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Skeletal muscle fatty acid transporter protein expression in type 2 diabetes patients compared with overweight, sedentary men and age-matched, endurance-trained cyclists.

Authors :
Pelsers, M.M.
Pelsers, M.M.
Tsintzas, K.
Boon, H.
Jewell, K.
Norton, L.
Luiken, J.J.F.P.
Glatz, J.F.
van Loon, L.J.
Pelsers, M.M.
Pelsers, M.M.
Tsintzas, K.
Boon, H.
Jewell, K.
Norton, L.
Luiken, J.J.F.P.
Glatz, J.F.
van Loon, L.J.
Source :
Acta Physiologica vol.190 (2007) date: 2007-01-01 nr.3 p.209-219 [ISSN 1748-1708]
Publication Year :
2007

Abstract

AIM: Membrane fatty acid transporters can modulate the balance between fatty acid uptake and subsequent storage and/or oxidation in muscle tissue. As such, skeletal muscle fatty acid transporter protein expression could play an important role in the etiology of insulin resistance and/or type 2 diabetes. METHODS: In the present study, fatty acid translocase (FAT/CD36), plasma membrane-bound fatty acid-binding protein (FABPpm) and fatty acid transport protein 1 (FATP1) mRNA and protein expression were assessed in muscle tissue obtained from 10 sedentary, overweight type 2 diabetes patients (60 +/- 2 years), 10 sedentary, weight-matched normoglycemic controls (60 +/- 2 years) and 10 age-matched, endurance trained cyclists (57 +/- 1 years). RESULTS: Both FAT/CD36 and FATP1 mRNA and protein expression did not differ between groups. In contrast, FABPpm mRNA and protein expression were approx. 30-40% higher in the trained men compared with the diabetes patients (P < 0.01) and sedentary controls (P < 0.05). CONCLUSIONS: Skeletal muscle FAT/CD36, FABPpm and FATP1 mRNA and protein expression are not up- or downregulated in a sedentary and/or insulin resistant state. In contrast, FABPpm expression is upregulated in the endurance trained state and likely instrumental to allow greater fatty acid oxidation rates.

Details

Database :
OAIster
Journal :
Acta Physiologica vol.190 (2007) date: 2007-01-01 nr.3 p.209-219 [ISSN 1748-1708]
Notes :
DOI: 10.1111/j.1748-1716.2007.01698.x, English
Publication Type :
Electronic Resource
Accession number :
edsoai.on1280125623
Document Type :
Electronic Resource