NAG-1/GDF-15 prevents obesity by increasing thermogenesis, lipolysis and oxidative metabolism
Open accessAbstract
Objective Obesity is a major health problem associated with high morbidity and mortality. NSAID-activated gene (NAG-1) is a TGF-β superfamily member reported to alter adipose tissue levels in mice. We investigated whether hNAG-1 acts as a regulator of adiposity and energy metabolism.Design/subjects hNAG-1 mice, ubiquitously expressing hNAG-1, were placed on a control or high-fat diet for 12 weeks. hNAG-1-expressing B16/F10 melanoma cells were used in a xenograft model to deliver hNAG-1 to obese C57BL/6 mice.Results As compared with wild-type littermates, transgenic hNAG-1 mice have less white fat and brown fat despite equivalent food intake, improved glucose tolerance, lower insulin levels and are resistant to dietary- and genetic-induced obesity. hNAG-1 mice are more metabolically active with higher energy expenditure. Obese C57BL/6 mice treated with hNAG-1-expressing xenografts show decreases in adipose tissue and serum insulin levels. hNAG-1 mice and obese mice treated with hNAG-1-expressing xenografts show increased thermogenic gene expression (UCP1, PGC1α, ECH1, Cox8b, Dio2, Cyc1, PGC1β, PPARα, Elvol3) in brown adipose tissue (BAT) and increased expression of lipolytic genes (Adrb3, ATGL, HSL) in both white adipose tissue (WAT) and BAT, consistent with higher energy metabolism.Conclusion hNAG-1 modulates metabolic activity by increasing the expression of key thermogenic and lipolytic genes in BAT and WAT. hNAG-1 appears to be a novel therapeutic target in preventing and treating obesity and insulin resistance.
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Overexpressing GDF-15 decreases body weight, fat mass and food intake, and improves glucose tolerance in mouse models.
“On the contrary, overexpressing GDF-15 led to decreased body weight, fat mass and food intake, improving the glucose tolerance in mouse models (83, 108–110).”
From GDF-15 as a Weight Watcher for Diabetic and Non-Diabetic People Treated With Metformin (2020) · cites this paper as [83]
Expression of human GDF15 improves glucose tolerance and insulin sensitivity, lowers body weight and leptin levels, and increases oxidative metabolism and energy expenditure in mice.
“The expression of human GDF15 (hGDF15) improved glucose tolerance and insulin sensitivity, lowered body weight and leptin levels, and increased oxidative metabolism and energy expenditure in mice [207,208] (Figure 2).”
From Hepatokines and metabolism: Deciphering communication from the liver (2021) · cites this paper as [208]
Two studies found GDF15 transgenic mice were protected against obesity and had increased insulin sensitivity and energy expenditure without changes in food consumption compared to control mice.
“Two studies found that GDF15 transgenic mice were protected against obesity and had increased insulin sensitivity and energy expenditure without any changes in food consumption compared to control mice [207,208].”
From Hepatokines and metabolism: Deciphering communication from the liver (2021) · cites this paper as [208]
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References 53 · Cited by 241
- Authors
- Chrysovergis, K., Wang, X., Kosak, J., Lee, S.-H., Kim, J. S., Foley, J. F., Travlos, G., Singh, S., Baek, S. J., & Eling, T. E.
- Affiliations
- National Institutes of Health (US)
- University of Tennessee at Knoxville (US)
- Corresponding author
- Eling, T E
- Venue
- International Journal of Obesity
- Published
- 2014-02-17
- Volume
- 38
- Issue
- 12
- Pages
- 1555-1564
- ISSN
- 0307-0565 (ISSN-L)
- 1476-5497
- PMC
- PMC4135041
- OpenAlex
- W1963540704
- Cited by
- 241
- References
- 53
- Citations by year
- 2026: 12 · 2025: 20 · 2024: 27 · 2023: 25 · 2022: 29 · 2021: 32 · 2020: 32 · 2019: 20 · 2018: 16 · 2017: 9 · 2016: 8 · 2015: 9 · 2014: 2
- FWCI
- 6.22
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- International Journal of Obesity (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute of Environmental Health Sciences (ZIAES010016, Z01ES010016)
- Topics
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Keywords
- NAG-1, GDF15, obesity, thermogenesis, lipolysis, brown adipose tissue, white adipose tissue, energy metabolism, insulin resistance, glucose tolerance, high-fat diet, TGF-beta superfamily, PGC-1α, UCP1, adipose tissue, transgenic mice
- MeSH terms
- Adipose Tissue, Animals, Eating, Energy Metabolism, Enzyme-Linked Immunosorbent Assay, Humans, Insulin Resistance, Lipolysis, Mice, Inbred C57BL, Mice, Obese, Obesity, Blotting, Western, Oxidative Stress, Thermogenesis, Mice, Growth Differentiation Factor 15, Diet, High-Fat, Real-Time Polymerase Chain Reaction
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