Antioxidant role of L-carnitine in an experimental model of oxidative stress induced by increased fructose consumption

Abstract

Objectives: To evaluate the role of L-carnitine (LC) on fructose-induced oxidative stress in Holtzman
rats. Materials and methods: An experimental study was carried out during 56 days, in patients assigned
to 4 groups: control, control+LC, fructose and fructose+LC. Patients in the fructose group received treatment
during 56 days, and those in the LC groups were treated during the last 28 days. Fructose was given
on demand and LC was administered orally at a dose of 500 g/kg/24 h. Lipid peroxidation (MDA), superoxide
dismutase activity, free LC and mitochondrial and post-mitochondrial proteins were measured in
liver tissue. Glycemia, insulin and the homeostasis model assessment of insulin resistance (HOMA-IR)
were measured in blood plasma. We measured insulin concentration and studied the histology of pancreatic
tissue. Results: LC treatment showed a decrease (p < 0.05) of MDA when compared to the control
group (21.73 ± 5.36 nmol/g tissue vs. 64.46 ± 7.87 nmol/g tissue). Mitochondrial and post-mitochondrial
proteins increased (p < 0.05) in comparison to the control group; pancreatic insulin also increased when
compared to the control (341.8 ± 42.3 μUI/ml vs. 70.1 ± 9.6 μUI/ml, p<0.05). The role of LC against fructose-
induced oxidative stress did not show any decrease of MDA, but decreased (p < 0.05) SOD Cu/Zn
activity (9.39 ± 1.5 USOD/mg protein vs. 13.52 ± 1.5 USOD/mg protein). We observed that LC improves
HOMA-IR in blood plasma. Histological analysis of the pancreas showed that the presence of LC increased
the number and size of the islets of Langerhans. Conclusions: LC favors changes in the oxidative
metabolism and it also contributes to glycemic homeostasis when fructose is consumed.