Abstract
Background Macrophages infiltrate adipose tissue at the onset of weight gain and directly contribute to adipose inflammation, insulin resistance, and obesity [1]. The type of fuel substrate utilized by macrophages is central to the formation of obesity, a global epidemic [2]. Our goal is to understand the role of macrophage glucose metabolism in the promotion of inflammation and insulin resistance during high fat diet-induced obesity. We hypothesize that macrophages with blunted or elevated glucose metabolism will display limited or exaggerated immune responses, and modulate susceptibility to insulin resistance and obesity, respectively.
Highlights
Macrophages infiltrate adipose tissue at the onset of weight gain and directly contribute to adipose inflammation, insulin resistance, and obesity [1]
Materials and methods GLUT1 is the glucose transporter expressed by macrophages [3]
GLUT1 over-expression resulted in elevated glucose uptake and metabolism, as well as a hyper-inflammatory state characterized by elevated secretion of MCP-1 and PAI-1, all of which could be blunted with a pharmacologic inhibitor of glycolysis
Summary
Macrophages infiltrate adipose tissue at the onset of weight gain and directly contribute to adipose inflammation, insulin resistance, and obesity [1]. The type of fuel substrate utilized by macrophages is central to the formation of obesity, a global epidemic [2]. Our goal is to understand the role of macrophage glucose metabolism in the promotion of inflammation and insulin resistance during high fat diet-induced obesity. We hypothesize that macrophages with blunted or elevated glucose metabolism will display limited or exaggerated immune responses, and modulate susceptibility to insulin resistance and obesity, respectively
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