McGillicuddy et al. (2009) demonstrated that IFNγ may play an important role in T-cell modulation of diet-induced obesity, insulin resistance, and type 2 diabetes via activation of the adipocyte JAK-STAT pathway [ 32].
Among a number of proposed innovative approaches targeting novel pathomechanisms, probiotics appear an interesting and reasonable option acting on gut-liver axis malfunction through the modulation of diet-driven, obesogenic, and inflammatory intestinal microbiota.
We believe that the modulation of the diet composition in Pank2 knockout mice has generated a useful model system in which to test not only pantethine, but also additional compounds, which could be beneficial for patients.
Genotype and diet modulation of activity followed different paths and interactions were not significant.
Thus, we hypothesized that modulation of animal performance by diet could be explained by modulation of the population of ruminal microorganisms.
The association of the TCF7L2- rs7903146 polymorphism with plasma lipids is controversial, and we found great variability in results depending on the different populations analyzed (26– 30), suggesting a possible modulation of this association by diet.
Importantly, the appetite-suppressing effect of NENF was abrogated in obese mice fed a high-fat diet, demonstrating a diet-dependent modulation of NENF function [ 68].
Thus, further understanding of the role of diet on immune modulation and CVD risk in SLE may be key in vascular damage prevention.
The latter may involve modulation of the microbiota, by means of diet, probiotics and/or prebiotics, to try to restore normality.
The modulation of the gut microbiota by diet could be effective in improving the low-grade inflammation associated with obesity and related diseases [ 7, 8].
