Daily rhythms of metabolic function are supported by molecular circadian clock systems that are strongly regulated by feeding and fasting. Intermittent fasting diets have been associated with weight loss and improved metabolism. However, the effects of time-restricted eating (TRE) on glycemic parameters are still under debate. In this review, we aim to systematically analyze the effects of TRE on glycemic parameters. We searched on PubMed, EMBASE, and the Cochrane Library for controlled studies in which subjects followed TRE for at least 4 weeks. 20 studies were included in the qualitative systematic review, and 18 studies (n = 1169 subjects) were included in the meta-analysis. Overall, TRE had no significant effect on fasting glucose (Hedges’s g = -0.08; 95% CI:-0.31,0.16; p = 0.52), but it did reduce HbA1c levels (Hedges’s g = -0.27; 95% CI: -0.47, -0.06; p = 0.01). TRE significantly reduced fasting insulin (Hedges’s g = -0.40; 95% CI: -0.73,-0.08; p = 0.01) and showed a tendency to decrease HOMA-IR (Hedges’s g = -0.32; 95% CI:-0.66,0.02; p = 0.06). Interestingly, a cumulative analysis showed that the beneficial effects of TRE regarding glucose levels were less apparent as studies with later TRE windows (lTRE) were being included. Indeed, a subgroup analysis of the early TRE (eTRE) studies revealed that fasting glucose was significantly reduced by eTRE (Hedges’s g = -0.38; 95% CI:-0.62, -0.14; p < 0.01). Our meta-analysis suggests that TRE can reduce HbA1c and insulin levels, and that timing of food intake is a crucial factor in the metabolic benefit of TRE, as only eTRE is capable of reducing fasting glucose levels in subjects with overweight or obesity.PROSPERO registration number CRD42023405946.

The purpose of the study was to determine the impact of weight loss through calorie restriction on metabolic profile, and inflammatory and oxidative stress parameters in metabolically healthy (MHO) and unhealthy (MUHO) obese individuals. A total of 74 subjects (34 MHO and 40 MUHO) received two cycles of a very low-calorie diet, alternating with a hypocaloric diet for 24 weeks. Biochemical, oxidative stress, and inflammatory markers, as well as serum metabolomic analysis by nuclear magnetic resonance, were performed at baseline and at the end of the intervention. After the diet, there was an improvement in insulin resistance, as well as a significant decrease in inflammatory parameters, enhancing oxidative damage, mitochondrial membrane potential, glutathione, and antioxidant capacity. This improvement was more significant in the MUHO group. The metabolomic analysis showed a healthier profile in lipoprotein profile. Lipid carbonyls also decrease at the same time as unsaturated fatty acids increase. We also display a small decrease in succinate, glycA, alanine, and BCAAs (valine and isoleucine), and a slight increase in taurine. These findings show that moderate weight reduction leads to an improvement in lipid profile and subfractions and a reduction in oxidative stress and inflammatory markers; these changes are more pronounced in the MUHO population.

Polycystic ovary syndrome (PCOS) is a complex condition associated with chronic inflammation and oxidative stress and is often linked to periodontal diseases. This study aimed to determine whether gingivitis modulates the NLRP3 inflammasome in peripheral blood mononuclear cells (PBMCs) from women with PCOS. Following a case-control design, 104 women were divided into three groups: controls (n = 36), PCOS without gingivitis (PCOS, n = 44) and PCOS with gingivitis (PCOS+, n = 24). Periodontal parameters, proinflammatory regulators (NFκB p65, JNK), NLRP3 components (NLRP3, ASC, procaspase-1, caspase-1) and oxidative stress markers (superoxide, NRF2, GCLC and GSR) were determined. The PCOS+ group presented elevated values for bleeding on probing (BOP) and plaque and calculus indices, both of which were associated with increased protein levels of NFκB p65 and JNK, thus indicating NLRP3 inflammasome priming. Higher protein levels of NLRP3, ASC, procaspase-1 and caspase-1 in the PCOS+ group confirmed that priming had occurred, suggesting an engagement in assembly. When potential assembly signals of inflammasome were evaluated, the patients with PCOS generally presented enhanced total superoxide and an impaired antioxidant response (NRF2, GCLC and GSR). Moreover, BOP was independently associated with JNK, ASC and procaspase-1. These findings suggest that gingival inflammation modulates the innate immune response in leukocytes of women with PCOS via the NLRP3 inflammasome pathway, which is regulated by proinflammatory factors and oxidative damage.

