|Year : 2022 | Volume
| Issue : 3 | Page : 199-209
Effect of L-carnitine on the lipid profile, glycemic control, oxidative stress, and anthropometric indices of individuals with type 2 diabetes: A systematic review
Navideh Khodadadi1, Behnood Abbasi2
1 Department of Clinical Nutrition and Dietetics, Faculty of Nutrition Science and Food Technology, Shahid Beheshti University of Medical Sciences, Tehran, Iran
2 Department of Nutrition, Electronic Health and Statistics Surveillance Research Center, Science and Research Branch, Islamic Azad University, Tehran, Iran
|Date of Submission||06-May-2022|
|Date of Decision||13-Jul-2022|
|Date of Acceptance||27-Jul-2022|
|Date of Web Publication||26-Sep-2022|
Dr. Behnood Abbasi
Department of Nutrition, Science and Research Branch, Islamic Azad University, 275 Daneshgah Boulevard, Simon Bolivar Street, Tehran 1477893855
Source of Support: None, Conflict of Interest: None
Diabetes mellitus is one of the most prevalent metabolic diseases in existence. With more than 536.6 million cases having been diagnosed globally, its prevalence is reported to be 10.5% in 2021. In individuals with diabetes, plasma L-carnitine is low and metabolized abnormally. In this review, we aimed to assess whether L-carnitine supplementation is correlated with a reduction of the risk of cardiovascular diseases in individuals with diabetes by improving the compositions of lipid profiles, indicators of oxidative stress, glycemic control, and anthropometric indices. A literature search in major databases such as Web of Science, PubMed, Google Scholar, Scopus, and Scientific Information Database was conducted until November 2021. This was done in conjunction with a search in Elsevier and SpringerLink databases, resulting in the inclusion of relevant articles in this review. To construct the search strategy, “Carnitine” OR “glycine propionyl carnitine” OR “Acetylcarnitine” in combination with “Diabetes Mellitus” OR “Diabetes Complications” OR “Lipid Profile” and all of its components were used to search for and within the articles and databases. After screening, 10 articles published between 1998 and 2017 were identified. They evaluated the effect of L-carnitine on lipid profile metabolism, glycemic control, anthropometric indices, and oxidative stress markers in individuals with diabetes. In this systematic review, we concluded that L-carnitine had no notable effect on lipid profile as well as glycemic control and anthropometric indices. Therefore, using L-carnitine probably has no notable effect on metabolic status in individuals with diabetes. Meanwhile, some articles suggested that L-carnitine may have positive effects on some oxidative stress indicators.
Keywords: Carnitine, diabetes mellitus, glycemic control, lipid metabolism, metabolic parameters
|How to cite this article:|
Khodadadi N, Abbasi B. Effect of L-carnitine on the lipid profile, glycemic control, oxidative stress, and anthropometric indices of individuals with type 2 diabetes: A systematic review. J Diabetol 2022;13:199-209
|How to cite this URL:|
Khodadadi N, Abbasi B. Effect of L-carnitine on the lipid profile, glycemic control, oxidative stress, and anthropometric indices of individuals with type 2 diabetes: A systematic review. J Diabetol [serial online] 2022 [cited 2022 Dec 7];13:199-209. Available from: https://www.journalofdiabetology.org/text.asp?2022/13/3/199/357131
| Introduction and Aim|| |
Diabetes mellitus (DM) is one of the metabolic disorders with high prevalence. With more than 536.6 million cases in 20–79-year-olds having been diagnosed, diabetes prevalence is reported to be 10.5% in 2021 globally and it is estimated that the number will rise to 783.2 million in 2045. Complications of DM are rising all over the world, and are accounting for 5–20% of healthcare budgets in most countries and even in some developing countries. DM remains one of the main causes of myocardial infarction., Recent studies have shown a direct connection between levels of some plasma lipid profiles such as HDL cholesterol (HDL-C) level and apolipoprotein B (Apo B), apolipoprotein A1 (Apo A1), and some cardiovascular complications such as thoracic aortic atherosclerosis. These studies emphasize the importance of total cholesterol (TC) or LDL cholesterol (LDL-C) in raising the risk of cardiovascular disease in individuals with diabetes, which support the current recommendation to reduce LDL-C to prevent the onset of atherothrombotic vascular events in them., In patients with type 2 diabetes, the LDL-C catabolism is significantly reduced, resulting in an increase of the duration of the presence of LDL-C in the plasma, which