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Alterations in Oral [1-(14)C] 18:1n-9 Distribution in Lean Wild-type and Genetically Obese (ob/ob) Mice

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Journal PLoS One
Date 2015 Apr 1
PMID 25826747
Citations 1
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Abstract

Obesity may result from altered fatty acid (FA) disposal. Altered FA distribution in obese individuals is poorly understood. Lean wild-type C57BL/6J and obese C57BL/6Job/ob mice received an oral dose of [1-(14)C]18:1n-9 (oleic acid), and the radioactivity in tissues was evaluated at various time points. The (14)C concentration decreased rapidly in gastrointestinal tract but gradually increased and peaked at 96 h in adipose tissue, muscle and skin in lean mice. The (14)C concentration was constant in adipose tissue and muscle of obese mice from 4 h to 168 h. (14)C-label content in adipose tissue was significantly affected by genotype, whereas muscle (14)C-label content was affected by genotype, time and the interaction between genotype and time. There was higher total (14)C retention (47.7%) in obese mice than in lean mice (9.0%) at 168 h (P<0.05). The (14)C concentrations in the soleus and gastrocnemius muscle were higher in obese mice than in lean mice (P<0.05). Perirenal adipose tissue contained the highest (14)C content in lean mice, whereas subcutaneous adipose tissue (SAT) had the highest (14)C content and accounted for the largest proportion of total radioactivity among fat depots in obese mice. More lipid radioactivity was recovered as TAG in SAT from obese mice than from lean mice (P<0.05). Gene expression suggested acyl CoA binding protein and fatty acid binding protein are important for FA distribution in adipose tissue and muscle. The FA distribution in major tissues was altered in ob/ob mice, perhaps contributing to obesity. Understanding the disparity in FA disposal between lean and obese mice may reveal novel targets for the treatment and prevention of obesity.

Citing Articles

Depot-specific differences in fat mass expansion in WT and ob/ob mice.

Wang X, Yu C, Feng J, Chen J, Jiang Q, Kuang S Oncotarget. 2017; 8(28):46326-46336.

PMID: 28564636 PMC: 5542270. DOI: 10.18632/oncotarget.17938.

References
1.
Turcotte L, Swenberger J, Zavitz Tucker M, Yee A . Increased fatty acid uptake and altered fatty acid metabolism in insulin-resistant muscle of obese Zucker rats. Diabetes. 2001; 50(6):1389-96. DOI: 10.2337/diabetes.50.6.1389. View

2.
Macotela Y, Emanuelli B, Mori M, Gesta S, Schulz T, Tseng Y . Intrinsic differences in adipocyte precursor cells from different white fat depots. Diabetes. 2012; 61(7):1691-9. PMC: 3379665. DOI: 10.2337/db11-1753. View

3.
Masuzaki H, Paterson J, Shinyama H, Morton N, Mullins J, Seckl J . A transgenic model of visceral obesity and the metabolic syndrome. Science. 2001; 294(5549):2166-70. DOI: 10.1126/science.1066285. View

4.
Rinaldo P . Fatty acid transport and mitochondrial oxidation disorders. Semin Liver Dis. 2001; 21(4):489-500. DOI: 10.1055/s-2001-19037. View

5.
Huang H, Starodub O, McIntosh A, Kier A, Schroeder F . Liver fatty acid-binding protein targets fatty acids to the nucleus. Real time confocal and multiphoton fluorescence imaging in living cells. J Biol Chem. 2002; 277(32):29139-51. DOI: 10.1074/jbc.M202923200. View