SCOPE: Virgin olive oil is an essential component of the Mediterranean diet. Its antioxidant and anti-inflammatory properties are mainly linked to phenolic contents. This study aims to evaluate the beneficial effects of a polyphenol-rich virgin olive oil (HPCOO) or olive oil without polyphenols (WPOO) in rats fed high-fat diet (HFD). METHODS AND RESULTS: Male Sprague-Dawley rats were divided into four groups based on the different types of diet: (I) standard diet (STD); (II) HFD; (III) HFD containing WPOO, and (IV) HFD containing HPCOO. HPCOO and WPOO induced a significant improvement of HFD-induced impaired glucose homeostasis (by hyperglycemia, altered oral glucose tolerance, and HOMA-IR) and inflammatory status modulating pro- and anti-inflammatory cytokines (TNF-α, IL-1, and IL-10) and adipokines. Moreover, HPCOO and less extensively WPOO, limited HFD-induced liver oxidative and nitrosative stress and increased hepatic fatty acid oxidation. To study mitochondrial performance, oxidative capacity and energy efficiency were also evaluated in isolated liver mitochondria. HPCOO, but not WPOO, reduced H2 O2 release and aconitase activity by decreasing degree of coupling, which plays a major role in the control of mitochondrial reactive oxygen species emission. CONCLUSION: HPCOO limits HFD-induced insulin resistance, inflammation, and hepatic oxidative stress, preventing nonalcoholic fatty liver disease progression.
SCOPE: Virgin olive oil is an essential component of the Mediterranean diet. Its antioxidant and anti-inflammatory properties are mainly linked to phenolic contents. This study aims to evaluate the beneficial effects of a polyphenol-rich virgin olive oil (HPCOO) or olive oil without polyphenols (WPOO) in rats fed high-fat diet (HFD). METHODS AND RESULTS: Male Sprague-Dawley rats were divided into four groups based on the different types of diet: (I) standard diet (STD); (II) HFD; (III) HFD containing WPOO, and (IV) HFD containing HPCOO. HPCOO and WPOO induced a significant improvement of HFD-induced impaired glucose homeostasis (by hyperglycemia, altered oral glucose tolerance, and HOMA-IR) and inflammatory status modulating pro- and anti-inflammatory cytokines (TNF-α, IL-1, and IL-10) and adipokines. Moreover, HPCOO and less extensively WPOO, limited HFD-induced liver oxidative and nitrosative stress and increased hepatic fatty acid oxidation. To study mitochondrial performance, oxidative capacity and energy efficiency were also evaluated in isolated liver mitochondria. HPCOO, but not WPOO, reduced H2 O2 release and aconitase activity by decreasing degree of coupling, which plays a major role in the control of mitochondrial reactive oxygen species emission. CONCLUSION:HPCOO limits HFD-induced insulin resistance, inflammation, and hepatic oxidative stress, preventing nonalcoholic fatty liver disease progression.
Authors: Isy F de Sousa; Amanda P Pedroso; Iracema S de Andrade; Valter T Boldarine; Alexandre K Tashima; Lila M Oyama; Lillà Lionetti; Eliane B Ribeiro Journal: Eur J Nutr Date: 2020-07-25 Impact factor: 5.614
Authors: Marta Farràs; Laura Martinez-Gili; Kevin Portune; Sara Arranz; Gary Frost; Mireia Tondo; Francisco Blanco-Vaca Journal: Nutrients Date: 2020-07-23 Impact factor: 5.717
Authors: Paola Ditano-Vázquez; José David Torres-Peña; Francisco Galeano-Valle; Ana Isabel Pérez-Caballero; Pablo Demelo-Rodríguez; José Lopez-Miranda; Niki Katsiki; Javier Delgado-Lista; Luis A Alvarez-Sala-Walther Journal: Nutrients Date: 2019-11-19 Impact factor: 5.717