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.

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  • Additional Information
    • Source:
      Publisher: Springer Verlag Country of Publication: Germany NLM ID: 9200299 Publication Model: Print Cited Medium: Print ISSN: 0940-5429 (Print) Linking ISSN: 09405429 NLM ISO Abbreviation: Acta Diabetol Subsets: MEDLINE
    • Publication Information:
      Publication: Berlin : Springer Verlag
      Original Publication: Berlin : Springer International, c1991-
    • Subject Terms:
      Dietary Fats* ; Insulin Resistance*; Adipose Tissue/*metabolism ; Diabetes Mellitus, Type 2/*metabolism ; Liver/*metabolism ; Muscles/*metabolism ; Receptor, Insulin/*metabolism; Analysis of Variance ; Animals ; Blood Glucose/metabolism ; Cells, Cultured ; Female ; Glucose/metabolism ; Glucose Tolerance Test ; Glycogen Synthase/metabolism ; Insulin/blood ; L-Lactate Dehydrogenase/metabolism ; Liver Glycogen/metabolism ; Male ; Mice ; Mice, Inbred Strains ; Weight Gain
    • 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.
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    • Accession Number:
      0 (Blood Glucose)
      0 (Dietary Fats)
      0 (Insulin)
      0 (Liver Glycogen)
      EC 1.1.1.27 (L-Lactate Dehydrogenase)
      EC 2.4.1.11 (Glycogen Synthase)
      EC 2.7.10.1 (Receptor, Insulin)
      IY9XDZ35W2 (Glucose)
    • Publication Date:
      Date Created: 19920101 Date Completed: 19921015 Latest Revision: 20191028
    • Publication Date:
      20240627
    • Accession Number:
      10.1007/BF00572823
    • Accession Number:
      1520900