Recent studies have shown a growing interest in the complex relationship between the human gut microbiota, metabolism, and overall health. This review aims to explore the gut microbiota–host association, focusing on its implications for precision nutrition and personalized medicine. The objective is to highlight how gut microbiota modulate metabolic and immune functions, contributing to disease susceptibility and wellbeing. The review synthesizes recent research findings, analyzing key studies on the influence of gut microbiota on lipid and carbohydrate metabolism, intestinal health, neurobehavioral regulation, and endocrine signaling. Data were drawn from both experimental and clinical trials examining microbiota–host interactions relevant to precision nutrition. Our findings highlight the essential role of gut microbiota-derived metabolites in regulating host metabolism, including lipid and glucose pathways. These metabolites have been found to influence immune responses and gut barrier integrity. Additionally, the microbiota impacts broader physiological processes, including neuroendocrine regulation, which could be crucial for dietary interventions. Therefore, understanding the molecular mechanisms of dietary–microbiota–host interactions is pivotal for advancing personalized nutrition strategies. Tailored dietary recommendations based on individual gut microbiota compositions hold promise for improving health outcomes, potentially revolutionizing future healthcare approaches across diverse populations.

Oxidative stress is generated by the imbalance between reactive oxygen species (ROS) formation and antioxidant scavenger system’s activity. Increased ROS, such as superoxide anion, hydrogen peroxide, hydroxyl radical and peroxynitrite, likely contribute to the development and complications of atherosclerotic cardiovascular diseases (ASCVD). In genetically modified mouse models of atherosclerosis, the overexpression of ROS-generating enzymes and uncontrolled ROS formation appear to be associated with accelerated atherosclerosis. Conversely, the overexpression of ROS scavenger systems reduces or stabilizes atherosclerotic lesions, depending on the genetic background of the mouse model. In humans, higher levels of circulating biomarkers derived from the oxidation of lipids (8-epi-prostaglandin F_2α, and malondialdehyde), as well as proteins (oxidized low-density lipoprotein, nitrotyrosine, protein carbonyls, advanced glycation end-products), are increased in conditions of high cardiovascular risk or overt ASCVD, and some oxidation biomarkers have been reported as independent predictors of ASCVD in large observational cohorts. In animal models, antioxidant supplementation with melatonin, resveratrol, Vitamin E, stevioside, acacetin and n-polyunsaturated fatty acids reduced ROS and attenuated atherosclerotic lesions. However, in humans, evidence from large, placebo-controlled, randomized trials or prospective studies failed to show any athero-protective effect of antioxidant supplementation with different compounds in different CV settings. However, the chronic consumption of diets known to be rich in antioxidant compounds (e.g., Mediterranean and high-fish diet), has shown to reduce ASCVD over decades. Future studies are needed to fill the gap between the data and targets derived from studies in animals and their pathogenetic and therapeutic significance in human ASCVD.

UVA radiation induces oxidative stress, mitochondrial dysfunction, and cell death in human dermal fibroblasts, contributing to skin aging and damage. In this study, we investigated the protective effects of polydatin, a natural polyphenol, against UVA-induced cell damage. Our results show that polydatin preserves cell viability and reduces intracellular reactive oxygen species (ROS) levels after UVA exposure. In addition, polydatin maintains mitochondrial integrity by preserving mitochondrial membrane potential and improving mitochondrial respiration. From a molecular perspective, polydatin regulates the expression of Nrf2, a key regulator of the cellular antioxidant response, thereby promoting cellular defense mechanisms. Additionally, polydatin attenuates UVA-induced mitochondrial fission, supporting a balanced mitochondrial dynamic profile. These results suggest that polydatin exerts a protective effect on UVA-irradiated fibroblasts, highlighting its potential for cosmetic and dermatological applications aimed at preventing photoaging and oxidative skin damage.

Granulosa cell (GC) differentiation, stimulated by FSH and LH, drives oocyte maturation and follicle development. FSH promotes GC proliferation, and LH triggers ovulation. In clinical practice, hCG is used to mimic LH. Despite various controlled ovarian stimulation (COS) protocols employing exogenous gonadotropins and GnRH analogs to prevent premature ovulation, their effectiveness and safety remain debated. To identify markers predicting a positive treatment response, the secretome of gonadotropin-stimulated GC using the human granulosa-like tumor cell line (KGN) via proteomics was analyzed. Additionally, a novel 2D-FFT quantitative method was employed to assess cytoskeleton fiber aggregation and polymerization, which are critical processes for GC differentiation. Furthermore, the activation of key kinases, focal adhesion kinase (FAK), and Rho-associated coiled-coil-containing protein kinase 1 (ROCK-1), which are implicated in cytoskeleton dynamics and hormone signaling, was evaluated. The proteomic analysis revealed significant modulation of proteins involved in extracellular matrix organization, steroidogenesis, and cytoskeleton remodeling. Notably, the combined FSH/hCG treatment led to a dynamic upregulation of the semaphorin pathway, specifically semaphorin 7A. Finally, a significant reorganization of the cytoskeleton network and signaling was detected. These findings enhance our understanding of folliculogenesis and suggest potential novel molecular markers for predicting patient responses to gonadotropin stimulation.

Gestational diabetes mellitus (GDM) is a transient pregnancy disorder marked by insulin resistance and oxidative stress. In type 1 and 2 diabetes, reduced red blood cell (RBC) membrane fluidity, measured by Laurdan-GP, associates with vascular risk, but its role in GDM is unclear. This study compared GP with intrinsic RBC autofluorescence (green-to-red ratio, $AFG,R$⁠) to identify a better marker of metabolic stress in GDM. Forty-eight pregnant women were enrolled (31 GDM, 17 controls). High-resolution multispectral confocal imaging quantified RBC GP and $AFG,R$⁠. A machine-learning pipeline analyzed core, membrane, and whole-cell metrics, alongside clinical and biochemical data. Logistic regression assessed associations with GDM. GP did not differ between groups (0.60 ± 0.04 versus 0.61 ± 0.04; p = 0.168), unlike the reductions reported in chronic diabetes. Conversely, $AFG,R$ values were higher in GDM across compartments (core: −0.073 ± 0.202 versus −0.154 ± 0.060; membrane: 0.013 ± 0.198 versus −0.066 ± 0.075; p = 0.049). In multivariable analysis, $AFG,R$ Core independently predicted GDM status (p = 0.018), outperforming clinical and hematological markers. In GDM, membrane fluidity remains unchanged, but RBC autofluorescence reflects acute oxidative stress, supporting its use as a non-invasive, repeatable complement to OGTT for early risk assessment and monitoring.