Search Results (278)

Background/Objectives: The mediating role of the diverse range of screen-based sedentary behaviors (SBs) remains understudied, particularly at younger ages. The present study examined the direct and indirect effects of parental BMI and education on ultra-processed food (UPF) consumption among preschoolers, testing the potential mediating role of screen time. Methods: The cross-sectional study sample comprised 919 kindergarten children (484 boys, 52.7%), with ages ranging from 2.2 to 6.8 years (mean: 4.7 ± 1.0 years). Screen-based sedentary behaviors (television viewing, smartphone use, tablet use, computer use, and playing electronic games) were measured by proxy-report fulfilled by parents, separately for weekdays and weekends. UPF consumption (drinks/yogurts, packaged/fast foods, and sweet/salty snacks) was assessed via 24 h recall scales. Path analysis mediation models tested direct effects of maternal/paternal BMI and education on UPF intake, and indirect effects through screen time, controlling for child age and sex. Results: Lower parental education and higher parental BMI were associated with increased mobile device use and UPF consumption (r = 0.10–0.28). Screen-based sedentary behaviors mediated the association between maternal BMI and UPF pathways (15–90% of total effects), particularly for sweet and salty snacks (50–90%). Parental education effects were also mediated by screen time (9–23% indirect effects), with paternal education showing stronger protection against packaged/fast foods. Conclusions: Mobile devices and watching television partially mediate intergenerational transmission of obesogenic dietary patterns from parental BMI/education to preschoolers’ UPF consumption. Findings of the current study support family-centered interventions targeting screen-time limits and UPF exposure, mainly at the weekends, to prevent early obesity trajectories. Full article

Obesity is considered a chronic disease that co-occurs with other disorders, including type 2 diabetes; therefore, the prevention and treatment of obesity are of utmost importance. The present review analysed the effects of bioactive compounds found in culinary herbs on the regulation of inflammatory processes through the modulation of inflammation and microbiota-dependent metabolic pathways. A total of 137 publications from 2010 to 2025 were reviewed. Few studies address the impact of culinary herbs on the gut microbiota in relation to obesity; however, analysing data on the effects of active compounds present in various herbs allows an assessment of their potential role in obesity prevention. This is a significant issue, as obesity is widespread, and the introduction of readily usable everyday food products may represent an important element of preventive strategies. Plant secondary metabolites, such as polyphenols, saponins, alkaloids, and flavonoids, exert strong antioxidant and anti-inflammatory activity, thus contributing to their beneficial effects on human health. Effective weight loss depends on the consistent maintenance of a healthy lifestyle, a requirement that can often be highly challenging. The daily use of herbs in meal preparation may reduce the risk of developing obesity or mitigate its severity. Herbs enhance the flavour of dishes and, additionally, help to reduce salt intake, thereby lowering the risk of cardiovascular disease, which is also an integral component of a healthy lifestyle. Full article

Background: Childhood obesity has become a major public health concern worldwide. Increasing evidence suggests that alterations in the gut microbiome may play a significant role in the development and progression of pediatric obesity. This narrative review synthesizes and analyzes recent studies investigating microbiome alterations in children with obesity, highlighting emerging insights and their potential implications for disease management. Understanding the relationship between gut microbial composition and obesity may provide new perspectives for prevention and therapeutic strategies in overweight pediatric populations. This narrative review was conducted through a search of major biomedical databases, including PubMed and Web of Science, complemented by manual screening of reference lists of relevant articles. Key findings: Children affected by obesity exhibit significant changes in gut microbiome composition, characterized by reduced microbial diversity and predominance of the Firmicutes and Bacteroidetes phyla. The balance between these two bacterial groups appears critical for maintaining gut homeostasis. Studies consistently report an increased Firmicutes-to-Bacteroidetes ratio in children with elevated body weight, suggesting that disruption of this balance may contribute to metabolic dysregulation and obesity-related pathologies. Given the essential role of the gut microbiota in nutrient metabolism and energy extraction, dysbiosis in obesity is associated with enhanced energy harvest and lipid absorption. Certain bacterial populations may promote increased caloric uptake, thereby contributing to weight gain and adiposity. Multidimensional interventions, including dietary modification and physical activity, have demonstrated the potential to reduce obesogenic microbiota patterns and restore microbial diversity. Additionally, probiotic supplementation is being investigated as a strategy to reestablish microbial homeostasis and potentially support body mass index reduction. Despite promising findings, further research is required to clarify mechanisms, establish causality, and determine the clinical effectiveness of microbiome-targeted therapies before they can be fully integrated into the management of pediatric obesity. Full article