Brief daily “exercise snacks” improved metabolic health, cardiorespiratory fitness, and muscle oxygenation in sedentary women. These changes were accompanied by modulation of PBMC mitochondrial dynamics, autophagy-related markers, and neutrophil-endothelial interactions. Our findings provide mechanistic support for time-efficient exercise as a feasible strategy to counteract sedentary-induced cardiometabolic dysfunction.

To assess the impact of non-surgical periodontal treatment (NSPT) on the oxidative and endoplasmic reticulum (ER) stress response of leukocytes, and to examine whether obesity modulates the biological response to periodontal treatment. Eighty individuals with periodontitis were enrolled and classified according to the presence (n = 42) or absence (n = 38) of obesity. Periodontal parameters -probing pocket depth (PPD), clinical attachment level (CAL), bleeding on probing (BOP), plaque calculus indices and PISA were assessed, along with systemic inflammatory markers (hsCRP, C3c, absolute neutrophil count). Leukocyte oxidative stress (total ROS, cytosolic and mitochondrial superoxide, SOD1, and total antioxidant capacity) and ER stress markers (GRP78, ATF6, p-eIF2α, IRE1α, sXBP1, CHOP) were analysed at baseline and 3 months post-NSPT. NSPT significantly improved all periodontal parameters in both groups, but more so in patients without obesity. Improvement was inversely associated with inflammatory markers, including C3c, systolic blood pressure, and absolute neutrophil count. Obesity was associated with a prooxidative profile with elevated total intracellular ROS, cytosolic superoxide, and SOD1 levels. Following treatment, mitochondrial superoxide, CHOP, and ATF6 decreased, while SOD1, total antioxidant capacity, and GRP78 increased, particularly in the group without obesity. NSPT provides systemic benefits beyond periodontal health, attenuating oxidative and ER stress in leukocytes. Obesity modulates these responses, highlighting redox and ER stress pathways as potential therapeutic targets linking periodontal and metabolic health. This study reinforces the importance of periodontal care providers in the early identification of patients at increased risk of suboptimal periodontal healing. Obesity and systemic inflammatory burden emerge as relevant modifiers of treatment response, indicating that periodontal outcomes are influenced by factors beyond the oral cavity. Incorporating simple clinical information, such as blood pressure and inflammatory status, into routine periodontal assessment would support more individualized treatment planning, optimize follow-up strategies, and improve long-term outcomes in patients with chronic periodontitis.

Gingival inflammation has been increasingly linked to metabolic and endocrine disorders, such as polycystic ovary syndrome (PCOS). This connection may involve immune system activation and cellular stress mechanisms, particularly the unfolded protein response (UPR), which regulates endoplasmic reticulum (ER) stress. The aim of the study was to investigate whether gingivitis modulates UPR activation in peripheral blood mononuclear cells (PBMCs) of women with PCOS. In this case-control study, female subjects were divided into 2 groups: a control group (n = 48); and a PCOS group (n = 68), which included 24 individuals with gingivitis (PCOS+). Anthropometric, biochemical and periodontal parameters were determined, namely probing pocket depth (PPD), clinical attachment level (CAL), bleeding on probing (BOP), and plaque index. Markers of oxidative stress, including total superoxide and glutathione peroxidase 1 (GPx1), and UPR mediators, such as glucose-regulated protein 78 (GRP78), activating transcription factor 6 (ATF6), phosphorylated eukaryotic initiation factor 2 alpha subunit (p-eIF2α), and C/EBP homologous protein (CHOP), were evaluated in PBMCs. Polycystic ovary syndrome was associated with an increased plaque index and significantly higher BOP in PCOS+. Increased superoxide and reduced GPx1 levels were observed in women with PCOS, with no significant differences between subgroups. Gingivitis in PCOS was correlated with the activation of specific UPR pathways; higher levels of p-eIF2α and CHOP and lower GRP78 levels were detected in PCOS+, while ATF6 was increased in the overall PCOS group. Moreover, BOP demonstrated a direct correlation with p-eIF2α and the plaque index. The association of leukocyte ER stress responses in PCOS with gingival inflammation underscores the impact of periodontal disease on modulating systemic cellular stress in the context of multifactorial metabolic disorders.