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Monounsaturated Fatty Acids in a High‐Fat Diet and Niacin Protect from White Fat Dysfunction in the Metabolic Syndrome
Author(s) -
Montserratde la Paz Sergio,
Naranjo Maria C.,
MillanLinares Maria C.,
Lopez Sergio,
Abia Rocio,
Biessen Erik A. L.,
Muriana Francisco J. G.,
Bermudez Beatriz
Publication year - 2019
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.201900425
Subject(s) - niacin , medicine , endocrinology , metabolic syndrome , docosahexaenoic acid , eicosapentaenoic acid , white adipose tissue , adipose tissue , polyunsaturated fatty acid , chemistry , lipid metabolism , biology , fatty acid , biochemistry , obesity
Scope Obesity is a principal causative factor of metabolic syndrome. Niacin potently regulates lipid metabolism. Replacement of saturated fatty acids by MUFAs or inclusion of omega‐3 long‐chain PUFAs in the diet improves plasma lipid levels. However, the potential benefits of niacin in combination with MUFAs or omega‐3 long‐chain PUFAs against white adipose tissue (WAT) dysfunction in the high fat diet (HFD)‐induced metabolic syndrome are unknown. Methods and results Male Lep ob/ob LDLR −/− mice are fed a chow diet or HFDs based on milk cream (21% kcal), olive oil (21% kcal), or olive oil (20% kcal) plus 1% kcal from eicosapentaenoic and docosahexaenoic acids, including immediate‐release niacin (1% w/v) in drinking water, for 8 weeks. Mice are then phenotyped. Dietary MUFAs are identified as positive regulators of adipose NAD + signaling pathways by triggering NAD + biosynthesis via the salvage pathway. This coexists with overexpression of genes involved in recognition of NAD + and fatty acids, a surrounding lipid environment dominated by exogenous oleic acid and an alternatively activated macrophage profile, which culminate in a healthy expansion of WAT and improvement of several hallmarks that typify the metabolic syndrome. Conclusion Niacin in combination with dietary MUFAs can favor WAT homeostasis in the development of HFD‐induced obesity and metabolic syndrome.