itself may increase lipid deposition in the arterial wall. Moreover, the number of LDL-C B/E receptors on the cell surface is considerably diminished, which may be due to a decrease in the expression of insulin and can lead to disruption of LDL-C catabolism., Changing LDL-C compositions may cause conformational changes and probably results in higher exposure of fatty acids to oxygen-free radicals and changes in lipid peroxidation levels., In plasma or subendothelial arterial wall, uptake of LDL-C will increase via scavenger receptors present in macrophages, smooth muscle cells, and endothelial cells as consequences of LDL-C oxidation.,,, The formation of foam cells as well as the alteration of monocytes and macrophages in the arterial wall to cholesterol foam cells, which are essential parts of the atherosclerosis plaque, significantly increases with the oxidative changes in LDL-C., Moreover, in individuals with diabetes, levels of serum lipids are often elevated and are independently related to some complications of DM., Higher levels of insulin in the blood, the presence of non-oxidative glycation products, and increases in levels of blood glucose because of insulin resistance may increase the risk of cardiovascular morbidity in type 2 diabetes. The risk of oxidative stress, which has a vital role in LDL-C oxidation and hyperglycemia, is high in individuals with diabetes., Many pharmacological agents, such as calcium channel antagonists and antiplatelet agents, have been used in the treatment of peripheral arterial disease (PAD) in individuals with diabetes. It has been suggested that oxidative stress might worsen the complications of diabetes, whereas antioxidants may alleviate and impede mechanisms that cause diabetes at an early stage.
L-carnitine is an amino acid-based substance that has an important role in the transport of long-chain fatty acids through the internal mitochondrial membrane.,, In tissues such as skeletal muscle and heart, which use fatty acids as the main fuel, it can be seen in high concentrations. Additionally, as literature suggests, in individuals with diabetes, plasma L-carnitine concentrations are low. In addition, abnormal metabolism of carnitine has been reported in individuals with diabetes, and the higher prevalence of carnitine deficiency in muscle tissues of PAD patients has also been observed.,, Carnitine deficiency has been shown to correlate with cardiomyopathy. Therefore, decreased carnitine levels may impair myocardial function., It has been suggested that L-carnitine, especially with its antioxidant and lipid-lowering effects, may be able to reduce atherosclerotic lesions., Moreover, oxidation of lipids accelerates the formation of free radicals, thus carnitine may prevent oxidative stress by inhibiting the peroxidation of membranes’ fatty acids. So, due to limited amounts of L-carnitine, fatty acids cannot enter the mitochondria to oxidize and produce ATP. A study that used L-carnitine supplementation showed a rapid reduction in serum levels of oxidative LDL-C (ox LDL-C), suggesting that it could possibly reduce oxidative stress, and it has been claimed that carnitine consumption may lead to change in the metabolic pathway of the liver from esterification and synthesis of triglycerides (TGs) to the production of acetyl L-carnitine (ALC). This pathway may lead to increases in mitochondrial fatty acids beta-oxidation and reduction in the synthesis of TG and very-low-density lipoprotein (VLDL) cholesterol. Also, it was shown that increasing carnitine may have positive effects on body fat reduction and increment of oxidation of the fatty acids. Moreover, it has been suggested that the beneficial effects of improving vascular reactivity and antioxidant activity, which can be observed during the treatment with L-carnitine, may be due to decreased plasma lipid levels; therefore, it can be used as an effective therapeutic tactic to improve diabetes vascular complications., Also, arterial blood pressure, insulin resistance,, impaired glucose tolerance, and hypoadiponectinemia in individuals with diabetes can be safely improved by ALC. In this study, we aimed to summarize the results of previous studies that examined the effects of L-carnitine supplementation on lipid profiles, indicators of glycemic control and oxidative stress, and anthropometric indices, to assess the potential relationship between L-carnitine supplementation and metabolic status in individuals with diabetes.
| Materials and Methods|| |
PRISMA guideline was used for completing this review which was registered with the PROSPERO database (Code: [removed for blind peer review]).
