| Content Provider |
World Health Organization (WHO)-Global Index Medicus |
| Author |
Porter, David W. Irwin, Nigel Gault, Victor A. Flatt, Peter R. Moffett, Charlotte Lennox, Rachael R. Moffett, R. Charlotte Lennox, Rachel |
| Description |
Country affiliation: United kingdom Author Affiliation: Lennox R ( School of Biomedical Sciences, The SAAD Centre for Pharmacy and Diabetes, University of Ulster, Coleraine, Londonderry BT52 1SA, Northern Ireland, UK.); Moffett RC ( School of Biomedical Sciences, The SAAD Centre for Pharmacy and Diabetes, University of Ulster, Coleraine, Londonderry BT52 1SA, Northern Ireland, UK.); Porter DW ( School of Biomedical Sciences, The SAAD Centre for Pharmacy and Diabetes, University of Ulster, Coleraine, Londonderry BT52 1SA, Northern Ireland, UK.); Irwin N ( School of Biomedical Sciences, The SAAD Centre for Pharmacy and Diabetes, University of Ulster, Coleraine, Londonderry BT52 1SA, Northern Ireland, UK.); Gault VA ( School of Biomedical Sciences, The SAAD Centre for Pharmacy and Diabetes, University of Ulster, Coleraine, Londonderry BT52 1SA, Northern Ireland, UK.); Flatt PR ( School of Biomedical Sciences, The SAAD Centre for Pharmacy and Diabetes, University of Ulster, Coleraine, Londonderry BT52 1SA, Northern Ireland, UK.) |
| Abstract |
It has been previously demonstrated that compromise of glucose-dependent insulinotropic polypeptide receptor (GIPR) action and chronic consumption of a high-fat diet can independently impair memory and learning ability, however, the underlying pathology remain to be elucidated. The present study investigated the effects of GIPR knockout (KO), alone and in combination with a high-fat diet, on aspects of cognitive function and hippocampal gene expression in mice. In object recognition tests, normal mice exhibited effective memory, preferring to investigate the novel over the familiar object. However, wild-type (WT) mice fed a high-fat diet and GIPR KO mice fed a standard or high-fat diet demonstrated no such discrimination, suggesting the impairment of memory function. This decline in cognitive function was associated with marked changes in the expression levels of hippocampal genes involved in memory and learning. The chronic consumption of a high-fat diet decreased the hippocampal gene expression levels of mammalian target of rapamycin (mTOR), neurotrophic tyrosine kinase receptor type 2 (NTRK2) and synaptophysin. Notably, the GIPR KO mice fed a high-fat diet exhibited no reduction in the hippocampal expression of synaptophysin expression, however, the GIPR KO mice fed a standard rodent maintenance diet exhibited reduced hippocampal expression of mTOR compared with the WT controls. These data highlighted the importance of intact GIPR signalling and dietary composition in modulating memory and learning, and hippocampal pathways involved in the maintenance of synaptic plasticity, including mTOR and NTRK2, appear to be key in this regard. |
| ISSN |
17912997 |
| e-ISSN |
17913004 |
| Journal |
Molecular Medicine Reports |
| Issue Number |
1 |
| Volume Number |
12 |
| Language |
English |
| Publisher |
Spandidos Publications |
| Publisher Date |
2015-07-01 |
| Publisher Place |
Greece |
| Access Restriction |
Open |
| Subject Keyword |
Cognition Physiology Hippocampus Metabolism Obesity Genetics Receptors, Gastrointestinal Hormone Animals Diet, High-fat Gene Expression Insulin Memory Mice Mice, Knockout Neuronal Plasticity Pathology Research Support, Non-u.s. Gov't Discipline Molecular Biology |
| Content Type |
Text |
| Resource Type |
Article |
| Subject |
Genetics Biochemistry Molecular Biology Cancer Research Molecular Medicine Oncology |
