caa a22 4500 469128712 CHVBK 20180323133158.0 cr unu---uuuuu 170328e19920301xx s 000 0 eng 10.1007/BF00572823 doi (NATIONALLICENCE)springer-10.1007/BF00572823 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 [Elektronische Daten] [C. Hedeskov, K. Capito, H. Islin, S. Hansen, P. Thams] 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. Springer-Verlag, 1992 Type 2 diabetes nationallicence Insulin resistance nationallicence Postreceptor defects nationallicence Animal model nationallicence High fat diet nationallicence Hedeskov C. Department of Biochemistry A, The Panum Institute, University of Copenhagen, Blegdamsvej 3, DK-2200, Copenhagen N, Denmark aut Capito K. Department of Biochemistry A, The Panum Institute, University of Copenhagen, Blegdamsvej 3, DK-2200, Copenhagen N, Denmark aut Islin H. Department of Biochemistry A, The Panum Institute, University of Copenhagen, Blegdamsvej 3, DK-2200, Copenhagen N, Denmark aut Hansen S. Department of Biochemistry A, The Panum Institute, University of Copenhagen, Blegdamsvej 3, DK-2200, Copenhagen N, Denmark aut Thams P. Department of Biochemistry A, The Panum Institute, University of Copenhagen, Blegdamsvej 3, DK-2200, Copenhagen N, Denmark aut Acta Diabetologica Springer-Verlag 29/1(1992-03-01), 14-19 0940-5429 29:1<14 1992 29 592 https://doi.org/10.1007/BF00572823 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/BF00572823 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Hedeskov C. Department of Biochemistry A, The Panum Institute, University of Copenhagen, Blegdamsvej 3, DK-2200, Copenhagen N, Denmark aut NATIONALLICENCE 700 1- Capito K. Department of Biochemistry A, The Panum Institute, University of Copenhagen, Blegdamsvej 3, DK-2200, Copenhagen N, Denmark aut NATIONALLICENCE 700 1- Islin H. Department of Biochemistry A, The Panum Institute, University of Copenhagen, Blegdamsvej 3, DK-2200, Copenhagen N, Denmark aut NATIONALLICENCE 700 1- Hansen S. Department of Biochemistry A, The Panum Institute, University of Copenhagen, Blegdamsvej 3, DK-2200, Copenhagen N, Denmark aut NATIONALLICENCE 700 1- Thams P. Department of Biochemistry A, The Panum Institute, University of Copenhagen, Blegdamsvej 3, DK-2200, Copenhagen N, Denmark aut NATIONALLICENCE 773 0- Acta Diabetologica Springer-Verlag 29/1(1992-03-01), 14-19 0940-5429 29:1<14 1992 29 592 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer