QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Yu-Poth, S. Articles by Etherton, T. D. Search for Related Content PubMed PubMed Citation Articles by Yu-Poth, S. Articles by Etherton, T. D.

---

Nutrient-Gene Interactions
Research Communication

Conjugated Linoleic Acid Upregulates LDL Receptor Gene Expression in HepG2 Cells

Shaomei Yu-Poth^*, Dezhong Yin^**, Guixiang Zhao^*, Penny M. Kris-Etherton^,1 and Terry D. Etherton^*,**

^* Graduate Program in Nutrition, Department of Nutritional Sciences, and ^** Department of Dairy and Animal Science, The Pennsylvania State University, University Park, PA 16802

¹To whom correspondence should be addressed. E-mail: pmk3{at}psu.edu.

Conjugated linoleic acid (CLA) exerts anticarcinogenic and antiatherosclerotic effects in animals. The present study was conducted to examine the effects of CLA on LDL receptor (LDLr) expression in HepG2 cells, and to evaluate whether the sterol response element binding protein 1 (SREBP-1) and acyl CoA:cholesterol acyltransferase (ACAT) were involved in the regulation of LDLr expression by CLA. When HepG2 cells were cultured with serum-free DMEM for 48 h, there was a three- to fivefold (P < 0.05) increase in LDLr protein and mRNA levels. Incubation of HepG2 cells in serum-free medium supplemented with 25-hydroxycholesterol (25OH, 5 mg/L) for 24 h decreased LDLr protein and mRNA by 50–70% (P < 0.05) and mature SREBP-1 by 20–40% (P < 0.05). CLA, but not linoleic acid, antagonized the depressive effects of 25OH and increased both LDLr protein and mRNA abundance twofold (P < 0.05). LDLr protein and mRNA abundance were not different when HepG2 cells were cultured with CLA (0.4 mmol/L) plus 25OH in the presence or absence of an ACAT inhibitor (58–035, 1 mg/L). Furthermore, CLA had no effect on SREBP-1 abundance. These results suggest that CLA upregulates LDLr expression via a mechanism that is independent of ACAT and SREBP-1.

KEY WORDS: • cholesterol • conjugated linoleic acid • LDL • LDL receptor mRNA • LDL receptor protein

This article has been cited by other articles:

				K. G. Jackson, V. Maitin, D. S. Leake, P. Yaqoob, and C. M. Williams Saturated fat-induced changes in Sf 60-400 particle composition reduces uptake of LDL by HepG2 cells J. Lipid Res., February 1, 2006; 47(2): 393 - 403. [Abstract] [Full Text] [PDF]

				S. Yu-Poth, D. Yin, P. M. Kris-Etherton, G. Zhao, and T. D. Etherton Long-Chain Polyunsaturated Fatty Acids Upregulate LDL Receptor Protein Expression in Fibroblasts and HepG2 Cells J. Nutr., November 1, 2005; 135(11): 2541 - 2545. [Abstract] [Full Text] [PDF]

				M. Zang, A. Zuccollo, X. Hou, D. Nagata, K. Walsh, H. Herscovitz, P. Brecher, N. B. Ruderman, and R. A. Cohen AMP-activated Protein Kinase Is Required for the Lipid-lowering Effect of Metformin in Insulin-resistant Human HepG2 Cells J. Biol. Chem., November 12, 2004; 279(46): 47898 - 47905. [Abstract] [Full Text] [PDF]