Journal article

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

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

AJP Endocrinology and Metabolism | 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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University of Melbourne Researchers


Awarded by Department of Health, Australian Government | National Health and Medical Research Council (NHMRC)

Awarded by Augustinus Fonden (Augustinus Foundation)

Awarded by Novo Nordisk Fonden (NNF)

Awarded by EC | European Research Council (ERC)

Awarded by Canadian Network for Research and Innovation in Machining Technology, Natural Sciences and Engineering Research Council of Canada (NSERC Canadian Network for Research and Innovation in Machining Technology)