (Km 126 μM), kaempferol (Km 172 μM), isorhamnetin (Km 200 μM) and fisetin (Km 270 μM). With quercetin as substrate, the apparent Km value for uridine diphosphate-D-glucose was 0.3 M. Glucosylation of flavonols and flavones by this preparation occurred weakly also at the 7-position. No activity was found with dihydroquercetin, naringenin, 4,2′,4′-trihydroxychalcone, daidzein or texasin. The enzyme was specific for flavonoid compounds, since no activity was observed towards cinnamic acids or simple phenols. However, the preparation was contaminated by a vanillic acid glucosyltransferase, from which it could be partially separated by ionexchange chromatography. The specific activity of the flavonol 3-O-glucosyltransferase increased with age of the culture, reaching a maximum late in the growth cycle of the culture.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00387925
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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