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    Neuropeptide Y1 Receptor in Immune Cells Regulates Inflammation and Insulin Resistance Associated With Diet-Induced Obesity

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    Author
    Macia, L; Yulyaningsih, E; Pangon, L; Nguyen, AD; Lin, S; Shi, YC; Zhang, L; Bijker, M; Grey, S; Mackay, F; ...
    Date
    2012-12-01
    Source Title
    Diabetes
    Publisher
    AMER DIABETES ASSOC
    University of Melbourne Author/s
    Mackay, Fabienne
    Affiliation
    Microbiology and Immunology
    Metadata
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    Document Type
    Journal Article
    Citations
    Macia, L., Yulyaningsih, E., Pangon, L., Nguyen, A. D., Lin, S., Shi, Y. C., Zhang, L., Bijker, M., Grey, S., Mackay, F., Herzog, H. & Sainsbury, A. (2012). Neuropeptide Y1 Receptor in Immune Cells Regulates Inflammation and Insulin Resistance Associated With Diet-Induced Obesity. DIABETES, 61 (12), pp.3228-3238. https://doi.org/10.2337/db12-0156.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/257780
    DOI
    10.2337/db12-0156
    Abstract
    Recruitment of activated immune cells into white adipose tissue (WAT) is linked to the development of insulin resistance and obesity, but the mechanism behind this is unclear. Here, we demonstrate that Y1 receptor signaling in immune cells controls inflammation and insulin resistance in obesity. Selective deletion of Y1 receptors in the hematopoietic compartment of mice leads to insulin resistance and inflammation in WAT under high fat-fed conditions. This is accompanied by decreased mRNA expression of the anti-inflammatory marker adiponectin in WAT and an increase of the proinflammatory monocyte chemoattractant protein-1 (MCP-1). In vitro, activated Y1-deficient intraperitoneal macrophages display an increased inflammatory response, with exacerbated secretion of MCP-1 and tumor necrosis factor, whereas addition of neuropeptide Y to wild-type macrophages attenuates the release of these cytokines, this effect being blocked by Y1 but not Y2 receptor antagonism. Importantly, treatment of adipocytes with the supernatant of activated Y1-deficient macrophages causes insulin resistance, as demonstrated by decreased insulin-induced phosphorylation of the insulin receptor and Akt as well as decreased expression of insulin receptor substrate 1. Thus, Y1 signaling in hematopoietic-derived cells such as macrophages is critical for the control of inflammation and insulin resistance in obesity.

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