The DOI matches its Crossref record; 41 of the 41 references it cites were found in a registry or an index.
Carnitine revisited: potential use as adjunctive treatment in diabetes
Open accessAbstract
Aims/hypothesis This study examined the efficacy of supplemental L: -carnitine as an adjunctive diabetes therapy in mouse models of metabolic disease. We hypothesised that carnitine would facilitate fatty acid export from tissues in the form of acyl-carnitines, thereby alleviating lipid-induced insulin resistance.Materials and methods Obese mice with genetic or diet-induced forms of insulin resistance were fed rodent chow +/- 0.5% L: -carnitine for a period of 1-8 weeks. Metabolic outcomes included insulin tolerance tests, indirect calorimetry and mass spectrometry-based profiling of acyl-carnitine esters in tissues and plasma.Results Carnitine supplementation improved insulin-stimulated glucose disposal in genetically diabetic mice and wild-type mice fed a high-fat diet, without altering body weight or food intake. In severely diabetic mice, carnitine supplementation increased average daily respiratory exchange ratio from 0.886 +/- 0.01 to 0.914 +/- 0.01 (p < 0.01), reflecting a marked increase in systemic carbohydrate oxidation. Similarly, under insulin-stimulated conditions, carbohydrate oxidation was higher and total energy expenditure increased from 172 +/- 10 to 210 +/- 9 kJ kg fat-free mass(-1) h(-1) in the carnitine-supplemented compared with control animals. These metabolic improvements corresponded with a 2.3-fold rise in circulating levels of acetyl-carnitine, which accounts for 86 and 88% of the total acyl-carnitine pool in plasma and skeletal muscle, respectively. Carnitine supplementation also increased several medium- and long-chain acyl-carnitine species in both plasma and tissues.Conclusions/interpretation These findings suggest that carnitine supplementation relieves lipid overload and glucose intolerance in obese rodents by enhancing mitochondrial efflux of excess acyl groups from insulin-responsive tissues. Carefully controlled clinical trials should be considered.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“Moreover, recent evidence suggests that lowering of mitochondrial acyl CoAs, resulting in increased PDH activity and improved metabolic flexibility, can be achieved via dietary supplementation with L-carnitine (Noland et al., 2009; Power et al., 2007).”
From Lipid-Induced Mitochondrial Stress and Insulin Action in Muscle (2012) · cites this paper as Power et al., 2007
In the citing paper
“In another recent investigation we found that oral carnitine supplementation improved insulin sensitivity in diabetic mice, in parallel with a marked rise in plasma acylcarnitines (8).”
From Carnitine insufficiency caused by aging and overnutrition compromises mitochondrial performance and metabolic control (2009) · cites this paper as [8]
In the citing paper
“The antidiabetic actions of carnitine were accompanied by an increase in whole body glucose oxidation, a surprising result given that carnitine is best known for its essential role in permitting mitochondrial translocation and oxidation of long chain acyl-CoAs.”
From Carnitine insufficiency caused by aging and overnutrition compromises mitochondrial performance and metabolic control (2009) · cites this paper as [8]
In the citing paper
“Previous work suggested that tissue export of acetylcarnitine lowers local concentrations of acetyl-CoA, which in turn favors increased pyruvate dehydrogenase activity and higher rates of glucose oxidation (8,20).”
From Carnitine insufficiency caused by aging and overnutrition compromises mitochondrial performance and metabolic control (2009) · cites this paper as [8]
In the citing paper
“We previously reported that carnitine supplementation effectively restored insulin responsiveness in multiple mouse models of glucose intolerance (8).”
From Carnitine insufficiency caused by aging and overnutrition compromises mitochondrial performance and metabolic control (2009) · cites this paper as [8]
In the citing paper
“carnitine therapy improved glucose tolerance and insulin responsiveness in rodent models of aging, genetic diabetes and high fat feeding [65,71], while also reversing obesity-related derangements in mitochondrial fuel selection [65].”
From Intramuscular triacylglycerol and insulin resistance: guilty as charged or wrongly accused? (2010) · cites this paper as [71]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
A Flexible System of Enzymatic Analysis
Lowry, O. H., & Passonneau, J. V. (1972) · Elsevier eBooks · doi:10.1016/b978-0-12-457950-7.x5001-3 · Cited by 4,050
Cellular mechanisms of insulin resistance
Shulman, G. I. (2000) · Journal of Clinical Investigation · doi:10.1172/jci10583 · Cited by 2,714
Turnover of Inositol Phospholipids and Signal Transduction
Nishizuka, Y. (1984) · Science · doi:10.1126/science.6147898 · Cited by 1,614
McGarry, J. D. (2002) · Diabetes · doi:10.2337/diabetes.51.1.7 · Cited by 1,435
Kishimoto, A., Takai, Y., Terutoshi, M. O. R. I., Kikkawa, U., & Nishizuka, Y. (1980) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(19)85886-6 · Cited by 1,303
Boden, G., & Shulman, G. I. (2002) · European Journal of Clinical Investigation · doi:10.1046/j.1365-2362.32.s3.3.x · Cited by 1,300
Fuel selection in human skeletal muscle in insulin resistance: a reexamination.