Energy thriftiness and metabolic adaptations have had a crucial role in the emergence and spreading of the Homo lineage in the world. A higher-energy demand was required not only for the growing body mass, encephalization and human proliferation, but also for the survival adaptations to the environmental stresses. Because lean body mass lacks the energy-storage capacity required to supply the body’s demands, dedicated fat-storing cells originated. To feed such fat stores, the hominid evolution developed “meat-adaptive” genes to detect, digest and metabolize higher fat diets, and body-fat stores can be affected by lifestyle through hormonal-controlled daily energy balance. In energy surplus conditions, hypertrophy and hyperplasia of adipocytes can occur, with hypertrophic adipocyte signaling both a neo-adipocyte differentiation (leading to hyperplasia) and a local macrophage density (resident + infiltrated macrophages) for fat surplus scavenging. Adiposity-induced inflammation is caused by fat-overstored (hypertrophied) adipocytes that may operate as an overactive endocrine organ secreting an array of pro-inflammatory adipokines that, in combination with resident-macrophage activity and infiltrated blood-recruited, monocyte-derived macrophages, amplify the inflammatory process by spurting pro-inflammatory cytokines into the bloodstream. From an evolutionary perspective, obese humans represent a natural selection overexpressing the “thrifty” genes evolved for efficient food collection and fat deposition intended to help in survival in prolonged periods of famine. However, genetically speaking, obesity is a polygenic multifactorial disorder. Considering the rapidity of obesity-epidemic growth worldwide, epigenetic sets forth the key assumption of the mismatch between our human genome molded over thousands of generations, coping with the unprecedented dietary and physical conditions. Consequently, obesity would be due to our evolutionary-adapted polygenic-charge expressed by a deteriorated lifestyle characterized by high energy-dense food intake coupled with a reduction in caloric expenditure stemming from new mobility-reducing technologies. As a model of lifestyle change (LiSM), our 28-year on-going longitudinal study (“Moving for Health”) has shown effectiveness in the reduction not only of obesity but especially of its comorbidities, in a (10 week to 3 year) length-dependent LiSM. However, a disappointing progressive decrease in compliance with the study has been observed and attributed to the resistance of people to change their actual “obesogenic” lifestyle, basically represented by the individuals’ demand for labor-saving technologies and convenient, affordable, palatable foods. Full article

Background: Obesity is a multifactorial chronic disease resulting from sustained energy imbalance and modulated by environmental and demographic factors, and it is associated with numerous comorbidities. DNA methylation is an epigenetic modification associated with obesity. Modulation of DNA methylation is a viable target for obesity control strategies. The flavanol (-)-epicatechin (EC) exerts beneficial effects in overweight individuals, suggesting that EC may influence gene regulation through signaling pathways and epigenetic mechanisms. We evaluated whether EC modulates obesity-associated DNA methylation changes using complementary in silico, in vitro, and in vivo approaches. Methods. In silico analyses were performed to explore potential EC interactions with the DNA methyltransferases DNMT1, DNMT3A, and DNMT3B. DNMT activity was measured in nuclear extracts of 4T1 cells in the presence of EC. Finally, in a C57BL/6 mouse model of diet- induced obesity, we assessed global DNA methylation and the expression of the DNA methyltransferases, as well as metabolism-related genes; peroxisome proliferator-activated receptor gamma coactivator 1 alpha (Pgc-1α), pyruvate dehydrogenase kinase isozyme 4 (Pdk4), and nuclear factor erythroid 2–related factor 2 (Nrf2) and relative mitochondrial DNA content (mtDNA/nDNA ratio) in visceral adipose tissue (VAT) and skeletal muscle. Results. EC showed stable in silico interactions within catalytic/cofactor-binding regions of DNMTs and inhibited DNMT activity in vitro in a concentration-dependent manner. In vivo, the obesogenic diet reduced global DNA methylation and decreased transcript levels of Dnmt1, Dnmt3a, and Dnmt3b in skeletal muscle and adipose tissue. EC counteracted obesity-associated DNA methylation changes in skeletal muscle, restoring global methylation and Dnmt expression toward control levels, whereas effects in VAT were limited. EC increased mitochondrial DNA content. Discussion. In silico and enzymatic data suggest that EC may bind DNMT active sites and inhibit DNMT activity in a concentration-dependent manner, supporting a role for EC in obesity-related epigenetic remodeling, particularly in skeletal muscle. EC also increased relative mitochondrial DNA content in VAT and skeletal muscle despite no obesogenic diet effect on relative mitochondrial abundance, consistent with favorable mitochondrial modulation. In conclusion, EC is an epigenetic modulator and may have positive effects in obesity related dysfunctional tissues. Full article

