SFEBES2022 Poster Presentations Metabolism, Obesity and Diabetes (96 abstracts)
Differentially expressed genes in insulin resistant macrophages are shared across multiple diabetes associated morbidities
Katie Goodhew 1 , Kyriakos Grammatopoulos 1 , Amy Jackson 1 , Ayanteh Makahamadze 1 , Ines Pineda-Torra 2 , Nadira Yuldasheva 3 , Mark Kearney 3 & Matthew Gage 1
1Royal Veterinary College, London, United Kingdom; 2CABIMER, Seville, Spain; 3University of Leeds, Leeds, United Kingdom
Authors 1-4 contributed equally to this work.
Background: Insulin resistance is the central defining feature of type 2 diabetes and increases with age. People with type 2 diabetes are at an increased risk of cardiovascular disease, non-alcoholic fatty liver disease (NAFLD), Alzheimer’s disease and arthritis. Macrophages are phagocytotic leukocytes which play a central role in the development of type 2 diabetes and the chronic inflammatory diseases mentioned above.
Aim: Our aim was to determine if differentially expressed genes from aged insulin resistant macrophages may be conserved across macrophages from multiple diabetes associated morbidities.
Methods: Differentially expressed gene datasets from transcriptome analysis of bone marrow derived macrophages (BMDM) from aged insulin resistant mice gained through chronic hyper-stimulation of the PI3K arm of the insulin signalling pathway via hematopoietic SHIP2 knock-down (h-SHIP2KD) were compared to published transcriptome data sets of macrophages from mouse models of hyperglycaemia, atherosclerotic plaque progression and regression, NAFLD, Alzeimer’s disease and arthritis.
Results: Upregulated and downregulated differentially expressed genes were found to be shared between h-SHIP2KD BMDM and all diabetes associated morbidity macrophage datasets analysed. Ongoing analyses are revealing common intracellular signalling pathway regulation between these morbidities.
Conclusion: These data reveal signalling pathways in insulin resistant macrophages which may have the potential to be targeted by new therapeutic strategies to impact diabetes associated chronic inflammatory disease progression.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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