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Health Industry Is Lying To You About BerberineL-carnitine and blood sugar control -
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Zhang Z, Zhao M, Wang J, Ding Y, Dai X, Li Y. This effect is mediated by increased glucose storage and oxidative glucose consumption, which might be associated with improved lipid metabolism resulting from carnitine activity. Remuzzi and colleagues enrolled in their study 32 individuals at high risk of decreased insulin sensitivity.
In these participants, moreover, blood glucose concentration at 60 and 90 min following a standard glucose oral load decreased significantly. Furthermore, the researchers observed in all 32 participants 17 of whom had hypertension a significant decrease in systolic blood pressure.
By contrast, diastolic blood pressure decreased significantly only in patients in the high GDR group. The researchers say that these data might be the first evidence of an antihypertensive effect of acetyl- l -carnitine in humans. You can also search for this author in PubMed Google Scholar.
Reprints and permissions. Lucchese, B. Acetyl- l -carnitine therapy increases insulin sensitivity in individuals at high cardiovascular risk.
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Thank you for visiting nature. You are using a browser version with limited support for CSS. To obtain L-carniine best sugag, we abd you use a more bloos L-carnitine and blood sugar control date Best weight loss pills or turn off compatibility Improve your metabolism naturally in Internet Explorer. Diabetes prevention strategies the meantime, to ensure continued support, we are displaying the site without styles and JavaScript. Type 2 diabetes is a highly prevalent chronic metabolic disorder characterized by hyperglycemia and associated with several complications such as retinopathy, hyperlipidemia and polyneuropathy. The dysregulated fatty acid metabolism along with tissue lipid accumulation is generally assumed to be associated in the development of insulin resistance and T2D. Moreover, several studies suggest a central role for oxidative stress in the pathogenesis of the disease.
L-carnitine and blood sugar control -
The minimum sample size was calculated as 30 samples in each group totally 60 cases based on anthropometric index adiposity. Exclusion criteria were liver disease, kidney cancer, pregnancy, lactation, menopause, insulin injections and use of any nutritional supplements as well as any other medications which affect balance of lipids as vitamin C or B6.
The recommended amounts for using L-carnitine supplementation is 1 to 3 grams per day orally in divided doses Intervention period was 8 weeks. Case group received L-carnitine supplement 2 grams twice daily in the morning and evening with a low calorie diet.
Control group received placebo with a low-calorie diet. Low calorie diet was defined as a regimen with kcal lower than the patients required energy required energy is calculated by the formula proposed by the food and nutrition board FNB. Dietary as daily intake units were instructed to the cases, and also a 7-day dietary were provided for them.
From each of the subjects, 5 mL of venous blood samples was taken after 10 - 12 hours fasting before and after the intervention. After separation of plasma by centrifugation for ten minutes in g, samples were analyzed to measure fasting blood glucose, lipid profile and insulin resistance.
Collected samples from the patients were evaluated by Pars Azmun kits lot: and Abbott autoanalyzer model Alcyon , made in France. LDL-C levels were calculated by Equation 1 Insulin resistance was defined as the HOMA-IR index more than 3. The protocol of this study was approved by the ethics committee of Tabriz University of Medical Sciences and registered in Clinical Trial Registration System at www.
ir under the number IRCTN1. Obtained data are expressed as mean ± standard deviation, frequency and percentage. Quantitative variables were compared by Student t-test. The demographic variables measured in the case and control groups to determine the compliance rate of participation were presented in Table 1.
Anthropometric indices and body fat of all 60 cases were presented in Table 2. a Data are presented as Mean ± SD. b Abbreviation: BMI, body mass index. b Between groups analysis. e Abbreviations: BF, body fat; BMI, body mass index; HC, hip circumference; WC, waist circumference; WHR, waist-hip ratio.
The results of the experiments performed in the two groups before and after the intervention were presented in Table 3. As indicated in Table 2 , patients in both the case and control groups had no significant difference before the intervention regarding weight, BMI, waist circumference, hip circumference, waist-hip ratio, and body fat.
After the intervention reduction was seen in mentioned variables compared to their initial values in the both groups, but this reduction was statistically significant in the case group in weight, waist circumference, hip circumference, and body fat. b P value between groups analysis. c Abbreviations: FBS, fasting blood sugar; HDL-C, high-density lipoprotein-cholesterol; HOMA-IR, homeostasis model assessment for insulin resistance; LDL-C, low-density lipoprotein-cholesterol; TG, triglyceride.
d P value within groups analysis. It has been recognized that obesity is a disorder of energy balance, occurring when energy consumption and daily energy intake are not adequate.
L-carnitine and its esters have been proposed as a treatment for many conditions such as heart failure, angina and weight loss due to their roles in reducing oxidative stress 25 and plasma inflammatory markers 26 that is consistent with our result.
