Can type 2 diabetic serum alter macrophage phenotype

Inflammation, caused by obesity and metabolic changes, contributes to the pathogenesis of Type 2 diabetes (T2D) via many mechanisms and may be mediated by circulating cytokines and inflammatory markers produced by macrophages and other inflammatory cells. However, previous research has focused on...

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Main Author: Lim, Jia Ying Tanoto
Other Authors: Yusuf Ali
Format: Final Year Project
Language:English
Published: 2017
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Online Access:http://hdl.handle.net/10356/72627
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Institution: Nanyang Technological University
Language: English
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spelling sg-ntu-dr.10356-726272020-11-01T05:33:10Z Can type 2 diabetic serum alter macrophage phenotype Lim, Jia Ying Tanoto Yusuf Ali Lee Kong Chian School of Medicine (LKCMedicine) DRNTU::Science::Medicine Inflammation, caused by obesity and metabolic changes, contributes to the pathogenesis of Type 2 diabetes (T2D) via many mechanisms and may be mediated by circulating cytokines and inflammatory markers produced by macrophages and other inflammatory cells. However, previous research has focused on specific players presumed to trigger the inflammation, such as fatty acids and high glucose, and the phenotype of macrophages when exposed to diabetic serum itself remains unclear. In this project, mouse macrophages (RAW264.7) were exposed for 16h to serum from either diabetic or normoglycemic subjects, and their M1 and M2 gene expression analysed using quantitative PCR to determine any changes in macrophage phenotype. Results showed that there was a trend towards M1 phenotype in macrophages exposed to diabetic serum, although this was not statistically significant and limited by small sample size (n=5). Further elucidation of the phenotype of macrophages may help in the understanding of the pathogenesis of T2D and development of potential drug targets towards the underlying β-cell loss in T2D from inflammation. Bachelor of Medicine and Bachelor of Surgery 2017-08-31T02:30:02Z 2017-08-31T02:30:02Z 2017 Final Year Project (FYP) http://hdl.handle.net/10356/72627 en 12 p. application/pdf
institution Nanyang Technological University
building NTU Library
continent Asia
country Singapore
Singapore
content_provider NTU Library
collection DR-NTU
language English
topic DRNTU::Science::Medicine
spellingShingle DRNTU::Science::Medicine
Lim, Jia Ying Tanoto
Can type 2 diabetic serum alter macrophage phenotype
description Inflammation, caused by obesity and metabolic changes, contributes to the pathogenesis of Type 2 diabetes (T2D) via many mechanisms and may be mediated by circulating cytokines and inflammatory markers produced by macrophages and other inflammatory cells. However, previous research has focused on specific players presumed to trigger the inflammation, such as fatty acids and high glucose, and the phenotype of macrophages when exposed to diabetic serum itself remains unclear. In this project, mouse macrophages (RAW264.7) were exposed for 16h to serum from either diabetic or normoglycemic subjects, and their M1 and M2 gene expression analysed using quantitative PCR to determine any changes in macrophage phenotype. Results showed that there was a trend towards M1 phenotype in macrophages exposed to diabetic serum, although this was not statistically significant and limited by small sample size (n=5). Further elucidation of the phenotype of macrophages may help in the understanding of the pathogenesis of T2D and development of potential drug targets towards the underlying β-cell loss in T2D from inflammation.
author2 Yusuf Ali
author_facet Yusuf Ali
Lim, Jia Ying Tanoto
format Final Year Project
author Lim, Jia Ying Tanoto
author_sort Lim, Jia Ying Tanoto
title Can type 2 diabetic serum alter macrophage phenotype
title_short Can type 2 diabetic serum alter macrophage phenotype
title_full Can type 2 diabetic serum alter macrophage phenotype
title_fullStr Can type 2 diabetic serum alter macrophage phenotype
title_full_unstemmed Can type 2 diabetic serum alter macrophage phenotype
title_sort can type 2 diabetic serum alter macrophage phenotype
publishDate 2017
url http://hdl.handle.net/10356/72627
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