Effects of L-carnitine on Blood Lipid Metabolism and Antioxidation in Hyperlipidemia Rats
LUAN Hai-yun, YANG Ming*, XU Yong, WANG Gui-hua
(Institute of Materia Medica, College of Pharmacy, Binzhou Medical University, Yantai 264003,China)
Abstract [Objective]To study the effects of L-carnitine(LC) on lowering the high blood lipid and antioxidation in hyperlipidemia rats. [Method]50 healthy SD rats were randomly divided into 5 groups. They were fed with standard diet, high-cholesterol diet and high-cholesterol diet with 0.25, 0.5, 1.0 g/(kg·d) LC. After the LC groups were consecutivelyorally administered LC for 28 days, rat serum total cholesterol (TC), triglyceride (TG), highdensity lipoprotein (HDL-C), low density lipoprotein (LDL-C) content,as well assuper oxide dismutase (SOD) activity and malondialdehyde (MDA) content in serum and liver were determined.[Result] Compared with the high-fat model group, LC could significantly reduce the serum TC,TG,LDL-C levels, increase HDL-C level, and enhanceSOD activity in serum and liver, decrease the content of MDA (P<0.05). [Conclusion]LC might have a significant role in lowering the high blood lipid and improving internal antioxidant capacity in hyperlipidemia rats.
Keywords L-carnitine; Hyperlipidemia; Antioxidation
Hyperlipidemia has now become a common and multiple disease, and is an important factor inducing atherosckerosis, fatty liver, coronary heart disease, diabetes and so on[1]. With the increase in people’s living standards, the disease incidence of hyperlipidemia rose year by year, and has become the current hot research. L-carnitine (LC) is a kind of amino acid extensively in the body, its main function is to promote the β-oxidization of internal long-chain fatty acid[2], also with the function of antioxidant and cleaning free radical and so on. Because of the role of LC in fatty acid metabolism, it has already demonstrated clinical lipid-lowering effect[3]. Therefore, the author established the rat model of hyperlipidemia and observed the effects of LC on blood lipids in rats and its antioxidation, to provide test basis for the drug research.
1. Materials and Methods
1.1. Animals SD rats of half gender, (150±10) g, clean grade, were provided by the Animal Center of Shandong Lukang pharmaceutical Co., Ltd. (number of animal license SCXK 2005-0017).
1.2. Reagents L-carnitine crude drug (Northeast General Pharmaceutical Factory); cholate, propacil (Shanghai Ruji Biotechnology Development Inco.). Serum total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C), SOD, MDA and Coomassie brilliant blue protein quantitative determination kit (Nanjing Jiancheng Reagent Co.).
1.3. Prescription of high-fat diet 10% lard, 0.3% propacil, 10% egg yolk powder and 74.7% standard diet.
1.4. Methods
1.4.1. Group and Administration 50 SD rats were randomly and equally divided into 5 groups with half gender. The 1st group was normal group fed with standard diet and 10 ml/(kg·d) physiologic saline; the 2nd group was model group fed with high-fat diet and physiologic saline (for 4 weeks, determination of lipid indicators to detect the model successful or not, then model rats of hyperlipemia can be obtained); the 3rd to 5th group were LC low, middle and high dose group, respectively, fed with high-fat diet and 0.25, 0.5, 1.0 g/(kg·d) LC, total feeding for 4 weeks. Rats in each group were free of ingestion and drinking water during the intragastric administration.
1.4.2. Determination of indicators 12 h of fasting after the last administration, but water was not forbidden. The rats were anesthetized by 3% pentobarbital sodium, and blood samples from abdominal aorta were centrifuged to separate serum, of which TC, TG, HDL, LDL, SOD and MDA were determined according to Kit instructions. The rat livers were rapidly took from the ice bag and washed by cold saline, after blotted with filter paper and precise weigh, 10% tissue homogenate were made to centrifuge and the supernate were put in the centrifuge tube. All the indicators were determined strictly according to Kit instructions.
1.4.3. Statistical treatment The data were analyzed by SPSS 13.0 statistics software.
2. Results
2.1. Observation of rats weight  rats of the normal group were in good state with normal diet; rats of the model group were not that well, with the extension of high-fat diet, activity was reduced, weight was gained, hair color turned gradually yellow, but no death, while rats of the LC administration group were significantly better than the model group.
2.2. Effects of LC on rats serum TC, TG, HDL-C, LDL-C Compared with that of the normal group, the levels of TC, TG and LDL-C in the rat serum of model group were significantly elevated (P<0.05), showing a typical lipid metabolic disorder, which indicated that experimental hyperlipemia models were successfully copied. Compared with the model group, LC groups could significantly lower the contents of serum TC, TG and LDL-C (P<0.05 or P<0.01), and significantly increase serum HDL-C (P<0.01), presenting dose-dependent. The results are shown in Table 1.
Table 1. Effects of LC on rats serum TC, TG, HDL-C, LDL-C ( , n=10)

