Background: Abdominal obesity (AO) is involved in the development of cardiometabolic disorders, in which factors such as diet and genetics play crucial roles. In this context, interactions between genetic variants and dietary responses may influence metabolic processes associated with AO. Objective: This study aimed to evaluate the effects of a nutrigenetic diet incorporating 21 genetic variants related to lipid metabolism and cardiovascular risk on anthropometric and biochemical parameters and antioxidant capacity in adults with AO. Methods: An eight-week randomized controlled trial was conducted in 58 adults with AO, who were randomly assigned to either a nutrigenetics-guided diet or a standard diet. Participants in the nutrigenetic group underwent genotyping for 21 variants associated with lipid metabolism and cardiometabolic risk in the ABCA1, APOA1, APOA2, APOA5, APOB, APOC3, APOE, CETP, CDKN2B-AS1, CD36, FABP2, FTO, LIPC, LPL, MTTP, MTHFR, NFKB1, PON1, SIRT1, and ZPR1 genes. Anthropometric and biochemical measurements were performed. Antioxidant and oxidative stress biomarkers were measured using colorimetric assays and ELISA, respectively. Results: In baseline-adjusted ANCOVA models controlling for age and sex, with false discovery rate (FDR) correction, both groups achieved comparable reductions in body weight and fat mass under equivalent energy restriction. However, the nutrigenetic group demonstrated significantly greater improvements in insulin levels, HOMA-IR, and high-sensitivity C-reactive protein (hs-CRP) compared with the standard diet group. The nutrigenetic intervention also resulted in greater reductions in the prevalence of elevated TyG index (−20% vs. −10.8%) and HOMA-IR (−33.3% vs. −10.7%), along with a trend toward a greater increase in catalase activity. Conclusions: Compared with a standard dietary intervention, a nutrigenetic diet was associated with greater improvements in fasting insulin, estimated insulin resistance (HOMA-IR), and systemic inflammation (hs-CRP) in adults with AO.

Background/Objectives: Coronary artery disease (CAD) is influenced by diet; however, the role of micronutrients remains underexplored. This study aimed to evaluate differences in dietary micronutrient intake between patients with and without CAD. Methods: A cross-sectional study was conducted with 107 participants (51 CAD, 56 non-CAD). Dietary intake was assessed using habitual 24-h dietary recalls and analyzed for micronutrient content. Biochemical, anthropometric, and clinical data were also evaluated. Results: CAD patients exhibited lower adequate intake of vitamins A, C, and K, as well as antioxidants such as lycopene and lutein, compared to the non-CAD group. While micronutrient inadequacy was prevalent in both groups, it was significantly more pronounced in subjects with CAD. Conclusions: Subjects with CAD had lower micronutrient intake than those without CAD, highlighting the potential importance of adequate micronutrient intake in the prevention and management of CAD.

Kidney transplantation (KT) remains the optimal therapy for end-stage kidney disease (ESKD), yet long-term graft survival is limited by unremitting allograft dysfunction and non-immune treatment toxicities. Sterile inflammation primarily drives graft failure. This inflammatory process releases damage-associated molecular patterns (DAMPs). DAMPs activate pattern recognition receptors (PRRs), such as Toll-like receptors (TLRs) 2 and 4, from proximal tubule epithelial cells, endothelial compartments, and infiltrating myeloid lineages. PRR signaling and the release of pro-inflammatory cytokines (IL-1β, IL-18, TNF-α) promote pro-inflammatory M1 macrophage polarization and accelerate interstitial fibrosis and tubular atrophy (IFTA). While maintenance immunosuppression prevents adaptive rejection, it causes severe metabolic, cardiovascular, and oncologic complications, including post-transplant diabetes mellitus, hypertension, and malignancies. Sodium-glucose cotransporter 2 (SGLT2) inhibitors (dapagliflozin, empagliflozin, canagliflozin) have emerged as novel disease-modifying, immunomodulatory adjuncts that act independently of glycemic control. SGLT2 inhibition reactivates tubuloglomerular feedback to relieve intraglomerular hypertension, blunts hyperfiltration, and reduces tubular transport workload. This alleviates cortical hypoxia, curtails mitochondrial ROS production, and activates AMP-activated protein kinase (AMPK) to suppress NF-κB and NLRP3 inflammasome assembly. SGLT2 inhibitors downregulate TLR expression, drive a phenotypic shift toward reparative M2 macrophages, reduce proteinuria, and provide sustained volume decongestion without triggering compensatory activation of the renin–angiotensin–aldosterone system. By targeting both upstream bioenergetic strain and downstream fibrotic remodeling (YAP/TAZ axis), SGLT2 inhibitors complement standard immunosuppression to protect allograft architecture, reduce cardiovascular morbidity, and improve long-term transplant outcomes.