Immune cells call macrophages accumulate in adipose tissue during obesity and appear to contribute to obesity-associated insulin resistance. Efforts to understand how macrophages accumulate have focused mostly on their recruitment to fat tissue.
Andrea Hill, a graduate student in the laboratory of Alyssa Hasty, Ph.D., and colleagues have explored another mechanism that could modulate macrophage number: regulation of cell survival/death.
The investigators report in Molecular Metabolism that activation of cell death signaling pathways (apoptosis) is reduced in adipose tissue macrophages in both diet-induced and genetically obese mice. They also found that levels of pro-survival proteins were elevated and that the increased pro-survival signaling was associated with elevated activation of the transcription factor NF-kappaB.
The findings demonstrate that activation of NF-kappaB in adipose tissue macrophages from obese mice promotes cell survival, suggesting that this mechanism may promote macrophage accumulation in fat tissue during obesity.
Understanding the control of adipose tissue macrophage number and function during obesity could lead to the development of novel therapeutics for the treatment of metabolic disorders.
This research was supported by a Department of Veterans Affairs Merit Award and by an American Heart Association Established Investigator Award.
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