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Increased Fasting Plasma Acylation-Stimulating Protein Concentrations in Nephrotic Syndrome

Departments of Endocrinology and Metabolism (M.O., I.C.O.), Internal Medicine (C.O., M.G., F.B.), Biochemistry (T.O.), and Nephrology (K.C., A.V.), Gulhane School of Medicine, Etlik-Ankara and Bayindir Medical Center (N.B.), TR-06018 Sogutozu-Ankara, Turkey

Address all correspondence and requests for reprints to: Metin Ozata, M.D., Department of Endocrinology and Metabolism, Gülhane School of Medicine, TR-06018 Etlik/Ankara, Turkey. E-mail: mozata{at}gata.edu.tr

Abstract

Acylation-stimulating protein (ASP) is an adipocyte-derived protein that has recently been suggested to play an important role in the regulation of lipoprotein metabolism and triglyceride (TG) storage. ASP also appears to have a role in the regulation of energy balance. In addition to its role as a hormonal regulator of body weight and energy expenditure, leptin is now implicated as a regulatory molecule in lipid metabolism. However, little is known about the alterations in fasting plasma ASP and leptin concentrations in the nephrotic syndrome. As hyperlipidemia is one of the most striking manifestations of the nephrotic syndrome, we have investigated fasting plasma ASP and leptin levels and their relation to lipid levels in this syndrome.

Twenty-five patients with untreated nephrotic syndrome and 25 age-, sex-, and body mass index-matched healthy controls were included in the study. Fasting plasma lipoproteins, TG, total cholesterol, lipoprotein(a), apolipoprotein AI (apoAI), apoB, urinary protein, plasma albumin, third component of complement (C3), ASP, and leptin levels were measured in both groups.

Total cholesterol, TG, low and very low density lipoproteins, lipoprotein(a), apoB, and urinary protein levels were increased in the patient group, whereas plasma albumin, high density lipoprotein cholesterol, and apoAI levels were decreased compared with those in the control group (P < 0.001). Plasma ASP levels were significantly higher in the patient group compared with the control subjects (133.72 ± 65.14 vs. 29.93 ± 12.68 nmol/liter; P < 0.001), whereas leptin (2.69 ± 2.06 vs. 3.99 ± 2.99 ng/ml; P = 0.118) and C3 (1.01 ± 0.25 vs. 1.06 ± 0.23 g/liter; P = 0.662) levels were not significantly different between the two groups. Plasma leptin levels were correlated with body mass index in both nephrotic patients (r_s = 0.86; P < 0.001) and controls (r_s = 0.98; P < 0.001), but were not correlated with the other parameters. Fasting ASP concentrations showed no correlation with body mass index, proteinuria, plasma albumin, leptin, or any lipid parameter in either group, but C3 levels (in patient group: r_s = 0.92; P < 0.001; in control group: r_s = 0.68; P < 0.001).

Our findings showed that plasma ASP levels were significantly elevated, whereas leptin levels were normal in the nephrotic syndrome. Increased ASP levels in the setting of dyslipidemia in the nephrotic syndrome raise the possibility of an ASP receptor defect in adipocytes, which also suggests the existence of so-called ASP resistance. Moreover, it is possible that ASP activity is maximal, but cannot keep up with increased rates of lipid production by the liver. Thus, further studies are needed to elucidate the mechanism or source (adipocytes, the liver, or both) of elevated ASP concentrations in the nephrotic syndrome.

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