Insulin-nonspecific reduction in skeletal muscle glucose transport in high-fat-fed rats
| Autor: | A. Y. I. Viana, Yan-Qing Han, Masaru Nagasaki, K. Koshinaka, Yoshiharu Oshida, Yuzo Sato, Masakazu Kubota |
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| Rok vydání: | 2004 |
| Předmět: |
Male
Nitroprusside medicine.medical_specialty Monosaccharide Transport Proteins Endocrinology Diabetes and Metabolism medicine.medical_treatment Blotting Western Biological Transport Active Muscle Proteins Stimulation In Vitro Techniques Biology Phosphatidylinositol 3-Kinases chemistry.chemical_compound Endocrinology Internal medicine medicine Animals Hypoglycemic Agents Insulin Nitric Oxide Donors Rats Wistar Muscle Skeletal Glucose Transporter Type 4 Glycogen Adenylate Kinase Glucose transporter AMPK Skeletal muscle Ribonucleotides Aminoimidazole Carboxamide Dietary Fats Adenosine Rats Glucose medicine.anatomical_structure chemistry Sodium nitroprusside medicine.drug |
| Zdroj: | Metabolism. 53:912-917 |
| ISSN: | 0026-0495 |
| DOI: | 10.1016/j.metabol.2003.12.026 |
| Popis: | High-fat feeding diminishes insulin-stimulated glucose transport in skeletal muscle. However, conflicting results are reported regarding whether phosphatidylinositol (PI)-3 kinase-independent glucose transport is also impaired in insulin-resistant high-fat-fed rodents. The aim of the present study was to study whether non-insulin-dependent mechanisms for stimulation of glucose transport are defective in skeletal muscle from high-fat-fed rats. Rats were fed normal chow diet or high-fat diet for 4 weeks and isolated epitrochlearis muscles were used for measuring glucose transport. Insulin-stimulated glucose transport was significantly lower in rats fed the high-fat diet compared with chow-fed rats (P < .05). Hypoxia-stimulated glucose transport was also reduced in high-fat-fed rats (P < .05). Nevertheless, hypoxia-stimulated adenosine monophosphate-activated protein kinase (AMPK) phosphorylation (Thr172) level was not affected by high-fat feeding. Glucose transport by sodium nitroprusside stimulation was reduced in high-fat-fed rats (P < .05). Protein content of glucose transporter (GLUT)-4 and AMPK-alpha, and glycogen content were comparable between both groups. Our findings provide evidence that high-fat feeding can affect not only insulin but also non-insulin-stimulated glucose transport. A putative defect in common steps in glucose transport may play a role to account for impaired insulin-stimulated glucose transport in rats fed a high-fat diet. |
| Databáze: | OpenAIRE |
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