LIVER ADAPTIVE INFLAMMATORY RESPONSE TO DIETARY INTERVENTION WITH VIRGIN OLIVE OIL IN A DIET-INDUCED OBESITY TNFR1-DEFICIENT MOUSE MODEL

GUZMÁN CF ; CHACÓN, I DEL V; BARRERA FS; LÓPEZ CM; PENNA FO; FORNES MW; RAMIREZ DC; GOMEZ MEJIBA SE

MAR DEL PLATA

Congreso; SAIC; 2023

The liver is a target of excessive dietary energetic balance-inducedinflammation. Inducible nitric oxide synthase (iNOS) and myeloperoxidase (MPO) in the liver are known to cause nitrosative and chlorinating stress, respectively. Moreover, upon binding to its ubiquitousreceptors (TNFR), TNFa can interfere with normal liver physiology.Virgin olive oil (VOO) is a complex mixture of nutrients, and an important component of the Mediterranean diet, which health benefitsare well known, but the effect on the inflammatory profile of the liveris rarely reported. Herein we tested whether a short- or long-periodof intervention with a VOO-supplemented diet (VOOSD, 11% bovinefat plus 11% VOO) can affect critical inflammatory parameters in theliver of diet-induced obese TNFR1-deficient mice. To accomplish ouraim, we fed TNFR1-/- mice with a control diet (CD, rodent chow) orobesogenic diet (OD, 22% bovine fat plus 10% fructose in tap water)for 24 weeks and intervened with VOOSD every 6 weeks. A VOOSDreduced the impact of an OD on insulin resistance and dyslipidemiacaused by an OB, but enhanced weight gain. Liver iNOS, TNFa,and MPO, three well-known inflammation markers were measuredby using ELISA. In the liver of TNFR1-deficient mice fed a CD, iNOSincreased in the groups intervened with VOOSD for 6 and 12 weeks,however, these changes were abolished when mice were intervenedwith VOOSD for 18 weeks. Compared to CD, MPO content in theliver was higher in the groups fed for 6, 12, and 18 weeks. Whereas no significant changes in hepatic TNFa content were found. Interestingly, in the liver of TNFR1-deficient mice fed an OD, iNOSincreased in the group fed a VOOSD for 6 weeks, meanwhile MPOincreased in the groups fed a VOOSD for 6 and 12 weeks, whereasTNFa was higher in 6 than in 18 weeks. Taken together these datasuggest an adaptive liver response to inflammatory stress causedby intervention with a VOOSD a diet induced TNFR1-deficient obesity mouse model.