Monounsaturated Fatty Acids in a High-Fat Diet and Niacin Protect from White Fat Dysfunction in the Metabolic Syndrome

Mol Nutr Food Res. 2019 Oct;63(19):e1900425. doi: 10.1002/mnfr.201900425. Epub 2019 Jul 31.


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 Lepob/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.

Keywords: adipose metabolism; metabolic syndrome; monounsaturated fatty acids; niacin; obesity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adipose Tissue, White / drug effects*
  • Adipose Tissue, White / immunology
  • Adipose Tissue, White / physiopathology*
  • Animals
  • Diet, High-Fat / adverse effects*
  • Fatty Acids, Monounsaturated / administration & dosage*
  • Female
  • Inflammation / prevention & control
  • Insulin Resistance
  • Leptin / deficiency
  • Leptin / genetics
  • Lipid Metabolism / drug effects
  • Male
  • Metabolic Syndrome / etiology
  • Metabolic Syndrome / physiopathology*
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Mutation
  • NAD / metabolism
  • Niacin / administration & dosage*
  • Obesity / etiology
  • Obesity / physiopathology
  • Obesity / prevention & control
  • Receptors, LDL / deficiency
  • Receptors, LDL / genetics
  • Receptors, LDL / physiology


  • Fatty Acids, Monounsaturated
  • Leptin
  • Receptors, LDL
  • NAD
  • Niacin