In our study, we observed a weight loss in both case and control groups, but this reduction was statistically significant in case group that received L-carnitine supplement compared to controls. It has been reported that L-carnitine has a useful effect on several diabetic risk parameters, including plasma lipids and lipoprotein This conversion could decrease triglycerides synthesis, and increase mitochondrial b-oxidation of fatty acids.
Studies that support this opinion indicated that L-carnitine decreases serum cholesterol, triglycerides, and free fatty acids 28 , the current study also observed a significant decrease in LDL-C, cholesterol and triglycerides in patients who received L-carnitine supplementation compared to the control group.
Our results are consistent with those of Gonzalez-Ortiz et al. Reduction of serum hypertriglyceridemia in diabetic patients who consumed L-carnitine resulted in decrease of triglycerides synthesis in the liver or inhibition of triglyceride release from the liver.
Moreover, L-carnitine induced significant reduction in total serum cholesterol in skeletal muscles of obese patients These results are consistent with our results, we observed a significant reduction in both case and control groups, but the reduction was stronger and clinically valuable in the case group, which shows the role of L-carnitine supplementation in this regard.
Increased fat mobilization from adipose tissue and insulin resistance to the antilipolytic actions cause diminished muscular uptake of glucose and lead to hyperlipidemia. Disordered insulin action is related to an oversupply of lipids.
Lipids increased availability causes elevated lipid stored in insulin target tissues e. muscle, liver adipose or increased plasma triglyceride Gonzalez-Ortiz et al.
in their study concluded that L-carnitine oral administration did not modify insulin sensitivity or the lipid profile. They administrated L-carnitine for a period of 4 weeks However, in our study, oral administration of L-carnitine with low calorie diet for a period of 8 weeks modified lipid profile, and also reduced insulin resistance.
In the current study, the weight loss due to oral administration of L-carnitine is associated with hypoglycemia because of elevated insulin sensitivity, thus decreasing insulin resistance in obese patients is due to regulating the cell energy metabolism or reducing free fatty acids.
These results are in agreement with those of Gonzalez-Ortiz et al. In addition, enhanced secretion of insulin from the beta-cells of the pancreatic islets or among an extra pancreatic mechanism is probably mediating hypoglycemia induced by L-carnitine.
Moreover, the inflammatory effect of cytokine release during diabetes is one of the causative agents for the insulin resistance; L-carnitine may reduce this effect of cytokines Based on the results of different studies, intestinal L-carnitine absorption is saturated within two grams, so the oral administration of L-carnitine more than 2 grams per meal, is not beneficial and not recommended.
It seems that L-carnitine supplementation before each meal has a good effect in its absorption Receiving 15 grams of L-carnitine orally per day has no side effects in healthy persons OSL, observed safe level.
The National Institutes of Health NIH has noted that L-carnitine supplementation is well tolerated by most individuals in the intervention up to six months. However, there is the possibility of side effects such as gastrointestinal disorders including nausea, vomiting, stomachache, mild diarrhea, and also in a small number of cases who received this supplement, changes in body odor as fishy smell or euphoric mode was reported 35 , Due to the effect of L-carnitine supplementation a dose of mg twice daily with low-calorie diet on reducing fasting blood glucose, triglycerides, cholesterol and LDL-C levels, and insulin resistance HOMA-IR , prescribing this supplement in obese diabetic patients is recommended.
Last but not least, there are some limitations to the study including lack of possibility to examine other indicators of oxidative stress and antioxidant system components such as oxidized LDL-C, MDA, enzymatic activity of SOD and GPx, lack of patient cooperation for long-term follow-up like 6 months, one year and financial constraints in the evaluation of various serum inflammatory markers such as IL and TNF-α.
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The present scientific contribution is dedicated to the th anniversary of the foundation of the University of Pécs, Hungary. We are grateful to Jon E. Marquette in support of the editorial consultation in the development of this research paper. Department of Medical Genetics, University of Pécs, Medical School, Szigeti 12, Pécs, H, Hungary.
Szentágothai Research Centre, University of Pécs, Ifjúság 20, Pécs, H, Hungary. You can also search for this author in PubMed Google Scholar.
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Reprints and permissions. Role of carnitine and its derivatives in the development and management of type 2 diabetes. Download citation. Received : 31 July Revised : 05 October Accepted : 28 December Published : 07 March Anyone you share the following link with will be able to read this content:.
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International Journal of Diabetes in Developing Countries Skip to main content Thank you for visiting nature. Download PDF. Subjects Diabetes complications Fatty acids Type 2 diabetes. Abstract Type 2 diabetes is a highly prevalent chronic metabolic disorder characterized by hyperglycemia and associated with several complications such as retinopathy, hyperlipidemia and polyneuropathy.
