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Updated: May 13, 2026
Isolation of Adipose Tissue Immune Cells
Published on: May 22, 2013
Neuropeptide Y is produced by adipose tissue macrophages and regulates obesity-induced inflammation
Kanakadurga Singer1, David L Morris, Kelsie E Oatmen
1Department of Pediatrics and Communicable Diseases, University of Michigan Medical School, Ann Arbor, Michigan, USA.
Abstract:
Neuropeptide Y (NPY) is induced in peripheral tissues such as adipose tissue with obesity. The mechanism and function of NPY induction in fat are unclear. Given the evidence that NPY can modulate inflammation, we examined the hypothesis that NPY regulates the function of adipose tissue macrophages (ATMs) in response to dietary obesity in mice. NPY was induced by dietary obesity in the stromal vascular cells of visceral fat depots from mice. Surprisingly, the induction of Npy was limited to purified ATMs from obese mice. Significant basal production of NPY was observed in cultured bone marrow derived macrophage and dendritic cells (DCs) and was increased with LPS stimulation. In vitro, addition of NPY to myeloid cells had minimal effects on their activation profiles. NPY receptor inhibition promoted DC maturation and the production of IL-6 and TNFα suggesting an anti-inflammatory function for NPY signaling in DCs. Consistent with this, NPY injection into lean mice decreased the quantity of M1-like CD11c(+) ATMs and suppressed Ly6c(hi) monocytes. BM chimeras generated from Npy(-/-) donors demonstrated that hematopoietic NPY contributes to the obesity-induced induction of Npy in fat. In addition, loss of Npy expression from hematopoietic cells led to an increase in CD11c(+) ATMs in visceral fat with high fat diet feeding. Overall, our studies suggest that NPY is produced by a range of myeloid cells and that obesity activates the production of NPY in adipose tissue macrophages with autocrine and paracrine effects.
Insights
Neuropeptide Y (NPY) production increases in adipose tissue macrophages during obesity. NPY signaling appears to have anti-inflammatory effects, regulating immune cell function in fat tissue.
Area of Science:
- Immunology
- Metabolic Disease
- Neuroendocrinology
Background:
- Neuropeptide Y (NPY) is found in peripheral tissues like adipose tissue during obesity.
- The precise role and mechanism of NPY induction in fat remain unclear.
- NPY is known to modulate inflammatory processes.
Purpose of the Study:
- To investigate the hypothesis that NPY regulates adipose tissue macrophage (ATM) function in response to diet-induced obesity in mice.
- To determine the cellular source and functional impact of NPY in the context of obesity and inflammation.
Main Methods:
- Induction of NPY in stromal vascular cells and purified ATMs from obese mice.
- In vitro studies on myeloid cells (macrophages, dendritic cells) with NPY and LPS stimulation.
- Assessment of myeloid cell activation profiles and cytokine production (IL-6, TNFα).
- In vivo experiments using NPY injection in lean mice and bone marrow chimeras from Npy(-/-) mice.
Main Results:
- NPY induction during obesity was primarily observed in ATMs.
- NPY signaling demonstrated anti-inflammatory effects on dendritic cells.
- NPY administration reduced M1-like ATMs and suppressed monocytes in lean mice.
- Hematopoietic NPY deficiency increased ATMs in visceral fat of diet-induced obese mice.
Conclusions:
- NPY is produced by various myeloid cells, including ATMs.
- Obesity triggers NPY production in ATMs, exerting autocrine and paracrine anti-inflammatory effects.
- NPY signaling plays a role in regulating immune cell populations within adipose tissue during obesity.
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