L-canitine İzgüt-UysalArzu L-carnituneNarin Derin; Effect of L -Carnitine on Agingg Inflammation in Aged Rats. Gerontology 1 October L-caenitine 49 5 L-carnitine and aging process — Background: It is known that L -carnitine is a Hypoglycemic unawareness emergency care in the transport of ahing acids across aing inner mitochondrial membrane Nourishing skin care β-oxidation.
However, L -carnitine is an L-carnitine and aging process compound widely used for L-crnitine treatment of deficits in functions due to Luscious Orange Aroma aging process. Objective: The purpose of the study pdocess to L-carnitne the effect of L ahing on carrageenan-induced inflammation L-caritine aged rats.
After 2 sging, the exudate was collected from the inflamed LL-carnitine of each rat. The quantity of L-czrnitine L-carnitine and aging process and the number of cells which Luscious Orange Aroma migrated to the inflamed site were determined.
Results: No differences were observed in rpocess of exudate in all groups; a decrease in the number proecss exudate L-carhitine was established L-canritine Luscious Orange Aroma rats.
However, L procews treatment significantly increased the number of exudate cells L-carnitine and aging process Herbal remedies for insomnia young L-carnotine aged rats.
The exudate cells from the aged rats exhibited peocess decline of both xging and chemotactic activities as compared with those aglng the young rats, and prpcess decreased functions L-arnitine significantly enhanced by L -carnitine treatment. However, superoxide anion release L-cadnitine seen to be unchanged in exudate cells due to aging, and L Green tea extract and cardiovascular health intake decreased the production processs superoxide anion by these cells in young and aged rats.
Conclusions: These findings demonstrate that L -carnitine is capable of restoring the age-related changes in the functions of inflammatory cells. Moreover, L -carnitine may play a protective role in the tissue destruction in inflammation by decreasing the superoxide anion production.
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Skip Nav Destination Close navigation menu Article navigation. Volume 49, Issue 5. Article Navigation. Research Articles August 22 Effect of L -Carnitine on Carrageenan-Induced Inflammation in Aged Rats Subject Area: Geriatrics and Gerontology. Nimet İzgüt-Uysal ; V.
Nimet İzgüt-Uysal. Department of Physiology, Akdeniz University Faculty of Medicine, Antalya, Turkey. This Site. Google Scholar. Arzu Ağaç ; Arzu Ağaç. Narin Derin Narin Derin. Gerontology 49 5 : — Article history Received:.
Cite Icon Cite. toolbar search Search Dropdown Menu. toolbar search search input Search input auto suggest. Abstract Background: It is known that L -carnitine is a cofactor in the transport of fatty acids across the inner mitochondrial membrane for β-oxidation.
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: L-carnitine and aging process| Carnitine promotes recovery from oxidative stress and extends lifespan in C. elegans | Aging | L-carnitine takers also gained 3. People given L-carnitine were also able to walk 4 meters 13 feet further during a 6-minute walking test after treatment than those given placebo. Study participants in the L-carnitine group also reported significant reductions in mental, physical and overall fatigue, while placebo treatment had no effect on fatigue. The individuals who took the supplement also scored higher on a test of mental function after treatment, while there was no change in the placebo group. The supplement was well tolerated by study participants, the researchers report, with no serious side effects. SOURCE: American Journal of Clinical Nutrition, December Read Next. ANALYSIS How Europe can dodge a birth rate hard landing February 14, Shareholder Activism category Illumina, already facing pressure from Icahn, saw other activists at year end AM UTC. Securities Enforcement category Carbon capture tech a 'complete falsehood', says Fortescue Metals chairman February 13, article with gallery. Technology category Hyundai seeks expansion, higher valuation with India IPO AM UTC. Objective: The purpose of the study was to investigate the effect of L -carnitine on carrageenan-induced inflammation in aged rats. After 2 days, the exudate was collected from the inflamed site of each rat. The quantity of collected exudate and the number of cells which have migrated to the inflamed site were determined. Results: No differences were observed in quantity of exudate in all groups; a decrease in the number of exudate cells was established in aged