Journal article

GIP receptor deletion in mice confers resistance to high-fat diet-induced obesity via alterations in energy expenditure and adipose tissue lipid metabolism

Geke Aline Boer, Stacey N Keenan, Paula M Miotto, Jens Juul Holst, Matthew J Watt

AJP Endocrinology and Metabolism | AMER PHYSIOLOGICAL SOC | Published : 2021


Glucose-dependent insulinotropic polypeptide (GIP) is best known as an incretin hormone that is secreted from K-cells of the proximal intestine, but evidence also implicates a role for GIP in regulating lipid metabolism and adiposity. It is well-established that GIP receptor knockout (GIPR KO) mice are resistant to diet-induced obesity; however, the factors mediating this effect remain unresolved. Accordingly, we aimed to elucidate the mechanisms leading to adiposity resistance in GIPR KO mice with a focus on whole-body energy balance and lipid metabolism in adipose tissues. Studies were conducted in age-matched male GIPR KO and wild-type (WT) mice fed a high-fat diet for 10 weeks. GIPR KO m..

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Awarded by National Health and Medical Research Council of Australia (NHMRC)

Awarded by Augustinus Fonden

Awarded by NovoNordisk Foundation

Awarded by European Research Council Advanced Grant

Funding Acknowledgements

This work was supported by infrastructure and technical assistance from the Melbourne Mouse Metabolic Phenotyping Platform (MMMPP) at the University of Melbourne. This work was supported by National Health and Medical Research Council of Australia (NHMRC) Grant APP1156508, Augustinus Fonden (19-2021), NovoNordisk Foundation Grant NNF15OC0016574, and European Research Council Advanced Grant 695069. P.M.M. was supported by a Canadian NSERC Post-doctoral Fellowship.