Sergio Montserrat-de la Paz1,2, Maria C Naranjo1, Maria C Millan-Linares3, Sergio Lopez1,4, Rocio Abia1, Erik A L Biessen5, Francisco J G Muriana1, Beatriz Bermudez1,4. 1. Laboratory of Cellular and Molecular Nutrition, Instituto de la Grasa, CSIC, 41013, Seville, Spain. 2. Department of Medical Biochemistry, Molecular Biology and Immunology, School of Medicine, University of Seville, 41009, Seville, Spain. 3. Cell Biology Unit, Instituto de la Grasa, CSIC, 41013, Seville, Spain. 4. Department of Cell Biology, School of Biology, University of Seville, 41012, Seville, Spain. 5. Experimental Vascular Pathology Group, Cardiovascular Research Institute of Maastricht (CARIM), University of Maastricht, 6200, Maastricht, The Netherlands.
Abstract
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.
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.
Authors: Carlos Vazquez-Madrigal; Soledad Lopez; Elena Grao-Cruces; Maria C Millan-Linares; Noelia M Rodriguez-Martin; Maria E Martin; Gonzalo Alba; Consuelo Santa-Maria; Beatriz Bermudez; Sergio Montserrat-de la Paz Journal: Nutrients Date: 2020-10-14 Impact factor: 5.717