Introduction Type 2 diabetes T2D is a complex heterogeneous group of metabolic conditions. Carnitine homeostasis in humans Carnitine is a vitamin-like water soluble small molecule featuring a number of essential roles in intermediary metabolism.
Carnitine and its derivatives and insulin resistance Diabetes mellitus is one of the most common chronic metabolic diseases with an underlying absolute or relative insulin deficiency.
Impact of L-carnitine supplementation on glucose metabolism The effect of L-carnitine supplementation on glucose metabolism in humans were widely investigated using a variety of methods Table 1.
Table 1 Effect of carnitine supplementation on glycemic and lipid parameters in human studies with and without diabetic subjects Full size table. Table 2 Analytical studies of acylcarnitines in humans with and without T2D Full size table.
Conclusions Several human and animal studies demonstrated in which L-carnitine supplementation has a beneficial effect on whole body glucose utilization, it improves several lipid parameters or oxidative stress markers as well, moreover, low levels of L-carnitine is associated with various diabetic complications.
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Only English publications were included. Inclusion criteria included: I randomized controlled trial RCT , II with Body Mass Index BMI information, III exact dose and duration of l-carnitine, acetyl-l-carnitine, and propionyl-l-carnitine.
Source, country, grouping, sample size, age, duration of treatment et al were extracted from the above-included studies. In order to eliminate the potential baseline effect, the efficacy of l-carnitine, acetyl-l-carnitine, and propionyl-l-carnitine were evaluated using BMI change rate from the baseline value.
The Formula 1 was as follows:. E t , the value of BMI at time t; E b , the value of BMI at baseline. The E max model was used to evaluate the effects of l-carnitine, acetyl-l-carnitine or propionyl-l-carnitine on Body Mass in T2DM patients.
In addition, in order to acquire the actual effects on BMI from l-carnitine, acetyl-l-carnitine, and propionyl-l-carnitine, the control effects need to be subtracted from the sum effects. The Formulas 2 and 3 were as follows:. E I,i,j , the sum effects on BMI from l-carnitine, acetyl-l-carnitine or propionyl-l-carnitine, including actual effects and control effects; E D,i,j , the actual effects on BMI; E C,i,j , the control effects on BMI; i, different studies; j, the time point of every study; E max , the maximal effects on BMI; ET 50 , the treatment duration to reach half of the maximal effects on BMI; ε i,j , the residual error of study i with j time; N i,j , the sample size in study i with time point j.
The inter-study variability was described by exponential error or additive error models. The Formulas 4 — 7 were as follows:. η 1,i , η 2,i were the inter-study variabilities, when available, they would be added into E max , and ET 50 , respectively.
η 1,i , η 2,i were assumed to be normally distributed, with a mean of 0 and variance of ω 1,i 2 , ω 2,i 2 , respectively. In addition, continuous covariates and categorical covariates were evaluated by Formulas 8 — 9 and 10 :. P p , the parameter for a patient with a covariate value of COV; P T , the typical value of the parameter; COV, covariate; COV m , the median value of covariable in the population.
θ c , a correction coefficient of the covariate to the model parameter. The model development was done using non-linear mixed-effect modeling NONMEM, edition 7, ICON Development Solutions, Ellicott City, MD, USA. When a basic model was built, potential covariates were considered for adding into E max.
The change of objective function value OFV was used as the covariate inclusion criteria. The goodness-of-fit plots of the model individual predictions vs. observations , distribution of conditional weighted residuals CWRES for the model density vs. CWRES, and quantiles of CWRES vs.
quantiles of normal , and individual plots from different studies were used to estimate the final model. Prediction-corrected visual predictive check VPC plots were used to assess the predictive performance of the final model. In addition, the medians and 2. The efficacy prediction of l-carnitine on BMI in T2DM patients was simulated by the Monte Carlo method.
Figure 1 was the retrieval process and a total of 10 RCT studies, comprising 1, T2DM patients were included for analysis, including 8 studies of l-carnitine 9 — 16 , 1 study of acetyl-l-carnitine 17 , and 1 study of propionyl-l-carnitine The risk of bias analysis was shown in Figure 2.
As both acetyl-l-carnitine, and propionyl-l-carnitine had only 1 study, model-based meta-analysis MBMA could not be performed at this time for them. Further analysis found that no significant effects on BMI in acetyl-l-carnitine or propionyl-l-carnitine in T2DM patients.
Therefore, the following MBMA analysis was mainly aimed at l-carnitine. In addition, no covariate in particular dosage was incorporated into the E max model, showing there was no significant dose-dependence from l-carnitine efficacy on BMI in T2DM patients in the present study.