Dose (g/kg)
TC (mmol/L)
TG (mmol/L)
HDL-C (mmol/L)
LDL-C (mmol/L)
Normal group
Model group

Compared with normal control group: aP<0.05, bP<0.01; compared with model group: cP<0.05, dP<0.01. Similarly hereinafter.
2.3. Effects of LC on SOD and MDA in rats serum and liver Compared with that of the normal group, SOD levels in rats serum and liver of model group were significantly reduced (P<0.01), but the contents of MDA were significantly elevated (P<0.01), which indicated that rats of model group were accompanied by lipid peroxidation injury. Compared with the model group, SOD in serum and liver can be significantly elevated by LC middle, high dose (P<0.01), but the contents of MDA were reduced (P<0.05 or P<0.01); however, compared with the normal group, levels of SOD and contents of MDA in serum and liver could be significantly elevated by LC middle, high dose (P<0.05 or P<0.01). Therefore, LC has a better resistance to lipid peroxidation on hyperlipemia rats, the results are shown in Table 2.
Table 2. Effects of LC on SOD and MDA in hyperlipemia rats serum and liver ( , n=10)

SOD (U/ml)
MDA (nmol/ml)
SOD (U/mg prot)
MDA (nmol/mg prot)
Normal group
Model group

3. Discussion
    L-carnitine is a necessary substance in energy metabolism in mammals, its main function is to promote fatty acid β-oxidation as well as the function of antioxidant and cleaning free radical. Liver is an important place for lipid metabolism, if the endogenous L-carnitine are insufficient, fatty acid would be impossible to enter mitochondria to energize, so it will accumulate with other harmful substances, leading to fatty degeneration, cell death and finally hepatic function damage. Epidemiological surveys have shown that most nonalcoholic fatty hepatopath often suffered from hyperlipemia, and the blood fat levels had some correlation with the severity of fatty liver[4]. The test results indicated that LC could significantly reduce TC, TG and LDL-C in high fat rats, but the content of HDL-C was elevated, which illustrated it may increase the transport process of the cholesterol from peripheral tissue cells of hyperlipemia rats to liver which promoted the fatty acid β-oxidation in the liver in order to reduce the aggregation of cholesterol in peripheral tissue cells, to achieve lipid-lowering effect.
When having hyperlipemia, the metabolism of free radicals in liver cells in vivo will overbalance, and defense capability against free radicals will decline, moreover, too many free radicals can have peroxidation with lipoid substances in cell membranes, resulting in membrane damage and cell death; simultaneously, the decomposition products of lipid peroxide (MDA) can also combine with substances such as proteins and phospholipids, then deposit in tissue cells, thus damaging cell membranes and causing cell dysfunction, eventually leading to unable to maintain normal metabolism and cell death. This study showed that SOD vigor in serum and liver of the model group was significantly smaller than that of the normal group, and MDA content was significantly larger, which indicated that the rise of blood fat presented correlation with lipid peroxidation, and besides, LC could significantly increase the SOD vigor in serum and liver of rats, reduce MDA caused by high-fat diet, illustrating the blood fat regulating effects was related to its antioxidation.
The study results indicated that after administration with LC in hyperlipemia rats, the TC, TG and LDL-C in rats were significantly reduced, while the content of HDL-C was elevated; MDA content in serum and liver was significantly reduced and SOD vigor was markedly elevated, which demonstrated LC promoted fatty acid metabolism, and had a certain effect of lipid regulating and liver protecting, in addition, its blood fat regulating effects may be related to its internal antioxidation.
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[2]  STRIJBIS K, VAZ FM, DISTEL B. Enzymology of the carnitine biosynthesis pathway [J]. IUBMB Life, 2010, 62 (5):357-362.
[3] GÜNE? B, YALÇIN SS, KALKANO?LU HS, et al. The effect of oral L-carnitine supplementation on the lipid profiles of hyperlipidaemic children [J]. Acta Paediatr. 2005, 94 (6):711-716.
[4] SHI J, LIU S, XIE WF. L-carnitine and hepatopathy [J]. Chinese Journal of Hepatology, 2005, 13 (7):556-558.
 Yantai Science and Technology Development Plan (2011074).
About the author
LUAN Haiyun (1979-), female, P. R. China, Master, lecturer, working at research on anti-aging pharmacology. Tel: 15905355268. E-mail: bluehy2000@126.com.
*Corresponding author: YANG Ming (1976-), female, P. R. China, Doctor, Tel: 13396383355. E-mail: yt.yming@gmail.com.

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