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dc.contributor.authorKim, Su-Jin
dc.contributor.authorNian, Cuilan
dc.contributor.authorKarunakaran, Subashini
dc.contributor.authorClee, Susanne M.
dc.contributor.authorIsales, Carlos M.
dc.contributor.authorMcIntosh, Christopher H. S.
dc.date.accessioned2012-10-26T20:30:47Z
dc.date.available2012-10-26T20:30:47Z
dc.date.issued2012-07-3en_US
dc.identifier.citationPLoS One. 2012 Jul 3; 7(7):e40156en_US
dc.identifier.issn1932-6203en_US
dc.identifier.pmid22802954en_US
dc.identifier.doi10.1371/journal.pone.0040156en_US
dc.identifier.urihttp://hdl.handle.net/10675.2/803
dc.description.abstractGlucose-dependent insulinotropic polypeptide (GIP) is a gastrointestinal hormone that potentiates glucose-stimulated insulin secretion during a meal. Since GIP has also been shown to exert b-cell prosurvival and adipocyte lipogenic effects in rodents, both GIP receptor agonists and antagonists have been considered as potential therapeutics in type 2 diabetes (T2DM). In the present study, we tested the hypothesis that chronically elevating GIP levels in a transgenic (Tg) mouse model would increase adipose tissue expansion and exert beneficial effects on glucose homeostasis. In contrast, although GIP Tg mice demonstrated enhanced b-cell function, resulting in improved glucose tolerance and insulin sensitivity, they exhibited reduced diet-induced obesity. Adipose tissue macrophage infiltration and hepatic steatosis were both greatly reduced, and a number of genes involved in lipid metabolism/inflammatory signaling pathways were found to be down-regulated. Reduced adiposity in GIP Tg mice was associated with decreased energy intake, involving overexpression of hypothalamic GIP. Together, these studies suggest that, in the context of over-nutrition, transgenic GIP overexpression has the potential to improve hepatic and adipocyte function as well as glucose homeostasis.
dc.rightsKim et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.en_US
dc.subjectResearch Articleen_US
dc.subjectBiologyen_US
dc.subjectAnatomy and Physiologyen_US
dc.subjectEndocrine Systemen_US
dc.subjectEndocrine Physiologyen_US
dc.subjectInsulinen_US
dc.subjectModel Organismsen_US
dc.subjectAnimal Modelsen_US
dc.subjectMouseen_US
dc.subjectMedicineen_US
dc.subjectEndocrinologyen_US
dc.subjectDiabetic Endocrinologyen_US
dc.subjectDiabetes Mellitus Type 2en_US
dc.subjectEndocrine Physiologyen_US
dc.subjectHormonesen_US
dc.subjectGastroenterology and Hepatologyen_US
dc.subjectMetabolic Disordersen_US
dc.subjectNutritionen_US
dc.subjectObesityen_US
dc.titleGIP-Overexpressing Mice Demonstrate Reduced Diet-Induced Obesity and Steatosis, and Improved Glucose Homeostasisen_US
dc.typeArticleen_US
dc.identifier.pmcidPMC3388996en_US
dc.contributor.corporatenameDepartment of Orthopaedic Surgery
dc.contributor.corporatenameDepartment of Cellular Biology and Anatomy
refterms.dateFOA2019-04-10T00:55:45Z
html.description.abstractGlucose-dependent insulinotropic polypeptide (GIP) is a gastrointestinal hormone that potentiates glucose-stimulated insulin secretion during a meal. Since GIP has also been shown to exert b-cell prosurvival and adipocyte lipogenic effects in rodents, both GIP receptor agonists and antagonists have been considered as potential therapeutics in type 2 diabetes (T2DM). In the present study, we tested the hypothesis that chronically elevating GIP levels in a transgenic (Tg) mouse model would increase adipose tissue expansion and exert beneficial effects on glucose homeostasis. In contrast, although GIP Tg mice demonstrated enhanced b-cell function, resulting in improved glucose tolerance and insulin sensitivity, they exhibited reduced diet-induced obesity. Adipose tissue macrophage infiltration and hepatic steatosis were both greatly reduced, and a number of genes involved in lipid metabolism/inflammatory signaling pathways were found to be down-regulated. Reduced adiposity in GIP Tg mice was associated with decreased energy intake, involving overexpression of hypothalamic GIP. Together, these studies suggest that, in the context of over-nutrition, transgenic GIP overexpression has the potential to improve hepatic and adipocyte function as well as glucose homeostasis.


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