Journal
AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY
Volume 312, Issue 5, Pages R816-R820Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpregu.00520.2016
Keywords
Cpt1a; Cpt1b; adipose tissue; lipid oxidation; obesity
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Funding
- National Institute of Diabetes and Digestive and Kidney Diseases Fellowship [T32DK-6458413]
- COBRE (National Institute of General Medical Sciences) [8P20GM-103528]
- Nutrition Obesity Research Centers (National Institute of Diabetes and Digestive and Kidney Diseases) [2P30-DK-072476-11A1]
- [R01DK-089641]
- [K01DK-106307]
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Carnitine palmitoyltransferase 1 (CPT1) is essential for the transport of long-chain fatty acids into the mitochondria for oxidation. Recently, it was reported that decreased CPT1b mRNA in adipose tissue was a contributing factor for obesity in rats. We therefore closely examined the expression level of Cpt1 in adipose tissue from mice, rats, and humans. Cpt1a is the predominate isoform in adipose tissue from all three species. Rat white adipose tissue has a moderate amount of Cpt1b mRNA, but it is very minor compared with Cpt1b expression in muscle. Total CPT1 activity in adipose tissue is also minor relative to other tissues. Both Cpt1a and Cpt1b mRNA were increased in gonadal fat but not inguinal fat by diet-induced obesity in mice. We also measured CPT1a and CPT1b expression in subcutaneous adipose tissue from human subjects with a wide range of body mass indexes (BMIs). Interestingly, CPT1a expression positively correlated with BMI (R = 0.46), but there was no correlation with CPT1b (R = 0.04). Our findings indicate that white adipose tissue fatty acid oxidation capacity is minor compared with that of metabolically active tissues. Furthermore, given the already low abundance of Cpt1b in white adipose tissue, it is unlikely that decreases in its expression can quantitatively decrease whole body energy expenditure enough to contribute to an obese phenotype.
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