General Information:

Id: 3,503 (click here to show other Interactions for entry)
Diseases: Diabetes mellitus, type II - [OMIM]
Insulin resistance
Mus musculus
PPARalpha-/- mouse
Reference: Makowski L et al.(2009) Metabolic profiling of PPARalpha-/- mice reveals defects in carnitine and amino acid homeostasis that are partially reversed by oral carnitine supplementation FASEB J. 23: 586-604 [PMID: 18945875]

Interaction Information:

Comment In wild-type mice, fasting-induced lipolysis was accompanied by increased plasma levels of several long-chain acylcarnitine species, including C16, C18:1, and C18:2. These same metabolites were elevated an additional 2- to 3-fold in PPARalpha -/- mice. Several of the hydroxylated acylcarnitine intermediates followed a similar pattern. Likewise, in the liver of PPARalpha -/- compared to wild-type mice, fasting levels of C16 and C18:1 were elevated, but medium-chain intermediates such as C8, C10, and C12 were present at lower levels. Skeletal muscle levels of C16, C18:1, and C18:2 were also elevated in fasted PPARalpha -/- mice, whereas the medium- and shorterchain species were either unchanged or decreased relative to their wild-type counterparts. This reciprocal long- to medium/short-chain acylcarnitine profile typically reflects a metabolic block that resides distal to carnitine palmitoyltransferase 1 (CPT1), the enzyme that synthesizes long-chain acylcarnitines and that functions as the first committed step in beta-oxidation. When long-chain products of this enzyme cannot be processed efficiently they accumulate within tissues and can be subsequently exported into the general circulation.
Formal Description
Interaction-ID: 32559



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