Abstract
Conjugated linoleic acid (CLA), a mixture of isomers of linoleic acid, has previously been shown to be able to decrease porcine subcutaneous (SC) adipose tissue levels while increasing the count of intramuscular (IM) adipose tissue in vivo. However, the underlying mechanisms through which it acts are poorly understood. The objective of this study was to investigate the different effects of CLA on adipogenesis in cultured SC adipose tissue and IM stromal vascular cells obtained from neonatal pigs. As shown here, trans-10, cis-12 CLA decreased the expression of adipocyte-specific genes as well as adipose precursor cell numbers and the accumulation of lipid in cultured SC adipose tissue stromal vascular cells. However, the cis-9, trans-11 CLA did not alter adipogenesis in SC cultures. On the other hand, both CLA isomers increased the expression of adipocyte-specific genes in IM cultures, together with the increasing accumulation of lipid and Oil Red O-stained cells. Collectively, these data show that CLA decreases SC adipose tissue but increases IM adipose tissue by different regulation of adipocyte-specific gene expression. These results suggest that adipogenesis in IM adipocytes differs from that in SC adipocytes.
Highlights
Conjugated linoleic acid (CLA), a mixture of isomers of linoleic acid, has previously been shown to be able to decrease porcine subcutaneous (SC) adipose tissue levels while increasing the count of intramuscular (IM) adipose tissue in vivo
Porcine stromal vascular cells from subcutaneous adipose tissue and longissimus muscle reached confluence in proliferation medium, cells were grown in differentiation medium containing BSA, 50 mmol/l CLA-mixture (Mix), c9,t11-CLA, t10,c12-CLA, or linoleic acid for 6 days
This study is the first to show the different effects of CLA on the proliferation and differentiation of adipose precursor cells in SC adipose tissue and skeletal muscle in vitro
Summary
Conjugated linoleic acid (CLA), a mixture of isomers of linoleic acid, has previously been shown to be able to decrease porcine subcutaneous (SC) adipose tissue levels while increasing the count of intramuscular (IM) adipose tissue in vivo. Studies suggested that t10,c12-CLA but not c9,t11-CLA inhibits both the proliferation and the differentiation of 3T3-L1 preadipocytes and cultured stromal vascular cells from human subcutaneous (SC) adipose tissue, decreasing lipid accumulation [10, 16]. Indirect evidence indicated that increased IM fat was attributable to the recruitment of more stromal vascular cells to IM adipocytes by CLA [18] These studies suggested that the regulation of CLA in adipocyte development in SC and IM adipose tissue is in distinct mechanisms [19]. Chawla and Lazar [24] suggested that the sequential expression of Abbreviations: ADD-1, adipocyte determination and differentiation factor-1; aP2, adipocyte fatty acid binding protein; C/EBPa, CAAT/ enhancer binding protein a; CLA, conjugated linoleic acid; IM, intramuscular; IR, insulin receptor; OROSM, Oil Red O-stained material; PPARg, peroxisome proliferator-activated receptor g; SC, subcutaneous
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