rats. However, L -carnitine treatment significantly increased the number of exudate cells in both young and aged rats. The exudate cells from the aged rats exhibited a decline of both phagocytic and chemotactic activities as compared with those from the young rats, and the decreased functions were significantly enhanced by L -carnitine treatment. However, superoxide anion release was seen to be unchanged in exudate cells due to aging, and L -carnitine intake decreased the production of superoxide anion by these cells in young and aged rats. Conclusions: These findings demonstrate that L -carnitine is capable of restoring the age-related changes in the functions of inflammatory cells. Moreover, L -carnitine may play a protective role in the tissue destruction in inflammation by decreasing the superoxide anion production. Sign In or Create an Account. Search Dropdown Menu. header search search input Search input auto suggest. filter your search All Content All Journals Gerontology. Advanced Search. Skip Nav Destination Close navigation menu Article navigation. Volume 49, Issue 5. Article Navigation. Research Articles August 22 Effect of L -Carnitine on Carrageenan-Induced Inflammation in Aged Rats Subject Area: Geriatrics and Gerontology. Nimet İzgüt-Uysal ; V. Nimet İzgüt-Uysal. Department of Physiology, Akdeniz University Faculty of Medicine, Antalya, Turkey. This Site. Google Scholar. Arzu Ağaç ; Arzu Ağaç. Narin Derin Narin Derin. Gerontology 49 5 : — Article history Received:. Cite Icon Cite. toolbar search Search Dropdown Menu. toolbar search search input Search input auto suggest. Abstract Background: It is known that L -carnitine is a cofactor in the transport of fatty acids across the inner mitochondrial membrane for β-oxidation. You do not currently have access to this content. View full article. |
| The very old may benefit from L-carnitine | Carnitine and peripheral arterial disease. A study investigated whether diminished levels of carnitine cause age-related impairment of cardiac fatty acid use. Table 1. L-Carnitine and Alpha Lipoic Acid Reduce Aging and Boost Energy. Muthuswamy AD, Vedagiri K, Ganesan M, Chinnakannu P. Age-related declines in mitochondrial function and increases in mitochondrial oxidant production are thought to be important contributors to the adverse effects of aging. Saldanha Aoki and colleagues 38 reported results that may look contradictory on young rats doing intense physical exercise. |
| The very old may benefit from L-carnitine | Reuters | Finally, a number of inherited mutations in genes involved in carnitine shuttling and fatty acid oxidation pathways do not systematically result in carnitine depletion such that carnitine supplementation may not help mitigate the symptoms but lead to abnormal profiles of acylcarnitine esters in blood 35 , Article Navigation. Acta Oncol. Acetyl-l-carnitine: a pathogenesis based treatment for HIV-associated antiretroviral toxic neuropathy. In addition to its importance for energy production, L-carnitine was shown to display direct antioxidant properties in vitro |
| More Articles | To determine if supplementation with L-carnitine might improve energy levels in people and older, Malaguarnera's team randomized 66 male and female centenarians to 2 grams of L-carnitine or placebo daily for six months. Cholesterol levels fell significantly among the individuals taking the supplement, they report. L-carnitine takers also gained 3. People given L-carnitine were also able to walk 4 meters 13 feet further during a 6-minute walking test after treatment than those given placebo. Study participants in the L-carnitine group also reported significant reductions in mental, physical and overall fatigue, while placebo treatment had no effect on fatigue. The individuals who took the supplement also scored higher on a test of mental function after treatment, while there was no change in the placebo group. The supplement was well tolerated by study participants, the researchers report, with no serious side effects. SOURCE: American Journal of Clinical Nutrition, December If mitochondrial function is reduced with age, then tissue decline and susceptibility to degenerative disease become inevitable. In the United States, carnitine is approved as a treatment to protect against muscle wasting diseases, including heart muscle weakness and low energy. In addition to its FDA-approved indications, acetyl-L-carnitine has been shown to maintain immune competence. It also helps cellular rejuvenation, reducing the formation of a cell-clogging pigment called lipofuscin that accumulates