The benefits of walnut (Juglans regia) consumption for metabolic health are known, but the molecular background underlying their putative antioxidant and anti‐inflammatory/immunomodulatory effects is underexplored. We assessed that walnut supplementation (6 weeks) reverted unfavorable changes of the SIRT1/FoxO3a/MnSOD/catalase axis in the heart induced by fructose‐rich diet (FRD). Intriguingly, Nox4 was increased by both FRD and walnut supplementation. FRD increased the cytosolic fraction and decreased the nuclear fraction of the uniquely elucidated ChREBP in the heart. The ChREBP nuclear fraction was decreased in control rats subjected to walnuts. In addition, walnut consumption was associated with a reduction in systolic BP in FRD and a decrease in fatty acid AA/EPA and AA/DHA ratios in plasma. In summary, the protective effect of walnut supplementation was detected in male rats following the fructose‐induced decrease in antioxidative/anti‐inflammatory capacity of cardiac tissue and increase in plasma predictors of low‐grade inflammation. The current results provide a novel insight into the relationship between nutrients, cellular energy homeostasis, and the modulators of inflammatory/immune response in metabolic syndrome, emphasizing the heart and highlighting a track for translation into nutrition and dietary therapeutic approaches against metabolic disease.

Glutathione S-transferases (GSTs) are the family of enzymes involved in the second line of defense against oxidative stress (OS). The lack of GSTT1/GSTM1 enzyme quantity or activity, due to the presence of homozygous deletion compromises antioxidative defense resulting in OS. OS is the critical mechanism in the pathophysiology of atherosclerosis, coronary artery disease, and myocardial infarction (MI). The increase in reactive oxygen species together with the process of apoptosis plays a role in left ventricular remodeling (LVR) after MI. The associations of GSTT1 and GSTM1 gene polymorphisms with the risk of MI are inconsistent. The aim was to analyze the association of GSTT1/GSTM1 null genotypes with first MI and LVR 8 months after the MI. The study involved 330 controls and 438 consecutive patients with symptoms and signs of first MI. The subgroup of 150 MI patients was prospectively followed up for 6 months. Evidence of maladaptive LVR was obtained by 2D Doppler echocardiography 3–5 days and 6 months after the MI. A multiplex polymerase chain reaction was used to detect the deletion in GSTT1 and GSTM1 genes. GSTM1 null genotype was significantly and independently associated with first MI (adjusted OR = 1.45 95% CI 1.03–2.03, p = 0.03). Association of double null genotypes with maladaptive LVR in patients 6 months after the first MI was no longer significant after adjustment for factors that differed significantly between patients with and without maladaptive LVR. This study demonstrated the association of GSTM1 null genotypes with the risk of MI in the Serbian population.

Galectin-3 is encoded by LGALS-3, located in a unique haplotype block in Caucasians. According to the Tagger server, rs4040064, rs11628437, and rs7159490 cover 82% (r² > 0.8) of the genetic variance of this HapBlock. Our aims were to examine the association of their haplotypes with first myocardial infarction (MI), changes in left ventricular echocardiographic parameters over time, and impact on plasma galectin-3 and LGALS-3 mRNA in peripheral blood mononuclear cells, both 6 months post-MI. The study group consisted of 546 MI patients and 323 controls. Gene expression was assessed in 92 patients and plasma galectin-3 in 189 patients. Rs4040064, rs11628437, rs7159490, and LGALS-3 mRNA expression were detected using TaqMan^® technology. Plasma galectin-3 concentrations were determined by the ELISA method. We found that the TGC haplotype could have a protective effect against MI (adjusted OR 0.19 [0.05–0.72], p = 0.015) and that the GAC haplotype had significantly higher galectin-3 concentrations (48.3 [37.3–59.4] ng/mL vs. 18.9 [14.5–23.4] ng/mL, p < 0.0001), both in males and compared to the referent haplotype GGC. Higher plasma Gal-3 was also associated with higher NYHA class and systolic dysfunction. Our results suggest that variants tagging LGALS-3 HapBlock could reflect plasma Gal-3 levels 6 months post-MI and may have a potential protective effect against MI in men. Further replication, validation, and functional studies are needed.

Background/Objectives: Dietary lifestyle, particularly the intake of fatty acids (FAs), may be useful in alleviating the key pathogenic processes in multiple sclerosis (MS); however, the data are still scarce, particularly with regard to the course of disease. Therefore, the objectives of this study were to investigate the erythrocyte profile of FAs in patients with relapsing-remitting (RR)MS and progressive (P)MS, and to examine whether dietary supplementation with n-3 PUFAs could influence the FA profile, according to the course of disease. Methods: The FA profile was determined in erythrocytes by gas–liquid chromatography, in 153 patients with RRMS and 69 with PMS, whereas the group on dietary supplementation with n-3 PUFAs consisted of 36 RRMS and 17 PMS patients. Individual FAs were quantified as a percentage of the total identified FAs and analyzed in relation to the demographic and clinical parameters. Results: Compared to RRMS, the PMS patients had higher saturated (S)FAs, n-7 mono-unsaturated (MU)FAs, and n-3 polyunsaturated (PU)FAs, and lower n-6 PUFAs. In the group on omega-3 supplementation, the only difference in FA profile was higher MUFA 16:1n-7 (POA) in PMS than RRMS patients. In PMS patients, there was a positive correlation of disability (EDSS) with the total SFA levels, whereby 16:0 (PA) correlated positively with EDSS and MS severity (MSSS). Also, in PMS, the MSSS correlated negatively with the total and individual n-6, and positively with the total and individual n-3 PUFAs. In PMS patients on n-3 supplementation, there was a negative correlation between MSSS and total n-6/n-3 ratio, and a positive one between MSSS and 22:6n-3 (DHA). The observed decrease in levels of circulating lipid peroxidation product 4-HNE in PMS patients was not found in the n-3 PUFA supplementation group. Conclusions: The present findings suggest that the changes in the levels of FAs and their correlations are specific for the course of MS. Detected FA profile differences can be influenced by n-3 supplementation, primarily in regard to SFAs and PUFAs, supporting an option for the use of dietary supplements in managing the clinical course and progression of MS.