A Combination of Nutriments Improves Mitochondrial Biogenesis and Function in Skeletal Muscle of Type 2 Diabetic Goto–Kakizaki Rats
Open accessAbstract
BACKGROUND: Recent evidence indicates that insulin resistance in skeletal muscle may be related to reduce mitochondrial number and oxidation capacity. However, it is not known whether increasing mitochondrial number and function improves insulin resistance. In the present study, we investigated the effects of a combination of nutrients on insulin resistance and mitochondrial biogenesis/function in skeletal muscle of type 2 diabetic Goto-Kakizaki rats. METHODOLOGY/PRINCIPAL FINDINGS: We demonstrated that defect of glucose and lipid metabolism is associated with low mitochondrial content and reduced mitochondrial enzyme activity in skeletal muscle of the diabetic Goto-Kakizaki rats. The treatment of combination of R-alpha-lipoic acid, acetyl-L-carnitine, nicotinamide, and biotin effectively improved glucose tolerance, decreased the basal insulin secretion and the level of circulating free fatty acid (FFA), and prevented the reduction of mitochondrial biogenesis in skeletal muscle. The nutrients treatment also significantly increased mRNA levels of genes involved in lipid metabolism, including peroxisome proliferator-activated receptor-alpha (Ppar alpha), peroxisome proliferator-activated receptor-delta (Ppar delta), and carnitine palmitoyl transferase-1 (Mcpt-1) and activity of mitochondrial complex I and II in skeletal muscle. All of these effects of mitochondrial nutrients are comparable to that of the antidiabetic drug, pioglitazone. In addition, the treatment with nutrients, unlike pioglitazone, did not cause body weight gain. CONCLUSIONS/SIGNIFICANCE: These data suggest that a combination of mitochondrial targeting nutrients may improve skeletal mitochondrial dysfunction and exert hypoglycemic effects, without causing weight gain.
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Oral administration of CoQ10 improves mitochondrial biogenesis and function in skeletal muscle of Goto-Kakizaki rats.
“Oral administration of coenzyme Q10 (CoQ10), a vitamin-like substance, improves mitochondrial biogenesis and function in skeletal muscle of Goto–Kakizaki rats [66].”
From Nutraceuticals in the Prevention and Treatment of the Muscle Atrophy (2021) · cites this paper as [66]
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References 62 · Cited by 63
Research works printed but not linked: 1
- [18]Ames BN Suh JH Liu J 2006 Enzymes lose binding affinity for coenzymes and substrates with age: A strategy for remediation. Kaput J Nutrigenomics: Concerpts and Technologies Hoboken, NJ John Wiley and Sons, Inc 277 291
- Authors
- Shen, W., Hao, J., Tian, C., Ren, J., Yang, L., Li, X., Luo, C., Cotma, C. W., & Liu, J.
- Affiliations
- Chinese Academy of Sciences (CN)
- University of California, Irvine (US)
- Corresponding author
- Liu, Jiankang
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2008-06-04
- Volume
- 3
- Issue
- 6
- Pages
- e2328
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC2391295
- OpenAlex
- W1982021390
- Cited by
- 63
- References
- 62
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 1 · 2023: 1 · 2022: 1 · 2021: 4 · 2020: 3 · 2018: 1 · 2017: 2 · 2016: 2 · 2015: 5 · 2014: 7 · 2013: 6 · 2012: 8
- FWCI
- 2.74
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- PLoS ONE (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- eScholarship (California Digital Library) (submittedVersion, cc-by)
- Funders
- Chinese Academy of Sciences
- Science and Technology Commission of Shanghai Municipality (04DZ14007)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Keywords
- mitochondrial biogenesis, skeletal muscle, type 2 diabetes, insulin resistance, Goto-Kakizaki rats, R-alpha-lipoic acid, acetyl-L-carnitine, nicotinamide, biotin, mitochondrial dysfunction, glucose tolerance, lipid metabolism, PPARα, PPARδ, carnitine palmitoyltransferase 1, pioglitazone, weight gain
- MeSH terms
- Animals, Diabetes Mellitus, Experimental, Diabetes Mellitus, Type 2, DNA, Mitochondrial, Fatty Acids, Nonesterified, Glucose Tolerance Test, Mitochondria, Muscle, Muscle Proteins, Rats, Mutant Strains, Muscle, Skeletal, Dietary Supplements, Rats
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