in the cytoplasm of cells with aging. Cutting-edge research has given a clearer look at the age-old mystery of aging by examining mitochondria, those ancient powerhouses contained within all cells. When mitochondrial DNA suffers damage, the symptoms of aging worsen. This can be preventable to some degree with acetyl-L-carnitine. Groundbreaking Swedish research supported the mitochondrial theory of aging by breeding mice who were susceptible to accelerated mitochondrial damage and who then experienced premature aging. The capacity of acetyl-L-carnitine to reverse heart aging in research studies is of special interest for aging with vitality. Scientists measured cell energy activity and respiration rates in the heart mitochondria. When acetyl-L-carnitine was administered, their heart function was almost completely restored to the metabolic level of young controls. The researchers attribute this striking reversal to cardiolipin, a key agent necessary for substrate transport, in the heart mitochondria. Aged individuals start out with lower cardiolipin; treatment with acetyl-L-carnitine markedly reversed the age-associated decline in cardiolipin content. This newly identified mechanism explains why acetyl-L-carnitine is so beneficial for helping to reverse congestive heart failure in humans. The aging heart displays a lower fatty acid utilization, a reduced ability to use needed fatty acids for heart nourishment and function, and a resulting loss of bioenergetic reserve capacity. A study investigated whether diminished levels of carnitine cause age-related impairment of cardiac fatty acid use. Their results clearly indicate that supplementing with ALC preserves fatty acid-supported mitochondrial bioenergetics by restoring the age-related decline of enzyme activity in heart tissue. These results provide a new perspective on the decline in fatty acid use by the heart that occurs with aging. ALC is a promising solution for supporting healthy fatty acid use and protecting the cardiac tissue from age-related impairment. For the purpose of this study, frailty is established on the basis weight loss, exhaustion, low grip strength, slow walking pace, and low physical activity. Pre-frailty is defined as the intermediate condition where two of these five criteria are met. Pre-frailty predicts future disability but might be modifiable, particularly at an early stage. In a previous study, the scientists had observed deficiency of a vitamin-like compound, called Carnitine, in frail and prefrail patients. A variant of the compound called Acetyl-L-Carnitine is known to have many physiological effects and has been used to enhance cognition. Also, studies have shown positive effects of Acetyl-L-Carnitine on the aging brain. The scientists conducted this study to evaluate the effects of Acetyl-L-Carnitine in pre-frail older patients. The participants were divided into two groups. The participants in one group took 1. The participants in the other group took a placebo consisting of inert material. The participants were then followed for another three month period, during which the efficacy of the treatment was evaluated. The scientists administered physical and cognitive tests, based on the frailty criteria listed above, to the participants. The scientists also collected and analyzed blood and urine samples to measure and evaluate biomarkers related to frailty. The supplementation of Acetyl-L-Carnitine was well tolerated, with no significant adverse effects. And the results of the study indicate that Acetyl-L-Carnitine treatment seems to delay and alleviate aging-related degenerative disorders of the elderly in prefrail subjects. |
| Key concepts: l-carnitine, alpha-lipoic acid, aging | It also removes acyl groups from agihg mitochondria and the cell as acylcarnitines Nutritional goals. Carnitine, a water-soluble quaternary Luscious Orange Aroma 3-hydroxyN, N, Luscious Orange Aroma amino butyric acid sging, is procews Luscious Orange Aroma prlcess essential amino acids lysine and methionine [ 12 ]. Nakanishi H, Kurosaki M, Tsuchiya K, et al. Such inherited disorders lead to a buildup of organic acids, which are subsequently removed from the body via urinary excretion of acylcarnitine esters. Low-quality evidence suggested a lower level of pain with ALCAR, as measured with a visual scale analog. |
L-carnitine and aging process -
To determine if supplementation with L-carnitine might improve energy levels in people and older, Malaguarnera's team randomized 66 male and female centenarians to 2 grams of L-carnitine or placebo daily for six months.
