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Beneficial effects of l-arginine on reducing obesity: potential mechanisms and important implications for human health
Abstract
Over the past 20 years, growing interest in the biochemistry, nutrition, and pharmacology of L-arginine has led to extensive studies to explore its nutritional and therapeutic roles in treating and preventing human metabolic disorders. Emerging evidence shows that dietary L-arginine supplementation reduces adiposity in genetically obese rats, diet-induced obese rats, finishing pigs, and obese human subjects with Type-2 diabetes mellitus. The mechanisms responsible for the beneficial effects of L-arginine are likely complex, but ultimately involve altering the balance of energy intake and expenditure in favor of fat loss or reduced growth of white adipose tissue. Recent studies indicate that L-arginine supplementation stimulates mitochondrial biogenesis and brown adipose tissue development possibly through the enhanced synthesis of cell-signaling molecules (e.g., nitric oxide, carbon monoxide, polyamines, cGMP, and cAMP) as well as the increased expression of genes that promote whole-body oxidation of energy substrates (e.g., glucose and fatty acids) Thus, L-arginine holds great promise as a safe and cost-effective nutrient to reduce adiposity, increase muscle mass, and improve the metabolic profile in animals and humans.
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Collective data suggest L-arginine, and by inference NO, has the capacity to reduce fat mass by increasing mitochondrial biogenesis, regulating brown adipose tissue signaling, and increasing expression of genes that promote oxidation of energy substrates.
“Overall, the collective data suggest that L-arginine, and by inference, NO, has the capacity to reduce fat mass by increasing mitochondrial biogenesis, regulating brown adipose tissue signaling, and increasing the expression of genes that promote oxidation of energy substrates [282].”
From Regulation of obesity and insulin resistance by nitric oxide (2014) · cites this paper as [282]
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Metadata
- Authors
- McKnight, J. R., Satterfield, M. C., Jobgen, W. S., Smith, S. B., Spencer, T. E., Meininger, C. J., McNeal, C. J., & Wu, G.
- Affiliations
- Texas A&M University (US)
- Texas A&M Health Science Center (US)
- Baylor Scott & White Medical Center - Temple (US)
- Corresponding author
- Wu, Guoyao
- ORCID
- Venue
- Amino Acids
- Published
- 2010-05-01
- Volume
- 39
- Issue
- 2
- Pages
- 349-357
- ISSN
- 0939-4451 (ISSN-L)
- 1438-2199
- OpenAlex
- W2057765693
- Cited by
- 376
- References
- 72
- Citations by year
- 2026: 6 · 2025: 6 · 2024: 10 · 2023: 13 · 2022: 24 · 2021: 18 · 2020: 19 · 2019: 9 · 2018: 13 · 2017: 14 · 2016: 27 · 2015: 43 · 2014: 39 · 2013: 38 · 2012: 32
- FWCI
- 3.83
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Amino Acids (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Heart, Lung, and Blood Institute (R21 HL094689)
- Topics
- Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
- Health Sciences › Nursing › Nutrition and Dietetics › Muscle metabolism and nutrition
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- L-arginine, obesity, dietary supplementation, type 2 diabetes, energy expenditure, white adipose tissue, brown adipose tissue, mitochondrial biogenesis, nitric oxide, polyamines, cyclic GMP, cyclic AMP, muscle mass, metabolic disorders
- MeSH terms
- Animals, Arginine, Adipose Tissue, Brown, Gene Expression Regulation, Humans, Nitric Oxide, Obesity, Signal Transduction, Adipocytes, Muscle, Skeletal, Dietary Supplements, Adiposity, Lipid Metabolism, Adipose Tissue, White
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