We used a systematic search approach to investigate electronic databases such as Web of Science, PubMed, Google Scholar, Scopus, and Scientific Information Database (SID) to retrieve articles that examine the effect of L-carnitine on lipid profile composition, indicators of oxidative stress and glycemic control, and anthropometric indices in individuals with diabetes from inception until November 2021. Our search was supplemented with the search of publisher databases Elsevier and SpringerLink. The following MeSH and non-MeSH terms were used to construct the search strategy for screening electronic papers: “Carnitine” OR “glycine propionyl carnitine” OR “Acetylcarnitine” in combination with “Diabetes Mellitus” OR “Diabetes Complications” and “Lipid Peroxides” OR “Cholesterol, LDL” OR “Cholesterol, HDL” OR “Cholesterol” OR “Triglycerides” OR “Cholesterol VLDL” OR “Apolipoprotein A-I” OR “Apolipoproteins B” OR “Lipoprotein(a)” OR “Oxidative Stress” OR “4-hydroxy-2-nonenal” OR “Nitrites” OR “Nitrates” OR “Thiobarbituric Acid Reactive Substances” OR “Malondialdehyde” OR “Glycemic Control” OR “ Insulin” OR “Glycated Hemoglobin A” OR “Blood Glucose” OR “Anthropometry” OR “Waist-Hip Ratio” OR “Body Mass Index” OR “Body Weight”. Details of the search strategy can be found in Supplementary File 1.
Inclusion and exclusion criteria
All articles addressing the effect of L-carnitine on lipid profiles components and indicators of oxidative stress, glycemic control, and anthropometry in individuals with diabetes were eligible to enter the study after screening the titles and abstracts. There were no restrictions regarding the language of publications. Also, the minimum acceptable criterion for blood glucose level was 126 mg/dL. Animal and other studies not providing our primary outcomes were excluded. Duplicated articles and studies with supplementation through injection were removed as well.
Data extraction and quality assessment
Two independent authors (NK and BA) identified articles and then extracted the following data regarding general characteristics of the study and population (study’s first author, year of publication, study design and location, number of participants and their gender and age, intervention duration, and supplement dosage); lipid metabolism such as HDL-C, LDL-C, TC, TG, VLDL, Apo A1, Apo B, lipoprotein (a) [Lp (a)]; oxidative stress markers such as 4-hydroxynonenal (4-HNE), nitric oxide (NO), nitrite/nitrate (NO2/3), glutathione peroxidase (GPx), thiobarbituric acid-reactive substances (TBAR), malondialdehyde (MDA), superoxide dismutase (SOD), glutathione-S-transferase (GST), total antioxidant capacity (TAC); glycemic control index such as insulin levels, glycosylated hemoglobin A1 C (HbA1C) and levels of fasting blood sugar (FBS), fasting plasma glucose (FPG), post-prandial plasma glucose (PPG), and fasting plasma insulin (FPI); and anthropometric indices such as body mass index (BMI), waist-to-hip ratio (WHR), and percent of body fat. The adequacy of selected trials was measured by using the quantitative 5-point Jadad scale. EndNote software was used to import and classify all the articles.
Quality assessment of included studies
The risk of bias in the eligible included studies was assessed using the Cochrane criteria. The quality of all studies was assessed by two different authors (NK and BA) for following items: sequence generation, allocation sequence concealment, blinding of participants and researchers, and outcomes reporting to evaluate possible sources of bias [Figure 1].
| Results|| |
From the 22 eligible studies, 10 articles were selected for studying after checking the full text carefully [Figure 2].
These articles were conducted from 1998 to 2017. The size of target groups ranged from 12 (in which 3 men and 3 women received L-carnitine) to 94 (in which 24 men and 22 women were in the L-carnitine group) patients. The longest period of the study was 12 months,, and the minimum length of the study was 4 weeks., In these 10 articles, the lowest dose of L-carnitine was 500 mg, and the highest dose was 3 g/day.,, Studies were conducted in five countries: Iran,,,, Italy,,,, Mexico, Iraq, and China. One study did not mention the gender of participants, and two studies were done exclusively on women,: one on men and the other study included both genders. In two of the studies, patients were taking oral antidiabetic drugs in addition to L-carnitine treatment, glyburide, and metformin in one paper, the results of which indicated an increment in TG, Apo A, and Apo B and no changes in LDL-C, HDL-C, and TC, and metformin and sulfonylurea in another study, the results of which showed significant reductions in FBS levels. The relevant factors to the title of this article, which have been reviewed in those 10 papers, are LDL-C, HDL-C, TC, TG, VLDL, and Lp (a). In addition, factors such as Apo B, Apo A1, HbA1C, and levels of FBS, FPG, PPG, and FPI and 4-HNE, MDA, insulin levels, NO2, NO3, and TBARs, BMI, WHR, body weight, and fat were also reviewed [Table 1].