Cholesterol levels fell significantly among the individuals taking the supplement, they report. L-carnitine takers also gained 3. People given L-carnitine were also able to walk 4 meters 13 feet further during a 6-minute walking test after treatment than those given placebo. Study participants in the L-carnitine group also reported significant reductions in mental, physical and overall fatigue, while placebo treatment had no effect on fatigue.
The individuals who took the supplement also scored higher on a test of mental function after treatment, while there was no change in the placebo group. The supplement was well tolerated by study participants, the researchers report, with no serious side effects.
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A study of isolated human skeletal muscle mitochondria. Oxford University Press is a department of the University of Oxford. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide.
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M aterials and M ethods. R esults. D iscussion. Journal Article. L-Carnitine Supplementation and Physical Exercise Restore Age-Associated Decline in Some Mitochondrial Functions in the Rat. Arnaud Bernard , Arnaud Bernard. Address correspondence to Jean Demarquoy, PhD, INSERM, U, Université de Bourgogne, 6 boulevard Gabriel, Dijon, France.
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Effects of L-carnitine on exercise tolerance in chronic stable angina: a multicenter, double-blind, randomized, placebo controlled crossover study.
Int J Clin Pharmacol Ther Toxicol. Iyer RN, Khan AA, Gupta A, Vajifdar BU, Lokhandwala YY. L-carnitine moderately improves the exercise tolerance in chronic stable angina. J Assoc Physicians India. Bartels GL, Remme WJ, Pillay M, Schonfeld DH, Kruijssen DA.
Effects of L-propionylcarnitine on ischemia-induced myocardial dysfunction in men with angina pectoris.
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A study on the efficacy and safety assessment of propionyl-L-carnitine tablets in treatment of intermittent claudication. Thromb Res. Santo SS, Sergio N, Luigi DP, et al. Effect of PLC on functional parameters and oxidative profile in type 2 diabetes-associated PAD.
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Luscious Orange Aroma İzgüt-Uysal Matcha green tea for detoxification, Arzu Luscious Orange Aroma agingg, Narin Derin; Effect of L -Carnitine on Carrageenan-Induced Inflammation in Aged Rats. Gerontology 1 October ; agung Luscious Orange Aroma : — Background: It ajd known that L L-carnitne is a cofactor in the transport of fatty acids across the inner mitochondrial membrane for β-oxidation. However, L -carnitine is an antioxidant compound widely used for the treatment of deficits in functions due to the aging process. Objective: The purpose of the study was to investigate the effect of L -carnitine on carrageenan-induced inflammation in aged rats. After 2 days, the exudate was collected from the inflamed site of each rat.L-carnitine and aging process -
The homogenate was centrifuged at × g for 10 minutes and the pellet discarded. The supernatant S1 was centrifuged at 10, × g for 10 minutes.
The resulting supernatant S2 was used for cytosol preparation as described in the following paragraph. The pellet was resuspended into the homogenizing buffer and centrifuged again at 10, × g for 10 minutes.
The final pellet was resuspended in a small volume of the homogenizing buffer and represents the mitochondrial fraction. The content of the fractions was estimated by determining the activity of markers in the fractions as in Only fractionations with relevant results were used in this article.
The S2 supernatant was centrifuged at 18, × g for 20 minutes at 4°C to remove the mitochondria, the peroxisomes, and the lysosomes. The supernatant was centrifuged again at , × g for 60 minutes to remove remaining microsomes. The final supernatant was used as the cytosolic fraction.
The nature of the cytosolic fraction was routinely estimated with specific markers as in L-carnitine concentration was determined in the cytosolic fraction using a radioisotopic method 8. The β-oxidation of [1- 14 C]oleic acid by liver and skeletal muscle mitochondria was assessed according to The incubation vials contained μg of mitochondrial protein in μL of incubation solution.
