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  • Electronic Resource  (5)
  • Type 2 (non-insulin-dependent) diabetes mellitus  (3)
  • Cell & Developmental Biology  (2)
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  • Electronic Resource  (5)
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  • 1
    Electronic Resource
    Electronic Resource
    Localisation of islet amyloid polypeptide and its carboxy terminal flanking peptide in islets of diabetic man and monkey (1991)
    Springer
    Diabetologia 34 (1991), S. 449-451 
    Details
    ISSN: 1432-0428
    Keywords: Islet amyloid polypeptide ; islet amyloid ; Type 2 (non-insulin-dependent) diabetes mellitus ; Beta cell ; pancreas
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Islet amyloid polypeptide is a normal constituent of islet Beta cells and is derived from a larger precursor by removal of flanking peptides at the carboxy (C) and amino (N) terminals. The role of these flanking peptides in the formation of amyloid in Type 2 (non-insulin-dependent) diabetes mellitus and in insulinomas is unknown. The C-terminal flanking peptide of islet amyloid polypeptide was localised by immunocytochemistry in human and monkey pancreatic islets from Type 2 diabetic and non-diabetic individuals by use of specific polyclonal antisera. Immunoreactivity for the C-terminal peptide was found in insulincontaining cells in both diabetic and non-diabetic tissue: no antibody binding was detected in islet amyloid of Type 2 diabetic man or of monkeys although a positive reaction occurred with antisera for islet amyloid polypeptide. The C-terminal peptide was localised by immunogold electron microscopy in the insulin granules in both diabetic and nondiabetic individuals but, unlike islet amyloid polypeptide, was not detected in lysosomes. The absence of immunoreactivity for the C-terminal peptide in amyloid suggests that incomplete cleavage of this flanking peptide from islet amyloid polypeptide is not a factor in the formation of islet amyloid.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00403186
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  • 2
    Electronic Resource
    Electronic Resource
    Chronic overproduction of islet amyloid polypeptide/amylin in transgenic mice: lysosomal localization of human islet amyloid polypeptide and lack of marked hyperglycaemia or hyperinsulinaemia (1993)
    Springer
    Diabetologia 36 (1993), S. 1258-1265 
    Details
    ISSN: 1432-0428
    Keywords: Islet amyloid polypeptide ; amylin ; transgenic mouse ; islet beta cell ; islet amyloid ; glucose metabolism ; insulin resistance ; Type 2 (non-insulin-dependent) diabetes mellitus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Type 2 (non-insulin-dependent) diabetes mellitus is characterised by hyperglycaemia, peripheral insulin resistance, impaired insulin secretion and pancreatic islet amyloid formation. The major constituent of islet amyloid is islet amyloid polypeptide (amylin). Islet amyloid polypeptide is synthesized by islet beta cells and co-secreted with insulin. The ability of islet amyloid polypeptide to form amyloid fibrils is related to its species-specific amino acid sequence. Islet amyloid associated with diabetes is only found in man, monkeys, cats and racoons. Pharmacological doses of islet amyloid polypeptide have been shown to inhibit insulin secretion as well as insulin action on peripheral tissues (insulin resistance). To examine the role of islet amyloid polypeptide in the pathogenesis of Type 2 diabetes, we have generated transgenic mice with the gene encoding either human islet amyloid polypeptide (which can form amyloid) or rat islet amyloid polypeptide, under control of an insulin promoter. Transgenic islet amyloid polypeptide mRNA was detected in the pancreas in all transgenic mice. Plasma islet amyloid polypeptide levels were significantly elevated (up to 15-fold) in three out of five transgenic lines, but elevated glucose levels, hyperinsulinaemia and obesity were not observed. This suggests that insulin resistance is not induced by chronic hypersecretion of islet amyloid polypeptide. Islet amyloid polypeptide immunoreactivity was localized to beta-cell secretory granules in all mice. Islet amyloid polypeptide immunoreactivity in beta-cell lysosomes was seen only in mice with the human islet amyloid polypeptide gene, as in human beta cells, and might represent an initial step in intracellular formation of amyloid fibrils. These transgenic mice provide a unique model with which to examine the physiological function of islet amyloid polypeptide and to study intracellular and extracellular handling of human islet amyloid polypeptide in pancreatic islets.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400803
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Diabetes mellitus in Macaca mulatta monkeys is characterised by islet amyloidosis and reduction in beta-cell population (1993)
    Springer
    Diabetologia 36 (1993), S. 378-384 
    Details
    ISSN: 1432-0428
