The Increase of Apolipoprotein A-V During Postprandial Lipemia Parallels the Response of Triglyceride-Rich Lipoproteins in Type 2 Diabetes  

Oleh:

Kahri, Juhani ; Fruchart-Najib, Jamila ; Matikainen, Niina ; Fruchart, Jean-Charles ; Vakkilainen, Juha ; and Others

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Diabetes Care vol. 30 no. 08 (Aug. 2007), page 2083.
Topik: Pathophysiology; Complications

Ketersediaan

Perpustakaan FK Nomor Panggil: D05.K.2007.03 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

INTRODUCTION Postprandial lipemia is a distinct feature of diabetic dyslipidemia and may partly explain the atherogeneity of the lipid profile in type 2 diabetes. Several genetic factors contribute to the elevation of triglyceride-rich lipoproteins (TRLs). The role of apolipoprotein (apo)C-III as a regulator of TRL metabolism is well documented. Recently, apoA-V has been identified as a novel regulator of triglyceride metabolism. When the human APOA5 gene was expressed in transgenic mice, plasma triglyceride concentration was decreased by 70%, whereas apoA5 gene knockout mice had fourfold elevation of plasma triglyceride levels. Inherited apoA-V deficiency results in severe hypertriglyceridemia in humans. A mutation in the APOA5 gene causes hypertriglyceridemia due to decreased lipoprotein lipase (LPL) mass and activity. Thus, previous studies have proposed that apoA-V decreases triglycerides by stimulating lipolysis. The present study focused on the response of apoA-V and apoC-III during postprandial lipemia and the associations between apoA-V and apoC-III and postheparin plasma LPL and hepatic lipase activities in type 2 diabetes. RESEARCH DESIGN AND METHODS— The present study cohort was comprised of 39 men and 8 women with type 2 diabetes who were enrolled in the previously published nateglinide study with the same inclusion and exclusion criteria. A total of 17 patients were . . .

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