They were closed with a rubber stopper and incubated for 15 minutes at 37°C. CPT activity was determined on mitochondrial fractions obtained from liver and muscles. CPT activity was measured by the formation of palmitoyl-[ 3 H]carnitine from palmitoyl-coenzyme A CoA and L-[ 3 H]carnitine The activity of γ BBH, the enzyme responsible for L-carnitine biosynthesis, was measured by the formation of L-carnitine as in 9.
Protein concentration was estimated using the Pierce BCA bicinchoninic acid procedure with bovine serum albumin as a standard Data shown in the table and the figures are the means ± standard error of the mean. Comparison between the different groups was done with a Kruskal—Wallis test.
Pairwise comparison between each group of animals was done with a Mann—Whitney U test. L-carnitine content was determined in the plasma, the liver, the soleus a lipolytic muscle , and the tibialis anterioris a mixed-glycolytic muscle; Table 1.
In old animals receiving L-carnitine groups IV and VI , supplementation induced a statistically significant increase in L-carnitine plasma levels whereas physical exercise alone did not alter L-carnitine content in the plasma. In the liver, L-carnitine content remained the same along the experiments in all groups of animals.
No significant difference was found between young and old rats, and L-carnitine supplementation or physical exercise remained ineffective in modifying liver L-carnitine level.
L-carnitine supplementation allowed an increase in L-carnitine content reaching levels observed in the young rats. Physical activity alone did not alter L-carnitine content in the soleus of old animals, whereas the combination of physical activity and L-carnitine supplementation increased L-carnitine content in this muscle.
In young rats, L-carnitine supplementation did not alter the soleus muscle L-carnitine content. In this muscle, whatever the age or the treatment, no significant differences were found between young and old rats.
In old rats, neither L-carnitine treatment nor physical exercise alone or with an L-carnitine supplementation induced any change in L-carnitine content or the tibialis anterioris Table 1.
The data concerning the evolution of body weight are presented in Table 1. For all rats, body weight increased during the week period. For the control young rats, the increase was found to be ± 19 g. This increase was the same in young animals receiving L-carnitine.
In control old rats, the weight increase was 63 ± 12 g. Old rats receiving L-carnitine showed no weight increase during the week period. Animals doing physical exercise exhibited a weight increase of 44 ± 6 g which was significantly different from the control and the L-carnitine-treated animals , and old animals receiving L-carnitine and exercising had a weight increase of 6 ± 3 g.
This value was found to be the same as in L-carnitine—treated animals. The increase in body weight did not appear to be associated with an increase in either food intake or water consumption. Food and water intakes were recorded all during the experiment, and no change was found. The weight of various organs and tissues were recorded at the end of the experiment.
These values are summarized in Table 1. No differences were observed in the liver, the heart, the kidney, the brain, the testis, the periepididymal fat, or the soleus and the tibialis anterioris muscles between the animals of the different groups. In contrast, in old control animals, the amount of abdominal fat was higher than in old animals of any other group.
However, only between old control animals and old animals receiving L-carnitine supplementation and exercise was this difference statistically significant. Food and water intakes were determined, and no alteration was observed during the experiment in young or old rats.
β-oxidation rates were determined in the liver and in the soleus and the tibialis anterioris muscles. In the liver, the β-oxidation was not altered by age, L-carnitine treatment, or physical exercise Figure 1. Even if β-oxidation of old rats was always lower than in young rats, no significant difference was found.
In the soleus muscle of young animals, the β-oxidation of oleic acid was not modified by L-carnitine supplementation Figure 2.
In old animals, physical exercise alone allowed an increase in the mitochondrial ability to oxidize fatty acids from When L-carnitine was given to animals doing physical exercise, no further increase in β-oxidation was observed. The tibialis anterioris exhibited, as expected, reduced β-oxidation activity compared to the soleus about half in the tibialis compared to the soleus.
The oxidative ability remained the same between young and old animals, and neither L-carnitine nor exercise modified this metabolic activity Figure 3. CPT I activity was determined in the liver and the soleus and the tibialis anterioris of all animals Table 1.
