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The development of insulin resistance with high fat feeding in rats does not involve either decreased insulin receptor tyrosine kinase activity or membrane glycoprotein PC-1.
The development of insulin resistance with high fat feeding in rats does not involve either decreased insulin receptor tyrosine kinase activity or membrane glycoprotein PC-1.
- Source :
-
Biochemical and molecular medicine [Biochem Mol Med] 1996 Dec; Vol. 59 (2), pp. 174-81. - Publication Year :
- 1996
-
Abstract
- Recent studies have suggested that the insulin receptor tyrosine kinase inhibitor, membrane glycoprotein PC-1, may play a role in certain insulin resistant states. In the present study, we examined whether either insulin receptor function or PC-1 activity was altered during the development of insulin resistance that occurs with high fat feeding in normal rats. Over the course of 14 days of high fat feeding, both maximal and submaximal (physiological) insulin-stimulated skeletal muscle glucose uptake decreased gradually; after 14 days of high fat feeding, submaximal and maximal insulin-stimulated glucose uptake decreased by approximately 40 and approximately 50%, respectively. In contrast, in the same muscles (tibialis anterior) of these animals, neither insulin receptor content nor insulin-stimulated insulin receptor autophosphorylation was altered after 14 days of high fat feeding. PC-1 has both nucleotide pyrophosphatase (EC 3.6.1.9) and alkaline phosphodiesterase I (EC 3.1.4.1) enzyme activities. These enzyme activities showed no changes during the course of 14 days of high fat feeding. Individual data revealed that there was no significant correlation between insulin-stimulated glucose uptake and alkaline phosphodiesterase or nucleotide pyrophosphatase activity (P > 0.05). Together, these data indicate that neither defects in insulin receptor function nor elevated PC-1 activities are involved in the development of insulin resistance in rats with high fat feeding, and the insulin resistance induced with high fat feeding is likely due to postreceptor defects in skeletal muscle.
- Subjects :
- Animals
Insulin physiology
Male
Membrane Glycoproteins antagonists & inhibitors
Rats
Rats, Wistar
Receptor, Insulin antagonists & inhibitors
Dietary Fats administration & dosage
Insulin Resistance
Membrane Glycoproteins metabolism
Phosphoric Diester Hydrolases
Pyrophosphatases
Receptor, Insulin metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 1077-3150
- Volume :
- 59
- Issue :
- 2
- Database :
- MEDLINE
- Journal :
- Biochemical and molecular medicine
- Publication Type :
- Academic Journal
- Accession number :
- 8986641
- Full Text :
- https://doi.org/10.1006/bmme.1996.0084