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  • 1
    ISSN: 1432-0428
    Keywords: Spontaneously diabetic mice ; non-obese diabetic mice ; kidney glycosidase activities ; α- & β-glycosidase ; parabiosis ; diabetic control ; diabetes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Spontaneously diabetic non-obese mice of the ICR strain were newly inbred in Shionogi laboratory, Japan. Animals became diabetic suddenly, more frequently and severely in females. Blood glucose levels were 452±73 mg/100 ml with serum insulin levels of 〈 1.0 μU/ml in the fed state. Parabiosis with normal control ICR mice for 2 weeks decreased the blood glucose level to 260±51 mg/ 100ml (P〈0.01) and resulted in serum insulin levels of 46.0±18.0 μU/ml (P〈0.01). Kidney homogenate β-N-acetylglucosaminidase and β-galactosidase activities were reduced in diabetic mice (42% and 44% decrease respectively) (P〈0.025 and P〈0.001), and restored almost to normal after 2 weeks of parabiosis. Renal α-mannosidase activity was decreased 43% (P〈0.001) in the diabetic mice but unaffected by parabiosis. Serum β-N-acetylglucosaminidase, β-galactosidase and α-glucosidase activities were significantly increased in diabetic mice (179%; 233% and 58% increase respectively) (P〈0.005, P〈0.001 and P〈0.001), and returned to normal with parabiosis.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 27 (1984), S. 460-463 
    ISSN: 1432-0428
    Keywords: Non-obese diabetic mice ; pancreas ; stomach ; insulin ; glucagon ; intestine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To investigate the rôle of glucagon in the development of diabetes mellitus, spontaneously diabetic non-obese mice were studied before (group 1) and after the onset of diabetes mellitus (group 2). In group 1, fasting blood glucose and insulin in plasma and pancreas did not differ significantly, while plasma glucagon was elevated (48.9±10.4 versus control 18.6±6.0pmol/l). In group 2, the insulin content of plasma and the pancreas were markedly reduced, whereas plasma glucagon was elevated (180.9±59.1 pmol/l). When diabetic mice were treated with insulin for 4 weeks (group 3), plasma glucagon was markedly reduced compared with that of group 2 (30.3±9.0 pmol/l). In group 1, glucagon and glucagon-like immunoreactivity of the intestine were reduced. The glucagon content of the intestine was elevated in group 2. Group 3 elicited increased contents of gastric glucagon as well as intestinal glucagon-like immunoreactivity. We conclude that, in addition to insulin deficiency, hypersecretion of glucagon might contribute to the development and clinical course of diabetes mellitus in the non-obese diabetic mouse.
    Type of Medium: Electronic Resource
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