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MUFAs in High‐Fat Diets Protect against Obesity‐Induced Bias of Hematopoietic Cell Lineages
Author(s) -
LemusConejo Ana,
Medrano Mayte,
Lopez Sergio,
MillanLinares Maria C.,
Rosillo Maria A.,
PerezSimon Jose A.,
Muriana Francisco J. G.,
Abia Rocio
Publication year - 2021
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.202001203
Subject(s) - docosahexaenoic acid , immune system , bone marrow , haematopoiesis , eicosapentaenoic acid , medicine , biology , endocrinology , granulopoiesis , polyunsaturated fatty acid , fatty acid , chemistry , stem cell , immunology , biochemistry , microbiology and biotechnology
Scope The role of dietary fatty acids in the generation of bone marrow (BM) immune cells and their trafficking to extramedullary compartments in the obesity is not yet fully understood. Methods and Results C57BL/6J mice are randomly assigned to isocaloric high‐fat diets (HFDs) formulate with dietary fats rich in saturated fatty acids (SFAs), monounsaturated fatty acids (MUFAs) or MUFAs fortified with eicosapentaenoic and docosahexaenoic acids for 20 weeks, followed by profiling of the obese metabolic phenotype and immunophenotypic features of immune cells in blood, spleen, and BM. All HFDs induce an obese phenotype, but it becomes largely less disruptive after the HFDs are enriched in MUFAs, which also induce signs of granulopoiesis and an expansion of long‐term hematopoietic stem and granulocyte‐macrophage progenitor cells in BM. In contrast, a HFD enriched in SFAs disturbs the fitness of medullary lymphocytes and promotes monopoiesis in favor of pro‐inflammatory activated subsets. Conclusion The reshaping of the fatty acid pools with MUFAs from the diet serves to manipulate the generation and trafficking of immune cells that are biased during obesity. These findings reveal a novel strategy by which dietary MUFAs may be instrumental in combating HFD‐induced dysfunctional immune systems.