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Composition of fatty acids in a high-fat diet affects adipose tissue inflammation by inducing calreticulin on adipocytes and activating group 1 innate lymphoid cells.
Matsumura, Kazunori; Mori, Taizo; Dohi, Taeko; Kawamura, Yuki I; Takaki, Satoshi.
Afiliación
  • Matsumura K; Department of Immune Regulation, The Research Center for Hepatitis and Immunology, Research Institute, National Center for Global Health and Medicine, Chiba, Japan.
  • Mori T; Department of Immune Regulation, The Research Center for Hepatitis and Immunology, Research Institute, National Center for Global Health and Medicine, Chiba, Japan.
  • Dohi T; Department of Liver Disease, The Research Center for Hepatitis and Immunology, Research Institute, National Center for Global Health and Medicine, Chiba, Japan.
  • Kawamura YI; Clinical Research Advancement Section, Research Institute, National Center for Global Health and Medicine, Tokyo, Japan.
  • Takaki S; Clinical Research Advancement Section, Research Institute, National Center for Global Health and Medicine, Tokyo, Japan.
Eur J Immunol ; 54(4): e2350800, 2024 Apr.
Article en En | MEDLINE | ID: mdl-38282083
ABSTRACT
Obesity-induced adipose tissue inflammation plays a critical role in the development of metabolic diseases. For example, NK1.1+ group 1 innate lymphoid cells (G1-ILCs) in adipose tissues are activated in the early stages of inflammation in response to a high-fat diet (HFD). In this study, we examined whether the composition of fatty acids affected adipose inflammatory responses induced by an HFD. Mice were fed a stearic acid (C180)-rich HFD (HFD-S) or a linoleic acid (C182)-rich HFD (HFD-L). HFD-L-fed mice showed significant obesity compared with HFD-S-fed mice. Visceral and subcutaneous fat pads were enlarged and contained more NK1.1+KLRG1+ cells, indicating that G1-ILCs were activated in HFD-L-fed mice. We examined early changes in adipose tissues during the first week of HFD intake, and found that mice fed HFD-L showed increased levels of NK1.1+CD11b+KLRG1+ cells in adipose tissues. In adipose tissue culture, addition of 4-hydroxynonenal, the most frequent product of lipid peroxidation derived from unsaturated fatty acids, induced NK1.1+CD11b+CD27- cells. We found that calreticulin, a ligand for the NK activating receptor, was induced on the surface of adipocytes after exposure to 4-hydroxynonenal or a 1-week feeding with HFD-L. Thus, excess fatty acid intake and the activation of G1-ILCs initiate and/or modify adipose inflammation.
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Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Aldehídos / Ácidos Grasos / Dieta Alta en Grasa Límite: Animals Idioma: En Revista: Eur J Immunol Año: 2024 Tipo del documento: Article País de afiliación: Japón

Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Aldehídos / Ácidos Grasos / Dieta Alta en Grasa Límite: Animals Idioma: En Revista: Eur J Immunol Año: 2024 Tipo del documento: Article País de afiliación: Japón