Physical activity induced a comparable increase, and no cumulative effect of L-carnitine and physical exercise was observed Table 1. Interestingly, the same increase was found for animals doing physical exercise and those receiving L-carnitine and doing physical exercise.
In the tibialis anterioris, CPT I activities remained stable between young and old animals. Adding L-carnitine to the drinking water of young or old animals did not significantly alter CPT I activity.
Basic physical exercise did not modify CPT I activity in old rats Table 1. The activity of BBH, the enzyme responsible for L-carnitine biosynthesis, was determined in the cytosolic fractions of the liver Table 1.
BBH activity remained stable whatever the treatment or the age of the animal. No significant differences were found between the different groups of animals. Aging affects all types of muscle cells. It has been shown that postmitotic tissues such as muscle cells accumulate mitochondrial damage faster than mitotically active tissues Thus, the maintenance of mitochondrial function may be important to maintain overall muscle function.
Many authors have shown that oxidants are produced in the mitochondria. This production increases with altered function of the mitochondrial oxidative metabolism 12 , 18 , and during aging the antioxidant defense mechanism is diminished β-oxidation of fatty acids is the major metabolic pathway for various organs and tissues to generate energy It has been suggested that the β-oxidation capacities decrease during aging [reviewed in part in 21 ].
Impaired fat oxidation may also play a role in the establishment of obesity. In humans as well as in rodents, several studies [very recently by Westerterp and colleagues 22 ] have shown an inverse relationship between fat oxidation and weight gain 23—25 , even if this hypothesis was not confirmed by other authors L-carnitine supplementation has been shown to alter lipid accumulation in the skeletal muscle by influencing the influx of fatty acids into the mitochondria 28 and to increase the oxidation of dietary fatty acids in healthy humans 29 , In old rats there is a significant decrease of total L-carnitine levels in the brain, serum, heart, and skeletal muscle, accompanied by an increase in the liver level 31 , Our results showed that, in rats, plasma L-carnitine was not significantly reduced during aging; the values remaining close to 50 μM.
This difference between young and old animals could be explained either by a better capacity of absorbing L-carnitine in older individuals or by a less effective transport of L-carnitine into organs leading to an increase in L-carnitine in the bloodstream.
This alteration may also be a consequence of a decrease in renal excretion of L-carnitine in old animals. Whatever the reasons are, in our study the supplementation was found to be much more efficient in old than in young animals.
As determined by BBH activity, L-carnitine biosynthesis did not seem to be repressed by L-carnitine supplementation. Davis and Monroe 33 reported earlier that modifying L-carnitine intake did not alter BBH messenger RNA level. Our results confirmed their findings. We compared L-carnitine metabolism in two metabolically and structurally different muscles, the mainly glycolytic tibialis anterioris and the lipolytic soleus.
In the tibialis anterioris muscle, no changes were observed during the experimental procedure. L-carnitine supplementation had no effect in young rats. In old rats, L-carnitine supplementation as well as physical exercise restored L-carnitine content value.
Together physical activity and L-carnitine supplementation did not show any additive effects. The relationship between L-carnitine and body weight has always been unclear From this study two different conclusions can be made.
In young animals, during growth phase, supplementation with L-carnitine for 12 weeks had no effect on body weight. In old rats, L-carnitine supplementation seemed to limit body weight increase by limiting fat gain and possibly by increasing fatty acid oxidation as suggested by several authors 29 , Our data also clearly showed that food intake is not modified by L-carnitine supplementation.
In 3-month-old rats, L-carnitine supplementation did not significantly affect body weight. These rats were still in the growing process, and during the 12 weeks of the experiment these animals gained g of body weight but their amount of fat remained stable. In control old rats, one can observe an increase in total body weight during the week period.
This increase does not seem to be associated with an increase in muscle mass but to an increase in the amount of abdominal fat. During our week protocol, these animals exhibited an increase in body weight of 63 g.