The E max model of l-carnitine on BMI in T2DM patients was shown in Formulas 11 :. E, efficacy of l-carnitine on BMI; Time, l-carnitine treatment duration. The visual inspection of routine diagnostic plots, and individual predictions vs.
observations, are shown in Figure 3A. The distribution of CWRES for model density vs. CWRES, and quantilies of CWRES vs. quantiles of normal are shown in Figures 3B,C.
Individual plots from different studies are shown in Figure 3D. As we could see, there were good linear relationships between individual predictions and observations, and individual plots were also consistent meaning the good fitting of the final models. At the same time, the distribution of the model also satisfied the normal distribution.
Figure 3. Model evaluation. A individual predictions vs. observations for the model from the effect of l-carnitine on BMI. B distribution of conditional weighted residuals CWRES for model density vs.
C distribution of CWRES for model quantiles of CWRES vs. quantiles of normal. D individual plots for the model from the effect of l-carnitine on BMI. Figure 4. Visual predictive check of the model from the l-carnitine effect on BMI. Median, 2. We also simulated the curve of the final model for the effect of l-carnitine on BMI via the Monte Carlo method.
The trend of the efficacy of l-carnitine on BMI in T2DM patients is shown in Figure 5. As we could see from the curve, the efficacy of l-carnitine on BMI at 0.
Carnitine is derived from amino acids and is found in almost all cells in the body Its name comes from the Latin carnus , meaning meat, because the compound is extracted from meat Carnitine is a generic term, which includes l-carnitine, acetyl-l-carnitine, and propionyl-l-carnitine L-carnitine plays an important role in energy metabolism It transfers long-chain fatty acids to cell mitochondria for oxidation, which produces energy needed by the body 21 , It also transports harmful substances out of the organelle, preventing them from accumulating in the cell Because of these functions, carnitine is found in high concentrations in skeletal muscle and cardiac muscle cells, which allow them to use fatty acids as an energy source For most people, the body can make enough to meet its needs, but for some people, because of genetic or pharmaceutical reasons, the body cannot produce enough, it is, therefore, an essential nutrient for these individuals As is well-known, l-carnitine can adjust many events, such as metabolism of glucose and fatty acids, and has the potential to protect these cellular events in several manners including decreasing the production of reactive oxygen species at different points and maintaining mitochondrial functions In addition, it has been reported that l-carnitine had many important pharmacological actions 24 — 31 , for example, l-carnitine has a potential therapeutic effect in treating insulin resistance It is also reported that l-carnitine can improve glycemia in T2DM patients Wang et al.
The purpose of this study is to explore the effects of l-carnitine, acetyl-l-carnitine, and propionyl-l-carnitine on Body Mass in T2DM patients by MBMA.
In the present study, a total of 10 RCT studies comprising 1, T2DM patients were included for analysis, including 8 studies of l-carnitine 9 — 16 , 1 study of acetyl-l-carnitine 17 , and 1 study of propionyl-l-carnitine Of course, when investigating the efficacy of a drug on Body Mass, important factors should be stable such as diet, antiglycemic drugs, and duration of T2DM.
Fortunately, since our study was from RCTs, conditions in the intervention group and the control group were similar in each study. In this way, the control group effects were deducted from the intervention group, and the actual l-carnitine drug effects were obtained. In addition, we also considered the impact of various indicators in different studies on baseline values.
In addition, as for both acetyl-l-carnitine, and propionyl-l-carnitine had only 1 study, MBMA analysis could not be performed at this time for them. Further analysis found no significant effects on BMI in acetyl-l-carnitine or propionyl-l-carnitine in T2DM patients.
In addition, no covariate in particular dosage was incorporated into the E max model, showing there was no significant dose-dependence from l-carnitine efficacy on BMI in T2DM patients.
From the current view, l-carnitine could play an important role in glucose metabolism and increase energy expenditure, meanwhile, l-carnitine had a role in lipid metabolism as well 34 — For these two reasons, l-carnitine helps Body Mass loss by increasing energy expenditure However, this study had some limitations.
The number of studies currently included was limited, and additional studies were needed in the future.
However, there was Improve your metabolism naturally significant effect seen on L-carnitone blood sugar FBSsuga TGand high-density lipoprotein-cholesterol HDLc Improve your metabolism naturally comparing the intervention and placebo groups. Contrll is a suggar amino acid Team sports nutrition tips in meat, fish, milk, and dairy products. L-carnitine and blood sugar control plays a role in lipid metabolism by transporting long-chain fatty acids into the mitochondria and is a popular supplement for weight loss and fat burning. Said to be the first meta-analysis to investigate the effect of L-carnitine supplementation on the biomarkers of metabolic syndromes, the analysis examined nine RCTs that were published before February this year. The researchers searched for the RCTs from a number of databases, including PubMed, EMBASE, Cochrane, and CINAHL. An RCT was included in the analysis if it examined at least one of the biomarkers, including waist circumference, blood pressure, FBS, TG, or HDLc.
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