Kelley, D. E., & Mandarino, L. J. (2000) · Diabetes · doi:10.2337/diabetes.49.5.677 · Cited by 1,017
Unger, R. H. (2002) · Annual Review of Medicine · doi:10.1146/annurev.med.53.082901.104057 · Cited by 875
Carnitine biosynthesis in mammals
Vaz, F. M., & Wanders, R. J. A. (2002) · Biochemical Journal · doi:10.1042/0264-6021:3610417 · Cited by 769
Randle, P., Newsholme, E., & Garland, P. (1964) · Biochemical Journal · doi:10.1042/bj0930652 · Cited by 736
Flagged first, then by citations
Cited by
Sorted by citations
Items 101–113 of 113
Role of carnitine transporter in skeletal muscle energy metabolism
Furuichi, Y., & Masuda, K. (2012) · 体力科學 · doi:10.7600/jspfsm.61.289
Metabolsk fleksibilitet i humane skjelettmuskelceller
Fjørkenstad, A. (2008) · NORA - Norwegian Open Research Archives
Role of carnitine in modulation of muscle energy metabolism and insulin resistance
Altamimi, T., & Lopaschuk, G. D. (2014) · CRC Press eBooks · doi:10.1201/b17092-8
The influence of age and nutrients on insulin sensitivity
Chee, C. (2016) · Nottingham ePrints (University of Nottingham)
Диабетическая кардиальная автономная нейропатия: каковы перспективы в лечении?
Сергієнко, В. О., & Serhiyenko, O. (2016) · HYPERTENSION · doi:10.22141/2224-1485.1.45.2016.74137
The role of Toll-like Receptor 4 in the Modulation in Skeletal Muscle Metabolism
Wu, Y. (2011) · VTechWorks (Virginia Tech)
Bruls, Y. M. H. (2018) · Research Publications (Maastricht University) · doi:10.26481/dis.20180614yb
“Free carnitine availability is identified as being crucial in acetylcarnitine formation and maintaining metabolic flexibility (4, 5, 8).”
BackgroundNovel role of carnitine in skeletal muscle revealed using dynamics analysis
Furuichi, Y., Goto‐Inoue, N., & Masuda, K. (2018) · 体力科學 · doi:10.7600/jspfsm.67.261
Current literature in diabetes
(2007) · Diabetes/Metabolism Research and Reviews · doi:10.1002/dmrr.787
Сергієнко, В. О. (2012) · PROBLEMS OF ENDOCRINE PATHOLOGY · doi:10.21856/j-pep.2012.3.17
Flayyih, N. K. (2022) · Journal of Wasit for Science and Medicine · doi:10.31185/jwsm.230
Cai, H., Li, D., Han, X., Han, Y., Zhang, R., Meng, K., & Yang, P. (2026) · PeerJ · doi:10.7717/peerj.21627
“L-carnitine L-carnitine supplementation in obese mice improves glucose tolerance and increases total energy expenditure ( Power et al., 2007 ; Cave et al., 2008 ).”
Mitochondrial adaptations in insulin resistant muscle
Broek, N. N. (2010) · TU/e Research Portal · doi:10.6100/ir684831
Metadata
- Authors
- Power, R. A., Hulver, M. W., Zhang, J. Y., Dubois, J., Marchand, R. M., Ilkayeva, O., Muoio, D. M., & Mynatt, R. L.
- Affiliations
- Pennington Biomedical Research Center (US)
- Virginia Tech (US)
- Duke University (US)
- Corresponding author
- Mynatt, R. L.
- Venue
- Diabetologia
- Published
- 2007-02-20
- Volume
- 50
- Issue
- 4
- Pages
- 824-832
- ISSN
- 0012-186X (ISSN-L)
- 1432-0428
- PMC
- PMC5682624
- OpenAlex
- W2069095858
- Cited by
- 113
- References
- 40
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 1 · 2023: 1 · 2022: 3 · 2021: 5 · 2020: 3 · 2019: 4 · 2018: 6 · 2017: 4 · 2016: 9 · 2015: 5 · 2014: 15 · 2013: 7 · 2012: 11
- FWCI
- 3.84
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Diabetologia (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (DK072476, P30DK072476)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Keywords
- carnitine supplementation, insulin resistance, type 2 diabetes, acylcarnitines, acetyl-L-carnitine, fatty acid export, lipid overload, impaired glucose tolerance, carbohydrate oxidation, energy expenditure, respiratory exchange ratio, skeletal muscle, high-fat diet, obesity, adjunctive therapy
- MeSH terms
- Animals, Calorimetry, Carnitine, Diabetes Mellitus, Experimental, Fatty Acids, Glucose Tolerance Test, Glycerol, Insulin Resistance, Male, Mice, Obese, Mass Spectrometry, Vitamin B Complex, Pyruvate Dehydrogenase (Lipoamide), Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