Lipid panel parameters
In nine articles, it was shown that the levels of HDL-C did not significantly change with L-carnitine treatment when compared with the placebo group.,,,,,,,,, Based on these results, the consumption of L-carnitine may not have a significant effect on HDL-C levels. In nine articles that measured TC levels, there was no significant change via L-carnitine treatment in the TC levels in comparison with the placebo group.,,,,,,,,, Likely, L-carnitine has not affected the TC levels. In five assessed papers, treatment with L-carnitine did not result in significant changes in TG levels when compared with the placebo group.,,,,,, Two studies found that TG levels were notably lowered in comparison with the placebo group, but another study showed that TG levels significantly increased by 3 g of L-carnitine daily when compared with the placebo group. Therefore, according to the results; it seems that the use of L-carnitine does not affect TG levels. In seven studies that measured LDL-C level, it was shown that L-carnitine consumption could not change LDL-C level,,,,,,,; one paper found that levels of LDL-C were significantly decreased when compared with the placebo group. Based on these results, the use of L-carnitine does not affect LDL-C levels. Levels of VLDL cholesterol were investigated in one study and no significant relevance was found. So, further studies are necessary to reach a definitive conclusion. In one paper, concentration of the plasma Lp (a) was significantly reduced with the consumption of L-carnitine after 6 months compared with the placebo group, but two studies did not find any significant decrease compared with the placebo group., Because of the inconsistency of the findings, further studies are necessary to reach a conclusive result. Apo A and Apo B were discussed in four papers; one of the studies showed a significant effect of L-carnitine on the reduction of Apo A1 and Apo B100 levels when compared with the placebo group. Two studies found no significant change in L-carnitine compared with the placebo group after 6 months,, and one study showed that Apo B100 and Apo A1 levels significantly increased after intervention in comparison with the placebo group. Due to these contradictory findings, further studies with different durations of intervention, and doses, are necessary to reach a conclusive result.
Ten studies evaluated glucose levels. In four of them, compared with the placebo group, a significant decrease in glucose levels was observed after L-carnitine administration.,,, Moreover, six studies indicated a contrast reporting no significant change in glucose levels compared with the placebo group.,,,,,, Also, one paper indicated no statistically notable change in PPG and FPI in comparison to the placebo group after 6 months. Moreover, all of the eight studies that evaluated the HbA1C level showed that it did not have any significant change after the intervention when compared with the placebo group.,,,,,,,, Therefore, according to our results, supplementation of L-carnitine does not have any short-term or long-term effects on glycemic control.
Oxidative stress profile
Some studies investigated oxidative stress factors such as ox LDL-C, 4-HNE, NO2/NO3, TBARs, and MDA. One study found that levels of ox-LDL-C, TBARs, and conjugated dienes decreased compared with the placebo group. In addition, a paper observed a significant change in the LDL-C oxidation time in patients who were treated with 2 g/day propionyl L-carnitine (PLC). They showed that 4-HNE, MDA, and NO2/NO3 ratio (nitrite/nitrate) levels significantly decreased in the PLC-treated group when compared with the placebo group.,
In all nine articles that measured BMI,,,,,,,,, in three articles that measured WHR,,, in two articles that measured body fat,, and in all three articles that measured body weight,,, there was no significant decrease after L-carnitine treatment when compared with the placebo group, but Liang et al. detected a significant diminishment in WHR and body fat. Based on these results, L-carnitine treatment in diabetes probably does not correlate with anthropometric indices.
In the studies reviewed in this paper, some side effects were also observed. In one of the studies, one patient complains of nausea, which was resolved after 3 days of treatment. In another study, several cases of nausea, headache, and abdominal pain were observed in the L-carnitine-treated group. In the placebo group, several cases of diarrhea and nausea and headache were also observed. In addition to the aforementioned side effects, in one study, one subject from L-carnitine and one subject from the placebo group were excluded due to facial flushing and skin rash after 5 days and 4 weeks, respectively.
| Discussion|| |
A former review evaluated the metabolic effect of L-carnitine in individuals with diabetes. The present systematic review by providing additional evidence intends to update the previous results and to evaluate more parameters.
