Determining the role of the macrophage GLUT1 transporter and glucose metabolism in obesity-associated inflammation
Public Deposited- Last Modified
- February 26, 2019
- Creator
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Lim, Maili Frances
- Affiliation: Gillings School of Global Public Health, Department of Nutrition
- Abstract
- Obesity and diabetes are the most prevalent metabolic diseases in the United States, afflicting over 60% of the adult population. The immune system contributes to obesity and insulin resistance, which are likely linked to over-nutrition. The adipocyte is more than a static lipid storage unit, and plays a crucial role as an endocrine organ, inducing the recruitment of macrophages to adipose tissue in obesity. Macrophages, specifically pro-inflammatory or M1-polarized, are the immune cells most commonly associated with perpetuating inflammation in adipose tissue through the secretion of inflammatory cytokines. The number of macrophages is increased significantly in obese adipose tissue; the damaged tissue, potentially trigged by hypoxia, may attract macrophages to the site, as M1 macrophages have been observed to form “crown-like structures” (CLS) around dead or dying adipocytes. We reported that GLUT1 is the primary rate-limiting glucose transporter on type I macrophages, thus we hypothesize that GLUT1 is essential in the activation of the pro-inflammatory response of macrophages. To test this hypothesis, quantitative polymerase chain reaction (qPCR) was used to determine the expression of specific genes associated with the pro-inflammatory M1 response in both GLUT1M+ and GLUT1M- bone marrow-derived macrophages (BMDMs) and epididymal white adipose tissue (eWAT) of lean and obese mice. eWAT of GLUT1M+ and GLUT1M- mice fed either a high-fat diet (HFD) or low-fat diet (LFD) was collected to examine the effects of the GLUT1 deletion on diet-induced obesity (DIO). Preliminary data, qPCR results and histologic analysis of CLS in adipose tissue suggest that although macrophage infiltration is occurring, polarization to the pro-inflammatory M1 phenotype is inhibited, resulting in an attenuated inflammatory response. Ultimately, findings from this study yield insight into the contribution of glucose metabolism to macrophage polarization and obesity.
- Date of publication
- spring 2015
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- Rights statement
- In Copyright
- Note
- Funding: Michael P. and Jean W. Carter Research Fund
- Advisor
- Makowski, Liza
- Degree
- Bachelor of Science in Public Health
- Honors level
- Highest Honors
- Degree granting institution
- University of North Carolina at Chapel Hill
- Extent
- 28
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