L-Arginine improves multiple physiological parameters in mice exposed to diet-induced metabolic disturbances
Abstract
L-Arginine (L-Arg) is a conditionally essential amino acid and a natural constituent of dietary proteins. Studies in obese rats and type 2 diabetic humans have indicated that dietary supplementation with L-Arg can diminish gain in white adipose tissue (WAT) and improve insulin sensitivity. However, the effects of L-Arg on glucose homeostasis, body composition and energy metabolism remain unclear. In addition, no studies have, to our knowledge, examined whether L-Arg has beneficial effects as a dietary supplement in the mouse model. In the present study, we investigated the effects of L-Arg supplementation to male C57BL/6 mice on an array of physiological parameters. L-Arg supplemented mice were maintained on a low-protein diet and body composition, appetite regulation, glucose tolerance, insulin sensitivity and energy expenditure were evaluated. A significant reduction in epididymal WAT was observed in L-Arg supplemented mice compared with mice fed an isocaloric control diet. Surprisingly, the L-Arg supplemented animals were hyperphagic corresponding to a highly significant decrease in feed efficiency, as body weight developed in a similar pattern in both experimental groups. Glucose homeostasis experiments revealed a major effect of L-Arg supplementation on glucose tolerance and insulin sensitivity, interestingly, independent of a parallel regulation in whole-body adiposity. Increased L-Arg ingestion also raised energy expenditure; however, no concurrent effect on locomotor activity, substrate metabolism or expression of uncoupling proteins (UCP1 and UCP2) in adipose tissues was displayed. In conclusion, dietary L-Arg supplementation substantially affects an array of metabolic-associated parameters including a reduction in WAT, hyperphagia, improved insulin sensitivity and increased energy expenditure in mice fed a low-protein diet.
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L-arginine feeding reduces white adipose tissue mass, improves insulin sensitivity, and increases energy expenditure in mice despite promoting hyperphagia.
“Despite promoting hyperphagia, L-arginine feeding reduced white adipose tissue mass, improved insulin sensitivity, and increased energy expenditure in mice [278].”
From Regulation of obesity and insulin resistance by nitric oxide (2014) · cites this paper as [278]
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- Authors
- Clemmensen, C., Madsen, A. N., Smajilovic, S., Holst, B., & Bräuner-Osborne, H.
- Affiliations
- University of Copenhagen (DK)
- Venue
- Amino Acids
- Published
- 2011-12-27
- Volume
- 43
- Issue
- 3
- Pages
- 1265-1275
- ISSN
- 0939-4451 (ISSN-L)
- 1438-2199
- OpenAlex
- W2012999911
- Cited by
- 49
- References
- 50
- Citations by year
- 2026: 2 · 2024: 1 · 2023: 2 · 2022: 3 · 2021: 1 · 2020: 1 · 2019: 1 · 2018: 1 · 2017: 9 · 2016: 6 · 2015: 4 · 2014: 8 · 2013: 8 · 2012: 2
- FWCI
- 4.71
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Amino Acids (publishedVersion)
- PubMed (publishedVersion)
- Research at the University of Copenhagen (University of Copenhagen) (submittedVersion)
- Funders
- Ministerio de Ciencia e Innovación
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diet, Metabolism, and Disease
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- L-arginine, dietary supplementation, low-protein diet, white adipose tissue, glucose tolerance, insulin sensitivity, energy expenditure, hyperphagia, body composition, obesity, type 2 diabetes, uncoupling proteins, C57BL/6 mice
- MeSH terms
- Animals, Arginine, Blood Glucose, Energy Intake, Energy Metabolism, Glucose, Homeostasis, Hyperphagia, Hypoglycemic Agents, Insulin, Insulin Resistance, Male, Mice, Inbred C57BL, Mitochondria, Motor Activity, Oxygen Consumption, Gene Expression, Diet, Protein-Restricted, Dietary Supplements, Adiposity, Genes, Mitochondrial, Mice, Adipose Tissue, White
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