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 Malonyl-CoA is produced by activated ACC, and insulin is known to activate ACC by mediating its dephosphorylation. In the basal state, 40% of ACC was in the phosphorylated inactive form in the lean subjects. Additionally, in these subjects, insulin stimulation had a marked effect to dephosphorylate and activate ACC. In the insulin-resistant obese and type 2 diabetic subjects, basal ACC levels were already highly activated, and no further effect of insulin was noted. After rosiglitazone treatment, the type 2 diabetic subjects showed restoration of basal phospho-ACC levels toward normal, with a substantial recovery of the insulin effect to dephosphorylate ACC. These results are fully consistent with the role of ACC to convert acetyl-CoA to malonyl-CoA.
Formal Description
Interaction-ID: 61842

drug/chemical compound

Rosiglitazone

decreases_activity of

gene/protein

ACACA

in muscle
Drugbank entries Show/Hide entries for Rosiglitazone or ACACA