GIP receptor deletion in mice confers resistance to high-fat diet-induced obesity via alterations in energy expenditure and adipose tissue lipid metabolism
Abstract
GIPR KO mice fed a high-fat diet have reduced adiposity despite transporting more ingested lipids into adipose tissue. This can be partly explained by accelerated adipose tissue lipolysis and increased energy expenditure in GIPR KO mice. These new insights rationalize targeting the GIPR as part of a weight management strategy in obesity.
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GIP administration promotes preadipocyte differentiation and fat storage, and, in the brain, inflammation and insulin resistance.
“GIP administration promotes preadipocyte differentiation and fat storage, and, in the brain, inflammation and insulin resistance.”
From The carbohydrate-insulin model: A physiological perspective on the obesity pandemic (2021) · cites this paper as [78]
GIP receptor knockout mice are protected against diet-induced obesity.
“GIP receptor knockout mice are protected against diet-induced obesity (36, 75–78).”
From The carbohydrate-insulin model: A physiological perspective on the obesity pandemic (2021) · cites this paper as [78]
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References 43 · Cited by 38
- Authors
- Boer, G. A., Keenan, S. N., Miotto, P. M., Holst, J. J., & Watt, M. J.
- Affiliations
- University of Copenhagen (DK)
- The University of Melbourne (AU)
- Corresponding author
- Watt, Matthew J.
- Venue
- American Journal of Physiology-Endocrinology and Metabolism
- Publisher
- American Physiological Society
- Published
- 2021-04-01
- Volume
- 320
- Issue
- 4
- Pages
- E835-E845
- ISSN
- 0193-1849 (ISSN-L)
- 1522-1555
- OpenAlex
- W3135377013
- Cited by
- 38
- References
- 43
- Citations by year
- 2026: 6 · 2025: 6 · 2024: 9 · 2023: 7 · 2022: 8 · 2021: 2
- FWCI
- 3.41
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- American Journal of Physiology-Endocrinology and Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Research at the University of Copenhagen (University of Copenhagen) (submittedVersion)
- Funders
- Augustinus Fonden (19-2021)
- Canadian Network for Research and Innovation in Machining Technology, Natural Sciences and Engineering Research Council of Canada (Post-doctoral fellowship)
- Department of Health, Australian Government | National Health and Medical Research Council (APP1156508)
- EC | European Research Council (695069)
- Novo Nordisk Fonden (NNF15OC0016574)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Keywords
- GLP-1 receptor, high-fat diet-induced obesity, energy expenditure, adipose tissue lipolysis, adipose tissue lipid metabolism, lipid transport, obesity resistance, weight management
- MeSH terms
- Adipose Tissue, Animals, Energy Metabolism, Lipolysis, Male, Mice, Inbred C57BL, Obesity, Receptors, Gastrointestinal Hormone, Gene Deletion, Mice, Knockout, Adiposity, Lipid Metabolism, Mice, Diet, High-Fat
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