Abstract
Macrophages are abundant within adipose tissue depots where they are exposed to fatty acids, leading to lipid accumulation. Herein, we have determined the effects of various fatty acids on the macrophage lipidome. Using targeted mass-spectrometry, we were able to detect 641 individual lipid species in primary murine macrophages treated with a variety of saturated fatty acids and an un-saturated fatty acid, either alone or in combination. The most pronounced effects were observed for the long-chain saturated fatty acid palmitate, which increased the total abundance of numerous classes of lipids. While other medium- and long-chain saturated fatty acids, as well as the long-chain unsaturated fatty acid, had less pronounced effects on the total abundance of specific lipid classes, all fatty acids induced marked alterations in the abundance of numerous lipid species within given lipid classes. Fatty acid treatment markedly altered overall phospholipid saturation status; these effects were most pronounced for phosphatidylcholine and ether-phosphatidylcholine lipid species. Finally, treatment of macrophages with either palmitate or stearate in combination with oleate prevented many of the changes that were observed in macrophages treated with palmitate or stearate alone. Collectively, our results reveal substantial and specific remodelling of the macrophage lipidome following treatment with fatty acids.
Highlights
In the last decade, the immune system has been identified as a powerful regulator of adipose tissue (AT) biology and whole body metabolic homeostasis
AT macrophages are exposed to marked fluctuations in the levels of fatty acids
This can occur macrophages are exposed to marked fluctuations in the levels of fatty acids. This can occur in pathological conditions, such as obesity, or in physiological settings, such as fasting or cold in pathological conditions, such as obesity, or in physiological settings, such as fasting or cold exposure
Summary
The immune system has been identified as a powerful regulator of adipose tissue (AT) biology and whole body metabolic homeostasis. In the lean, insulin-sensitive state, AT is enriched in cells of both the innate and adaptive immune system, including eosinophils, group 2 innate lymphoid cells, regulatory T cells, invariant NK T (iNKT) cells, and M2 macrophages [1]. The concerted actions of these cells contribute to the maintenance of whole body metabolic homeostasis, and their loss from lean AT results in weight gain, impaired glucose metabolism, and insulin resistance [2,3,4,5]. The collective effect of these alterations is to induce a state of low-grade, chronic inflammation within AT, which disrupts whole body metabolism, as in impaired glucose tolerance and insulin resistance, for example
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