Lipid panel parameters
Based on the fact that Apo A1 has significantly increased whereas the HDL-C level remained unaffected, it seems that there is no correlation between L-carnitine and HDL-C levels. One possible hypothesis leading to this observation could be related to the increasing concentration of TG in the remaining VLDL and rising of TG antiport with HDL-C at the same time. One study showed a contrasting result by reporting the effect of carnitine on the HDL-C level; it found that ALC may increase the HDL-C levels probably via reducing HDL-C clearance and also by increasing the activity of lipoprotein lipase (LPL). The difference in results may be due to the type of the study conducted and/or the increase of dosage and duration of the intervention. L-carnitine may have cholesterol-lowering effects. This may be due to its effect on lowering TG as a result of changes in lipoprotein composition, which is damaged in diabetes. These different results may be caused by the difference in the types of studies conducted,, the way in which they were designed, and the duration of intervention applied. Also, TG levels may increase due to an elevated amount of fatty acids and Apo B100 that can lead to increased VLDL production. However, L-carnitine may in fact decrease TG levels. This may be based on the hypothesis that changes in the liver metabolic pathways of esterification and synthesis of TGs to ALC could reduce the production of TG. The LDL-C level may not decrease because cholesterol is not decreasing and also the Apo B100 level is increasing at the same time. In addition, the LDL-C receptor saturation and its regulatory reduction increase TG and abnormal VLDL that enriches in TG. Moreover, based on the Friedwald–Fredrickson formula [LDL-C= TC-(HDL-C+TG/5)], the levels of LDL-C depend on TC, HDL-C, and TG levels. If there is no significant change in cholesterol, TG, and HDL-C levels, there will not be any changes in the LDL-C level., However, supplementation with L-carnitine could probably decrease the LDL-C and TG levels by increasing the expression of the LDL-C receptor and LPL genes. The observed reduction in LDL-C levels may be due to the consumption of low-calorie diet and aerobic exercise along with the supplementation. González-Ortiz et al. assess the effect of L-carnitine on VLDL cholesterol level and no significant correlation was found. However, L-carnitine may change metabolic pathways from esterification in the liver and change TG synthesis to ALC, which can reduce the synthesis of TG and VLDL cholesterol. Also, catabolism of VLDL is reduced in individuals with diabetes, which is due to decreased activity of LPL in adipose tissue leading to augmented levels of TG in individuals with diabetes. Since insulin activates LPL, insulin resistance reduces the LPL activity. In addition, increasing plasma levels of Apo C-III, which inhibits the activity of LPL in individuals with diabetes, can reduce the catabolism of VLDL. Additionally, increasing the transfer of fatty acids to the liver, a common disorder in insulin-resistant diabetes, may increase the secretion of VLDL,, and also its concentration may rise by higher amounts of fatty acids and Apo B100. By stimulating and contributing to the decomposition of fatty acids in the mitochondria, L-carnitine can probably reduce the number of fatty acids to produce Lp (a) in patients who are likely to have high atherogenic lipoprotein production. In addition, it has been shown that strong inhibitory acyl cholesterol acyltransferase may be able to reduce plasma Lp (a) levels. Moreover, some studies measured the effect of L-carnitine on Apo B and Apo A1 levels, and their results were inconsistent.,,, This may be because apolipoproteins are genetically determined and dietary supplements are unlikely to have a significant effect on them. L-carnitine may affect Apo levels via its effect on oxidative stress. Apo A1 and Apo B100 levels may decrease because of the fact that L-carnitine reduces and inhibits oxidative stress. It also regulates cellular respiration, nitric oxidative stress, and nitric oxide and defends enzymes against oxidative damage. It also protects the enzymes catalase, succinate dehydrogenase, and superoxide dismutase and antioxidant enzymes. However, it has been proposed that high levels of carnitine may possibly induce fatty acids synthesis rather than their oxidation. Therefore, high doses of L-carnitine or its prolonged intake could probably play a role in increasing Apo B in a period of more than 3 months.
Most studies suggested that L-carnitine supplementation probably did not have any beneficial effect on the short-term depletion of glucose. In addition, there was no evidence of the ability of L-carnitine to regulate long-term hyperglycemia based on the HbA1C factor. L-carnitine may raise the hepatic homogenate glucose levels possibly by increasing beta-oxidation and producing excess hepatic glucose via gluconeogenesis. However, some studies indicated that carnitine could have a positive effect on glucose metabolism via modifying and altering the genes expression that contributes to its metabolism such as enzymes of gluconeogenic, glycolytic, and insulin signaling pathway, and also by increasing the activity of pyruvate dehydrogenase, producing more acetyl-CoA and stimulating the Krebs cycle.
