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See Latest ArticlesRegulatory enzymes of mitochondrial beta-oxidation as targets for treatment of the metabolic syndrome
Obesity Reviews, 08/27/09
Leij FRVD et al. – Stimulation of CPT1 can be achieved by elimination or inhibition of ACC2 activity and through activating transcription factors like peroxisome proliferator–activated receptors and their protein partners. The latter leads to enhanced CPT1 gene expression. Recent developments are discussed, including a recently identified CPT1 isoform, i.e. CPT1C. This protein is highly expressed in the brain and may provide a target for new tools to prevent obesity.
FR van der Leij, 08/28/09
| The traditional view on CPT1 as drug target was to prevent severe symptoms of diabetes, such as keto-acidosis, by inhibition of hepatic fatty acid oxidation. However, rather than focussing on symptom treatment, the prevention of diabetes, metabolic syndrome and related health problems now opens the perspective of systemic stimulation of fatty acid oxidation, especially in skeletal muscle. Higher activity of CPT1 has been shown promising. Actually, this enables modulation of the effects of metformin, as CPT1 stimulation is one of the indirect consequences of the action of metformin. Apart from these applications, the discovery of a brain-type family member of CPT1, called CPT1C, may contribute to further understand satiety control. It should be realized that all three CPT1 genes are expressed in the brain, however. |
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