General Information:

Id: 6,509 (click here to show other Interactions for entry)
Diseases: Diabetes mellitus, type II - [OMIM]
Insulin resistance
Homo sapiens
article
Reference: Bandyopadhyay GK et al.(2006) Increased malonyl-CoA levels in muscle from obese and type 2 diabetic subjects lead to decreased fatty acid oxidation and increased lipogenesis; thiazolidinedione treatment reverses these defects Diabetes 55: 2277-2285 [PMID: 16873691]

Interaction Information:

Comment Another control point for muscle fatty acid oxidation relates to the ability of muscle cells to take up fatty acids through fatty acid transporters/translocators. Therefore, FAT/ CD36 and FATP4 were measured in muscle homogenates plasma membrane and microsomal fractions obtained in both the basal and insulin-stimulated state. In the lean subjects, insulin had the expected effect to increase translocation of these two proteins from the microsomes to the plasma membrane, but this insulin effect was absent in the untreated type 2 diabetic subjects. Furthermore, basal levels of FAT/CD36 expression were substantially elevated in plasma membrane fractions of the type 2 diabetic subjects, and a modest increase in the FATP4 content was also noted. FATP1 levels were not different between any of the subject groups. After rosiglitazone treatment, basal fatty acid levels of FAT/CD36 and FATP4 remained elevated, but the effect of insulin to induce translocation to the plasma membrane fraction was completely restored. This is consistent with the view that fatty acid uptake is increased in insulin-resistant type 2 diabetic subjects, but that the intracellular fatty acids are preferentially directed toward lipogenesis rather than oxidation.
Formal Description
Interaction-ID: 61879

drug/chemical compound

Rosiglitazone

affects transport of

gene/protein

SLC27A4

to plasma membrane, in muscle
Drugbank entries Show/Hide entries for Rosiglitazone