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In vivo effects of dietary quercetin and quercetin-rich red onion extract on skeletal muscle mitochondria, metabolism, and insulin sensitivity
Open accessAbstract
Red onions and low doses of the flavonoid, quercetin, increase insulin sensitivity and improve glucose tolerance. We hypothesized that dietary supplementation with red onion extract (RO) would attenuate high fat diet (HFD)-induced obesity and insulin resistance similar to quercetin supplementation by increasing energy expenditure through a mechanism involving skeletal muscle mitochondrial adaptations. To test this hypothesis, C57BL/6J mice were randomized into four groups and fed either a low fat diet (LF), HFD (HF), HFD + quercetin (HF + Q), or HFD + RO (HF + RO) for 9 weeks. Food consumption and body weight and composition were measured weekly. Insulin sensitivity was assessed by insulin and glucose tolerance tests. Energy expenditure and physical activity were measured by indirect calorimetry. Skeletal muscle incomplete beta oxidation, mitochondrial number, and mtDNA-encoded gene expression were measured. Quercetin and RO supplementation decreased HFD-induced fat mass accumulation and insulin resistance (measured by insulin tolerance test) and increased energy expenditure; however, only HF + Q showed an increase in physical activity levels. Although quercetin and RO similarly increased skeletal muscle mitochondrial number and decreased incomplete beta oxidation, establishing mitochondrial function similar to that seen in LF, only HF + Q exhibited consistently lower mRNA levels of mtDNA-encoded genes necessary for complexes IV and V compared to LF. Quercetin- and RO-induced improvements in adiposity, insulin resistance, and energy expenditure occur through differential mechanisms, with quercetin-but not RO-induced energy expenditure being related to increases in physical activity. While both treatments improved skeletal muscle mitochondrial number and function, mtDNA-encoded transcript levels suggest that the antiobesogenic, insulin-sensitizing effects of purified quercetin aglycone, and RO may occur through differential mechanisms.
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“In this study, 17 mg/kg of quercetin aglycone treatment for nine weeks increased skeletal muscle mitochondria number and decreases incomplete β-oxidation, establishing mitochondrial function comparable to that of lean counterparts [98].”
From Mitochondrial Adaptation in Skeletal Muscle: Impact of Obesity, Caloric Restriction, and Dietary Compounds (2024) · cites this paper as [98]
Experimental — accuracy not yet measuredIn the citing paper
“Similarly, dietary quercetin supplementation was reported to decrease high-fat diet-induced fat accumulation and insulin resistance [98].”
From Mitochondrial Adaptation in Skeletal Muscle: Impact of Obesity, Caloric Restriction, and Dietary Compounds (2024) · cites this paper as [98]
In the citing paper
“Similarly, dietary quercetin supplementation was reported to decrease high-fat diet-induced fat accumulation and insulin resistance [98].”
From Mitochondrial Adaptation in Skeletal Muscle: Impact of Obesity, Caloric Restriction, and Dietary Compounds (2024) · cites this paper as [98]
In the citing paper
“In this study, 17 mg/kg of quercetin aglycone treatment for nine weeks increased skeletal muscle mitochondria number and decreases incomplete β-oxidation, establishing mitochondrial function comparable to that of lean counterparts [98].”
From Mitochondrial Adaptation in Skeletal Muscle: Impact of Obesity, Caloric Restriction, and Dietary Compounds (2024) · cites this paper as [98]
In the citing paper
“In this study, 17 mg/kg of quercetin aglycone treatment for nine weeks increased skeletal muscle mitochondria number and decreases incomplete β-oxidation, establishing mitochondrial function comparable to that of lean counterparts [98].”
From Mitochondrial Adaptation in Skeletal Muscle: Impact of Obesity, Caloric Restriction, and Dietary Compounds (2024) · cites this paper as [98]
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Metadata
- Authors
- Henagan, T. M., Cefalu, W. T., Ribnicky, D. M., Noland, R. C., Dunville, K., Campbell, W. W., Stewart, L. K., Forney, L. A., Gettys, T. W., Chang, J. S., & Morrison, C. D.
- Affiliations
- Purdue University West Lafayette (US)
- Pennington Biomedical Research Center (US)
- Rutgers, The State University of New Jersey (US)
- University of Northern Colorado (US)
- ORCID
- Venue
- Genes & Nutrition
- Published
- 2014-12-27
- Volume
- 10
- Issue
- 1
- Pages
- 451-451
- ISSN
- 1555-8932 (ISSN-L)
- 1865-3499
- PMC
- PMC4277553
- OpenAlex
- W2023989068
- Cited by
- 102
- References
- 34
- Citations by year
- 2026: 4 · 2025: 3 · 2024: 11 · 2023: 10 · 2022: 7 · 2021: 11 · 2020: 13 · 2019: 9 · 2018: 10 · 2017: 11 · 2016: 8 · 2015: 5
- FWCI
- 5.32
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Genes & Nutrition (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (DK072476)
- National Institute of General Medical Sciences (P20GM103528, P30GM118430)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK072476, DK064584, 8P20-GM103528-07, R01DK096311, 5T32-DK064584-09, T32DK064584, P30DK072476)
- National Center for Complementary and Alternative Medicine
- National Center for Research Resources (P20RR021945)
- National Center for Complementary and Integrative Health (P50AT002776)
- Topics
- Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Natural Antidiabetic Agents Studies
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Keywords
- quercetin, red onion extract, dietary flavonoids, insulin resistance, insulin sensitivity, high-fat diet, obesity, energy expenditure, skeletal muscle mitochondria, mitochondrial biogenesis, physical activity, glucose tolerance, fat mass
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