Necessity of carnitine supplementation in semistarved rats fed a high-fat diet

Feng, Yu; Guo, Changjiang; Wei, Jingyu; Yang, Jijun; Ge, Yuzhang; Lanxing, Gao

doi:10.1016/s0899-9007(01)00601-3

Cited by 14 publications

(6 citation statements)

References 15 publications

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“…Da‐Silva et al 30 and Aguiar et al 31, in studies of animals receiving a 20% ethanol solution and 50% of the control diet, obtained similar data, indicating that ethanol consumption attenuates the weight loss of malnourished animals. Weight gain was evident with the re‐feeding process, and both animal groups had similar weight at the end of the protocol, though it was 25% lower than control, in agreement with the data obtained by Feng et al 32 …”

Section: Discussionsupporting

confidence: 91%

Failure of carnitine in improving hepatic nitrogen content in alcoholic and non-alcoholic malnourished rats

Rodrigues

Portari

Padovan

et al. 2010

Clinics

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AIMS:To investigate the effect of carnitine supplementation on alcoholic malnourished rats' hepatic nitrogen content.METHODS:Malnourished rats, on 50% protein‐calorie restriction with free access to water (malnutrition group) and malnourished rats under the same conditions with free access to a 20% alcohol/water solution (alcohol group) were studied. After the undernourishment period (4 weeks with or without alcohol), both groups were randomly divided into two subgroups, one of them nutritionally recovered for 28 days with free access to a normal diet and water (recovery groups) and the other re‐fed with free access to diet and water plus carnitine (0.1 g/g body weight/day by gavage) (carnitine groups). No alcohol intake was allowed during the recovery period.RESULTS:The results showed: i) no difference between the alcohol/no alcohol groups, with or without carnitine, regarding body weight gain, diet consumption, urinary nitrogen excretion, plasma free fatty acids, lysine, methionine, and glycine. ii) Liver nitrogen content was highest in the carnitine recovery non‐alcoholic group (from 1.7 to 3.3 g/100 g, P<0.05) and lowest in alcoholic animals (about 1.5 g/100g). iii) Hepatic fat content (∼10 g/100 g, P>.05) was highest in the alcoholic animals.CONCLUSION:Carnitine supplementation did not induce better nutritional recovery.

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Section: Discussionsupporting

confidence: 91%

Failure of carnitine in improving hepatic nitrogen content in alcoholic and non-alcoholic malnourished rats

Rodrigues

Portari

Padovan

et al. 2010

Clinics

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“…Richter et al (45) reported that administration of l-carnitine reduced the sucrose-induced hypertriglyceridemia and the increase of free fatty acid levels in rat plasma. Carnitine supplementation of semistarved rats was recently found to significantly increase the activity of preheparin plasma lipoprotein lipase and to restore plasma triacylglycerol secretion rate to the normal level (46). If carnitine supplementation enhances the oxidation of fatty acids, there should be a concurrent increase in the production of ketone bodies.…”

Section: Discussionmentioning

confidence: 99%

Acetyl-l-carnitine supplementation restores decreased tissue carnitine levels and impaired lipid metabolism in aged rats

