Horm Metab Res 2008; 40(1): 69-71
DOI: 10.1055/s-2007-1004528
Short Communication

© Georg Thieme Verlag KG Stuttgart · New York

Changes in Hepatic ApoAV Expression are not Required for the Rapid Triglyceride Lowering Effect of Fish Oil Diet in Rats

B. P. Hagerty 1 , F. G. Schaap 2 , M. Hermann 3 , B. Krenn 1 , C. Eder 1 , B. Dorfmeister 1 , H. Stangl 1 , W. Patsch 4 , W. Strobl 1
  • 1Department of Medical Chemistry, Center for Physiology, Pathophysiology and Immunology, Medical University of Vienna, Vienna, Austria
  • 2AMC Liver Center, Amsterdam, The Netherlands
  • 3Max F. Perutz Laboratories, Department of Biochemistry, Medical University of Vienna, Vienna, Austria
  • 4Institute for Laboratory Medicine, Paracelsus Private Medical University, Salzburg, Austria
Further Information

Publication History

received 27.03.2007

accepted 28.06.2007

Publication Date:
07 January 2008 (eFirst)

Introduction

Diets rich in polyunsaturated ω-3 or ω-6 fatty acids (PUFA) reduce fasting and postprandial plasma triglyceride levels by a rapid suppression of hepatic VLDL secretion and possibly by accelerated chylomicron clearance. ApoAV is a newly identified apolipoprotein of hepatic origin circulating bound to triglyceride rich lipoproteins and HDL at very low plasma levels [1] [2]. Human APOA5 polymorphisms are associated with elevated plasma triglycerides [1]. ApoAV deficiency leads to severe hypertriglyceridemia [3]. In genetically modified mice apoAV has a marked triglyceride-lowering effect due to stimulation of proteoglycan-bound lipoprotein lipase and possibly due to reduction of hepatic VLDL production [1] [4] [5] [6]. Thus, an increase of Apoa5 expression conceivably could play a role in the rapid triglyceride-lowering effect of diets rich in PUFA.

The present study was designed to determine whether Apoa5 gene expression is altered during the initial phase of a fish oil diet using rats adapted to a single meal per day. Apoa4, the apolipoprotein most homologous to apoAV, and Spot 14 (S14) a nuclear protein involved in lipogenesis were studied as controls. Both are suppressed transcriptionally by PUFA feeding [7] [8].

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Correspondence

W. Strobl

Department of Medical chemistry, CPPI

Medical University of Vienna

Währingerstraße 10

1090 Vienna

Austria

Phone: +43/1/4277 608 22

Fax: +43/1/4277 608 81

Email: wolfgang.strobl@meduniwien.ac.at