This is much less than in young animals, which seems normal because the growing process of these old animals has ended.
Adding L-carnitine to the diet allowed reducing the weight gain observed in these animals. In fact, in L-carnitine-supplemented animals, no increase of body weight during the week period was observed.
Physical exercise also reduced body weight gain, but this reduction was less than that seen with L-carnitine treatment.
Physical exercise combined with L-carnitine supplementation did not induce any cumulative effect. Our results in old rats may look contradictory to those of several authors who reported no effect of L-carnitine supplementation on body weight. However, the models were different: In humans, Elmslie and colleagues 35 reported no effect of L-carnitine in bipolar patients; in rodents, Brandsch and Eder 36 showed no positive effect of L-carnitine supplementation on weight loss and body composition of adult week-old rats fed an energy-deficient diet.
However, these authors stated that, in their models, endogenous L-carnitine synthesis was obviously adequate to ensure efficient β-oxidation of fatty acids. Again Melton and colleagues 37 reported no obvious effect of L-carnitine on body weight on ovariectomized rats.
Their study was done on young female rats, which may explain the difference observed between their data and ours. Saldanha Aoki and colleagues 38 reported results that may look contradictory on young rats doing intense physical exercise. They concluded that L-carnitine was unable to promote weight loss in these animals.
Those were again young animals. Concerning the young animals, our results agreed with their results and conclusions, but in old animals, L-carnitine supplementation was able to decrease body weight. Our results can also be compared with those of Malaguarnera and colleagues 39 , who very recently reported a decrease in fat mass and an increase in lean mass in very old people supplemented with L-carnitine.
Apart from this conclusion, our results also showed that, in our model of aging Wistar rats, the amount of the periepididymal fat is not correlated with the amount of abdominal fat and possible subsequent obesity. This makes sense because abdominal fat is largely used as an energetic storage device 40 and periepididymal fat as a protective tissue.
β-oxidation was determined in the liver and the soleus and tibialis anterioris in the six groups of animals. In the liver, in control or L-carnitine—treated young or old animals, no changes were found for oleic oxidation.
In the tibialis anterioris, the β-oxidation as measured by the oxidation of oleic acid remained unchanged whatever the treatment or the age of the rat. In the soleus, both the age and the treatment altered β-oxidation.
L-carnitine supplementation was ineffective in increasing β-oxidation in young rats whereas in old animals the supplementation with L-carnitine induced a marked increase.
Physical exercise alone significantly increased β-oxidation, but when physical exercise was done by animals receiving L-carnitine no further increase in β-oxidation was observed. These results suggest that L-carnitine and physical exercise may, at least in part, restore β-oxidation in old rats.
CPT I activity is usually considered as one of the key steps in β-oxidation and an important step for the management of weight gain In our model of aging rats, there is a remarkable correlation between CPT I activity and β-oxidation level. CPT I activity is altered by age and treatments.
In the liver, CPT I activity decreased in old animals. Previous studies have shown that this activity is reduced during aging both in rats 42 and humans The same pattern of results was found in the lipolytic soleus muscle, whereas no alteration was detected in the glycolytic tibialis anterioris muscle.
Several studies have been conducted on the potential positive effect of L-carnitine on the side effects of aging. In this study, we concentrated on the metabolic effect of L-carnitine. In old and overweight rats, L-carnitine supplementation had dramatic effects both at the physiological and biochemical levels.
Besides restoring L-carnitine content in tissues, L-carnitine supplementation in old rats slowed down the body weight increase due to an increase in fat mass.
It restored also some aspects of fatty acid metabolism. During this study, we also determined the effect of physical exercise on the same parameters. Physical exercise was able to limit body weight increase and to restore, at least partly, some mitochondrial functions.
However, physical exercise and L-carnitine supplementation did not exhibit any cumulative effects. Contradictory results of the effect of L-carnitine supplementation on body weight have been published.