Tanaka

Sasaki

Fukui

et al. 2004

Journal of Lipid Research

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The effects of long-term carnitine supplementation on age-related changes in tissue carnitine levels and in lipid metabolism were investigated. The total carnitine levels in heart, skeletal muscle, cerebral cortex, and hippocampus were ‫ف‬ 20% less in aged rats (22 months old) than in young rats (6 months old). On the contrary, plasma carnitine levels were not affected by aging. Supplementation of acetyl-l -carnitine (ALCAR; 100 mg/kg body weight/day for 3 months) significantly increased tissue carnitine levels in aged rats but had little effect on tissue carnitine levels in young rats. Plasma lipoprotein analyses revealed that triacylglycerol levels in VLDL and cholesterol levels in LDL and in HDL were all significantly higher in aged rats than in young rats. ALCAR treatment decreased all lipoprotein fractions and consequently the levels of triacylglycerol and cholesterol. The reduction in plasma cholesterol contents in ALCAR-treated aged rats was attributable mainly to a decrease of cholesteryl esters rather than to a decrease of free cholesterol. Another remarkable effect of ALCAR was that it decreased the cholesterol content and cholesterol-phospholipid ratio in the brain tissues of aged rats. These results indicate that chronic ALCAR supplementation reverses the age-associated changes in lipid metabolism. Aging causes quantitative and compositional changes in body lipids. Analyses of plasma samples from humans and experimental animals indicate that cholesterol and triacylglycerol levels increase with aging (1-3). Aging increases total cholesterol and decreases phospholipids, leading to increased cholesterol-phospholipid molar ratios in hepatic mitochondria (4), brain (5), and cerebral synaptic membranes (6). These age-related changes in lipid composition in various tissues and organs are thought to account not only for the age-related accumulation of body fat, which is a risk factor for diabetes and atherosclerotic diseases, but also for age-related cellular hypofunction. Therefore, reversing age-related changes in lipid metabolism would help to maintain normal cellular function and prevent common diseases.Carnitine plays an essential role in transporting fatty acids into mitochondria, where they are oxidized to produce energy in tissues (7). Carnitine levels in cardiac and skeletal muscles, both of which are major storage sites of carnitine, appear to decrease with age (8-11). In plasma, however, it is unclear whether carnitine levels decease with age. Some studies have shown an increase in plasma carnitine levels with aging (12, 13), whereas others have found significant decreases in human (14) and rat (10). This inconsistency is a problem because plasma carnitine levels are often used as an index of body carnitine status. Concerning the age-related changes in carnitine levels in tissues and organs, cardiac and skeletal muscles have frequently been investigated (8-11), but other organs have not attracted much attention. One study reported a decrement of carnitine contents in the brain and a drast...

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“…Sigma-Tau, Spain, kindly provided both compounds. The selected dose was chosen taking into account previous reports that found that either LC or PLC at 200 mg kg 21 given to rats was able to significantly increase plasma free LC concentration [17,18]. Treatments were administered in the drinking water and the amount of either LC or PLC was adjusted as previously described [16].…”

Section: Animalsmentioning

confidence: 99%

l-carnitine and its propionate: Improvement of endothelial function in SHR through superoxide dismutase-dependent mechanisms

Sotomayor

Mingorance

Rodríguez‐Rodríguez

et al. 2007

Free Radical Research

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To clarify the mechanism underlying the antioxidant properties of l-carnitine (LC) and propionyl-l-carnitine (PLC) on spontaneously hypertensive (SHR) and normotensive WKY, animals were treated with either PLC or LC (200 mg kg(- 1)). Aorta was dissected and contraction to (R)-( - )-phenylephrine (Phe) and relaxation to carbachol (CCh) were assessed in the presence or not of the NO synthase (NOS) inhibitor, l-NAME. [image omitted] production was evaluated by lucigenin-enhanced chemiluminescence and its participation on relaxation was observed after incubation with superoxide dismutase (SOD) plus catalase. Protein expressions of eNOS, Cu/Zn-SOD and Mn-SOD were studied by western blot. Both LC and PLC treatments improved endothelial function of SHR through increasing NO participation and decreasing [image omitted] probably involving higher Cu/Zn-SOD expression. PLC treatment augmented eNOS expression in SHR. Surprisingly, LC increased [image omitted] produced by aorta from WKY and thus diminished NO and damaged endothelial function. Conversely, PLC did not affect CCh-induced relaxation in WKY. These results demonstrate that LC and PLC prevent endothelial dysfunction in SHR through an antioxidant effect.

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Necessity of carnitine supplementation in semistarved rats fed a high-fat diet

Cited by 14 publications

References 15 publications

Failure of carnitine in improving hepatic nitrogen content in alcoholic and non-alcoholic malnourished rats

Failure of carnitine in improving hepatic nitrogen content in alcoholic and non-alcoholic malnourished rats

Acetyl-l-carnitine supplementation restores decreased tissue carnitine levels and impaired lipid metabolism in aged rats

l-carnitine and its propionate: Improvement of endothelial function in SHR through superoxide dismutase-dependent mechanisms

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