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  • 1
    Electronic Resource
    Electronic Resource
    Long-term fat-feeding-induced insulin resistance in normal NMRI mice: postreceptor changes of liver, muscle and adipose tissue metabolism resembling those of type 2 diabetes (1992)
    Springer
    Acta diabetologica 29 (1992), S. 14-19 
    Details
    ISSN: 1432-5233
    Keywords: Type 2 diabetes ; Insulin resistance ; Postreceptor defects ; Animal model ; High fat diet
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Postreceptor insulin resistance was studied in liver, muscle and adipose tissue from NMRI mice of both sexes made diabetic by long-term fat-feeding. Intravenous glucose tolerance tests showed a combination of impaired glucose tolerance and increased plasma insulin concentrations consistent with insulin resistance and reduced peripheral and hepatic uptake of glucose. In the morning, the fat-fed mice were normoinsulinaemic and hyperglycaemic. Liver glucokinase activity and glycogen content were reduced whereas lactate dehydrogenase activity was enhanced. Fatty acid synthase activity was decreased but glucose 6-phosphate dehydrogenase and the rate limiting enzyme in fatty acid synthesis, acetyl CoA carboxylase, were both unaffected. In muscle, the proportion of glycogen synthase in the active I-form was decreased. Total glycogen synthase activity was not affected. In isolated adipocytes, basal and insulin-stimulated glucose oxidation, as well as basal and insulin-stimulated lipogenesis from glucose were all severely inhibited, oxidation more so than lipogenesis. It is concluded that insulin resistance and postreceptor metabolic disorders in liver, muscle and adipose tissue from mice made diabetic by long-term fat-feeding are very similar to those demonstrated in human type 2 diabetics and may be studied in more detail and with more ease in this particular animal model.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00572823
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Characteristics of an adenylate cyclase enhancing factor from mouse pancreatic islet cytosol (1984)
    Springer
    Diabetologia 26 (1984), S. 375-378 
    Details
    ISSN: 1432-0428
    Keywords: Adenylate cyclase ; cytosol ; pancreatic islets ; mouse
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The role of cytosolic components in the regulation of mouse pancreatic islet adenylate cyclase activity was studied. Addition of mouse islet cytosol (27000 g supernatant of mouse islet sonicate), devoid of adenylate cyclase activity itself, increased adenylate cyclase activity by 93±17% (n = 9) in the 27000 g total particulate fraction of mouse islets. Addition of GTP stimulated adenylate cyclase activity by 91±11% (n = 13) or to the same degree as cytosol. Like GTP, the substance causing the enhancing activity of the cytosol was found to be dialysable, resistant to heat, sensitive to charcoal treatment and alkaline phosphatase and insensitive to digestion with trypsin. However, in contrast to the stimulation by GTP, the stimulation by cytosol was not inhibited by guanosine 5′-0-(2-thiodiphosphate), and furthermore, the effects of cytosol and GTP were additive. Neither NAD nor phosphoenolpyruvate stimulated adenylate cyclase activity. The cytosolic factor did not confer sensitivity towards glucose, Ca2+ or Ca2+-calmodulin on adenylate cyclase. The results demonstrate that mouse pancreatic islets contain a phosphocompound (or several compounds) distinct from GTP and capable of markedly stimulating adenylate cyclase. The identity of the compound and its physiological significance remain to be established.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00266040
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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