Introduction
e metabolic syndrome is characterized by the
association of insulin resistance (IR) with alterations
in glucose tolerance or type 2 diabetes, central obes-
ity, hypertension and dyslipidemia. is condition
has an increasing incidence in human populations
consuming high calorie diets and with a tendency to
a sedentary behaviour (Reaven, 1988; Guthrie et al.,
2000). All the abnormalities involved in IR constitute
a high risk for developing cardiovascular disease, the
main cause of morbidity and mortality in developed
and developing countries.
Feeding rats with high sucrose (SRD) or fructose
(FRD) induces early changes in glucose and lipid
metabolism that resemble the profile of the human
metabolic syndrome, thus providing a useful model
to study its consequences as well as to design different
preventive strategies (Tobey et al., 1982; Gutman et al.,
1987; ornburn et al., 1989; Dai et al., 1994; Catena
et al., 2003). is experimental model is particularly
appropriate to study the development of IR and is
Archives of Physiology and Biochemistry, 2010; 116(1): 42-49
ORIGINAL ARTICLE
Glycoxidative stress-induced damage on lipid profile
in a fructose-enriched diet model of insulin resistance
in rats
M.E. García
1
, C.A. Marra
2
, and O.R. Rebolledo
1
1
CENEXA (Centro de Endocrinología Experimental y Aplicada, UNLP-CONICET La Plata, PAHO/WHO Collaborating
Center), and
2
INIBIOLP (Instituto de Investigaciones Bioquímicas de La Plata, UNLP-CONICET La Plata, Cátedra de
Bioquímica y Biología Molecular), Facultad de Ciencias Médicas, Universidad Nacional de La Plata, 60 y 120 (1900)
La Plata, Argentina
Abstract
Objective: To study alterations in plasma lipid profile and oxidative damage to lipoprotein fractions (LF) and
their fatty acids during an early insulin-resistant and increased oxidative state developed by a fructose-rich
diet (FRD).
Methods and results: Wistar rats were fed a commercial diet with (FRD) or without (CD) 10% fructose in the
drinking water. After 3 weeks, plasma glucose, triglyceride (TG), insulin (I), fructosamine (F), free fatty acids
(FFA) and lipid profile (total cholesterol [TC] and HDL-C, LDL-C and VLDL-C sub-fractions) were determined.
The insulin sensitivity HOMA index was assessed. FRD-fed rats had higher plasma TG, I, and F levels; increased
HOMA; decreased HDL-C and LDL-C; augmented VLDL-C and TC/HDL-C, and TG/HDL-C atherogenic risk
scores. LF of FRD rats had increased oxidative damage on the fatty acyl profile and in copper-induced
lipoperoxidation.
Conclusions: Fructose feeding early increases the atherogenic risk inducing an insulin resistant-glycoxidative
state that affects plasma lipid profiles.
Keywords: Oxidative stress; lipid peroxidation; lipoproteins; fructose diet; dyslipidemia
Non-conventional abbreviations: CETP, cholesteryl-ester-tansfer protein; c-GLC, capillary gas-liquid
chromatography; CD, control diet; FAMEs, fatty acid methyl esters; FFA, free fatty acids; FRD, fructose-rich
diet; LCAT, lecitine-cholesterol-acyltransferase; LPL, lipoprotein-lipase; PUFA, polyunsaturated fatty acids;
ROS, reactive oxygen species; TBARS, thiobarbituric acid reactive substances
Address for Correspondence: Prof. Dr. Oscar Rebolledo, CENEXA (Centro de Endocrinología Experimental y Aplicada) UNLP-CONICET LA PLATA,
PAHO/WHO Collaborating Center). Tel: +54 221 423 6712. Fax: +54 221 422 2081. E-mail: oscar_rebolledo@yahoo.com.ar
(Received 14 October 2009; revised 30 November 2009; accepted 03 December 2009)
ISSN 1381-3455 print/ISSN 1744-4160 online © 2010 Informa UK Ltd
DOI: 10.3109/13813450903527713 http://www.informahealthcare.com/arp
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