    Keywords: Type 2 (non-insulin-dependent) diabetes mellitus ; Macaca mulatta ; islet of Langerhans — pathology ; amyloid ; islet amyloid polypeptide ; beta cells ; obesity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Diabetes mellitus in Macaca mulatta rhesus monkeys is preceded by phases of obesity and hyperinsulinaemia and is similar to Type 2 (non-insulin-dependent) diabetes mellitus in man. To relate the progression of the disease to quantitative changes in islet morphology, post-mortem pancreatic tissue from 26 monkeys was examined. Four groups of animals were studied: group I — young, lean and normal (n=3); group II — older (〉10 years), lean and obese, normoglycaemic (n=9); group III — normoglycaemic and hyperinsulinaemic (n=6); group IV — diabetic (n=8). Areas of islet amyloid, beta cells and islets were measured on stained histological sections. Islet size was larger in animals from groups III (p〈0.01) and IV (p〈0.0001) compared to groups I and II. The mean beta-cell area per islet in Μm2 was increased in group III (p〈0.05) and reduced in group IV (p〈0.001) compared to groups I and II. Mean beta-cell area per islet correlated with fasting plasma insulin (r=0.76, p〈0.001) suggesting that hyper- and hypoinsulinaemia are related to the beta-cell population. Amyloid was absent in group I but small deposits were present in three of nine (group II) and in four of six (group III) animals, occupying between 0.03–45% of the islet space. Amyloid was present in eight of eight diabetic animals (group IV) occupying between 37–81% of the islet area. Every islet was affected in seven of eight diabetic monkeys. There was no correlation of degree of amyloidosis with age, body weight, body fat proportion or fasting insulin. Islet amyloid appears to precede the development of overt diabetes in Macaca mulatta and is likely to be a factor in the destruction of islet cells and onset of hyperglycaemia.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00402271
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  • 4
    Electronic Resource
    Electronic Resource
    Prospects for the genetic engineering of milk (1992)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 49 (1992), S. 121-127 
    Details
    ISSN: 0730-2312
    Keywords: milk/protein ; transgenic ; bovine ; dairy industry ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Milk and milk products comprise a substantial fraction of the protein intake of the industrialised West. The establishment of germline manipulation techniques in cows offers opportunities for directly manipulating milk composition to produce products with enhanced nutritional and processing properties. The major milk proteins are encoded by a small number of abundantly expressed single-copy genes and a number of possible manipulations are described. Milk proteins exhibit complex interactions with each other and with other constituents of milk. It will, therefore, be necessary to utilise model systems to evaluate the consequences of these proposed changes before embarking upon the costly and time-consuming process of manipulating the bovine genome.
    Additional Material: 2 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240490204
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    Paper (German National Licenses)
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  • 5
    Electronic Resource
    Electronic Resource
    The beginning of a genetic analysis of recombination proficiencyThis investigation was supported in part by a Public Health Service research grant (AI 05371) from the National Institute of Allergy and Infectious Diseases, and by a grant (GB 2981) from the National Science Foundation. (1967)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 70 (1967), S. 165-180 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Recombination-deficient mutants of Escherichia coli have been isolated as members of a class showing reduced ability to mother recombinants when crossed with a given Hfr strain. All those showing less than one-tenth the ability of their immediate ancestors in mothering merodiploids have been eliminated from consideration, as have those strains of reduced fertility with only one donor strain. The remainder are all more sensitive to ultraviolet light (UV) than were their immediate ancestors; differences in levels of sensitivity are evident. Mutants have been isolated from two distantly related ancestors, and the sets of mutants from each are divisible into three phenotypic groups. The strains in the first group are the least UV-sensitive (UVs), and lambda lysogens of these show normal spontaneous induction. The strains in the second and third groups are more UVs than those in Group 1, and lysogens of these show abnormally low spontaneous induction. Groups 2 and 3 are separable by their levels of fertility with the Hfr strain (KL16) found to transfer the rec+ allele of some of the strains early in conjugation. The strains more fertile with KL16 are in Group 2, and those less fertile are in Group 3. Two mutants (JC1553 and AB2463) of different parentage but both in phenotypic Group 2 have been analyzed by transduction; and a single mutation probably determines both their mutant UVs and Rec- phenotypes. When the mutants of different parentage are arranged together, a continuous ranking of fertilities is observed. Preliminary complementation tests show no complementation between those mutations carried by strains in Group 2 and Group 3 which have been tested. Complementation has been observed between those mutations carried by strains in Group 1 and those carried by strains in Groups 2 and 3.
    Additional Material: 3 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1040700412
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    Paper (German National Licenses)
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