Oxidative stress profile
Oxidative stress is caused by an imbalance in the production of reactive oxygen species and the cell’s own antioxidant defense, which may contribute to a number of diseases. Some studies showed that L-carnitine may be able to improve oxidative stress via affecting factors such as ox LDL-C, 4-HNE, NO2/NO3, TBARS, and MDA. A study, indicated that PLC could change the oxidative profile, as one of the roles of carnitine is facilitating the passage of fatty acids from cytosol to the matrix of mitochondria. Beta-oxidation of these fatty acids produces ATP, and any alteration in this pathway changes the oxidative metabolism. Also, in non-insulin-dependent diabetes mellitus (NIDDM) patients, increased blood glucose level and decreased insulin sensitivity lead to some changes in oxidative metabolism at the cellular level and endothelial dysfunction, which plays an important role in maintaining the balance of the circulatory system. L-carnitine is likely to improve oxidative-negative conditions in individuals with diabetes, as well as peripheral use of oxygen. A study indicated a notable decrease in ox LDL-C, which may be due to lower oxidative stress by the ability of L-carnitine to increase the mitochondria-mediated uptake of fatty acids to produce ATP. Additionally, this could be due to vasodilation of vessels that is related to the activity of acetylcholine, which is disrupted in NIDDM. By increasing the release of relaxation factors such as NO, acetylcholine induces vasodilation of the endothelium. Disturbance in NO production or response leads to the vascular and endothelium complications. Some studies showed that superoxide, hydroxyl, and free radicals can interact with NO. They produce weaker vasodilators such as peroxynitrite NO2 and NO3, which may interfere with endothelium-dependent vasodilators. L-carnitine improved acetylcholine and its response. However, in practice, a diet rich in nitrate can achieve the same plasma nitrate concentration as supplements. Also, another study, showed that the 4-HNE level significantly decreased in the PLC-treated group when compared with the placebo group. At a very low concentration, 4-HNE, which is the production of lipid peroxidation of unsaturated fatty acid on the cell membrane, can participate in the normal physiological cell functions. When its concentration is higher than normal, it can stimulate cell apoptosis, affecting cell signal transduction and creating a cytotoxic influence. Lipid peroxidation, created by free radicals attacking cell membranes, results in the production of lipid peroxidation derivatives, including 4-HNE, MDA, and many other toxic aldehydes. HNE can damage beta cells of the pancreas and impair the ability of muscle and the liver cells to respond to insulin. HNE may elevate the risk of atherosclerosis by altering lipoproteins. By impairing the metabolic enzymes, it can also damage the cardiac cells. Another study found that in hyperlipidemic individuals with diabetes, reducing antioxidants or improving their defensive function may correlate with a decrease in TBARs and conjugated dienes as lipid peroxidation indicators. The interaction between fatty acids and free radicals and, finally, changes in lipid peroxidation levels, could be altered by changes in LDL-C compounds. Hypertriglyceridemic and hypercholesterolemic individuals with diabetes are associated with protein glucose and glucose autoxidation and changes in the oxidative LDL-C, which increase lipid peroxidation. As a result, the amount of TBARs and conjugated dienes increases and, ultimately, elevates oxidative stress. Ox LDL-C is likely to cause atherogenesis by altering the TBARS level., Also, the results of one study indicated that L-carnitine could decrease MDA levels. MDA is an important indicator of lipid peroxidation and its increase in the liver may be the result of the stimulating effect of L-carnitine in the oxidation of fatty acids in mitochondria to produce ATP.
We could not find a significant correlation between L-carnitine and the reduction of anthropometric indices in individuals with diabetes, and also a recent systematic review did not support consumption of alternative dietary supplementation for weight loss. However, some studies showed that L-carnitine may reduce body weight through insulin resistance, appetite reduction, and food digestion by affecting the hypothalamus directly, for instance, Askarpour et al. found that L-carnitine could decrease body weight and BMI because the end product of beta-oxidation, acetyl coenzyme A, can be increased by L-carnitine, which can affect the supply of glucose to brain, thereby regulating energy expenditure and suppressing appetite and could effect on body weight; this different result may be due to that they consider weight as a secondary outcome variable in their study.,,
| Conclusion|| |
This systematic review concluded that the intake of L-carnitine had no significant effect on the lipid profile composition, glycemic control, and anthropometric indices in individuals with diabetes. However, it identified a significant enhancement in some oxidative stress indicators. It seems that the use of L-carnitine may not significantly affect metabolic status in individuals with diabetes. However, as only the intermediate parameters were evaluated in the papers reviewed in this study, further research is needed to recommend the use of L-carnitine in individuals with diabetes.
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Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2]