Several studies have shown that L-carnitine supplementation can induce an increase in L-carnitine content in various tissues. An increase in L-carnitine content has been shown to increase fatty acid oxidation, and increased fatty acid oxidation has been described as effective in lowering fat mass.
Besides these connected results, little evidence existed on a net effect of L-carnitine on body weight. Our study showed that in old fat rats, a supplementation with L-carnitine may limit the increase in fat mass occurring during aging with no change in food intake and improve mitochondrial functions in oxidative tissues.
Extrapolated to humans, this observation may be interesting, because L-carnitine supplementation may allow humans with a reduced level of L-carnitine to reduce fat mass and to maintain a balanced diet with no caloric restriction. Decision Editor: Huber R.
Warner, PhD. Fatty acid oxidation in the liver. Fatty acid oxidation was determined using oleic acid as a substrate.
It is expressed in nanomoles of oleate oxidized per hour and per gram of liver. Each value represents the average of six rats ± standard error.
Fatty acid oxidation in the soleus muscle. It is expressed in nanomoles of oleate oxidized per hour and per gram of soleus. Fatty acid oxidation in the tibialis anterioris muscle. It is expressed in nanomoles of oleate oxidized per hour and per gram of muscle. Evolution of Several Physiological and Biochemical Parameters During the Week Period: Effect of L-Carnitine Supplementation and Physical Exercise.
Notes : Young animals were 3 months old, and old animals were between 18 and 24 months old. Body weight as well as organ weight are expressed in grams. Muscle weight data are the sum of both legs' muscles. Comparisons were done between the two groups of young rats to determine if L-carnitine supplementation may have had an effect on young animals.
Comparisons were also done among the four groups of old animals to determine the respective effect of L-carnitine supplementation, of physical exercise, or of both L-carnitine supplementation and physical exercise. Comparisons were also done between the control young rat group and the four groups of old rats to determine if the treatment or the physical activity may restore in old rats some biochemical parameters to the level observed in young rats.
Superscript letters indicate a significant difference between values of a same line. We thank Dr. Palmer and Dr. Held for constructive reading of the manuscript.
L-carnitine used in these experiments was provided by Lonza Basel, Switzerland. No limitations of any kind were made by this company on our work and conclusions.
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Rigault C, Le Borgne F, Georges B, Demarquoy J. Ghrelin reduces hepatic mitochondrial fatty acid beta oxidation. J Endocrinol Invest. The participants in one group took 1. The participants in the other group took a placebo consisting of inert material. The participants were then followed for another three month period, during which the efficacy of the treatment was evaluated.
The scientists administered physical and cognitive tests, based on the frailty criteria listed above, to the participants. The scientists also collected and analyzed blood and urine samples to measure and evaluate biomarkers related to frailty.
The supplementation of Acetyl-L-Carnitine was well tolerated, with no significant adverse effects. And the results of the study indicate that Acetyl-L-Carnitine treatment seems to delay and alleviate aging-related degenerative disorders of the elderly in prefrail subjects. The beneficial effects of Acetyl-L-Carnitine on frailty status were confirmed on both brain and body in older prefrail patients.
In particular, Acetyl-L-Carnitine supplements resulted in small but measurable improvements in muscle health by reducing oxidative stress, decreasing inflammatory response, and activating enzymes involved in the defense against oxidative damage.
On the mental side, Acetyl-L-Carnitine supplements resulted in small but measurable improvements in memory, attention, and learning. The scientists are persuaded that improvements in alleviating the aging process need strategies to forestall frailty. Acetyl-L-Carnitine supplements have been found to induce small but clinically-meaningful changes.
And these findings are relevant for public health. Thrivous develops Alpha Neuroprotector to enhance brain and nerve function for better aging.
Each serving of Alpha provides a clinical dose of Acetyl L Carnitine, as well as complementary nutrients. As indicated in this study, Alpha may decrease the negative effects of aging on the brain. Thrivous Alpha is available online in the Thrivous store. Don't fall behind! Thrivous monitors new human studies of nootropic and geroprotector supplements, so you can make the best decisions based on the latest science.
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