Background: Obesity-associated inflammation arises from adipose dysfunction and intestinal disturbances, including altered microbiota and short-chain fatty acid (SCFA) metabolism. Beans (Phaseolus vulgaris) are rich in non-digestible carbohydrates and polyphenols, but whether kidney bean varieties differing in seed coat colour exert distinct effects on inflammation in obesity remains unclear. Objective: To determine whether supplementation of an obesogenic high-fat (HF) diet with white or dark red kidney beans modulates gut microbiota, SCFAs, and intestinal, systemic, and neuroinflammatory outcomes. Methods: Male C57Bl/6N mice (n = 12/group) were fed a basal diet (BD; modified AIN-93G), an HF diet (60% kcal from fat), or an HF diet supplemented with 15% cooked white (HF + WK) or dark red kidney beans (HF + DK) for nine weeks. Outcomes included cecal microbiota composition, predicted KEGG pathways with taxon contributors mapped with BURRITO (a tool for linking predicted microbial functions to contributing taxa), and SCFA-related pathways; cecal and fecal SCFA concentrations; colon histomorphometry and expression of gut barrier junction and inflammatory genes; serum cytokines and adipose hormones; and hippocampal inflammatory and barrier genes. Results: Mice consuming bean-supplemented HF diets had higher microbial diversity, enrichment of SCFA-producing taxa (Prevotella, Lactobacillus, Muribaculaceae), and lower obesity-associated genera versus HF alone (Mucispirillum, rc4-4). Bean diets elevated cecal acetate and butyrate concentrations, which aligned with increases in predicted acetate kinase in both bean groups versus HF and BD, and butyrate kinase in HF + DK versus BD. Bean supplementation attenuated HF-induced reduction of goblet cells and systemic interleukin (IL)-10. The HF + DK group had lower colonic tumour necrosis factor (TNF)-α and partially attenuated hippocampal IL-6. SCFAs were inversely associated with systemic and neuroinflammatory markers in HF + DK mice. Conclusions: Kidney bean supplementation mitigated HF diet-induced intestinal, systemic, and neuroinflammatory disturbances in male mice, with microbiota and SCFA modulation. Further, dark red beans exerted stronger anti-inflammatory effects, highlighting the role of seed coat colour in bean-mediated obesity outcomes. Full article

Obesity is associated with profound metabolic, inflammatory, and neurobehavioral dysfunctions. Dietary interventions leading to weight loss are commonly employed, yet it remains unclear whether all obesity-related alterations are fully reversed upon reaching normal body weight. Poor adherence to dietary regimens often results in weight cycling, or yo-yo dieting, characterized by repeated episodes of weight gain and loss, a phenomenon linked to adverse health outcomes. Here, we investigated the consequences of weight cycling in C57BL/6J mice. The Control Group was maintained on a standard chow diet throughout the protocol, whereas the experimental group underwent two alternating cycles of high-fat diet feeding (weight gain) and standard diet reversion (weight loss), until the end of the protocol where both groups reached 80 weeks of age. Despite achieving a final body weight and glucose and lipid metabolic profile comparable to lean controls, weight-cycled mice exhibited impaired sensorimotor function, increased anxiety-like behavior (evaluated through behavioral tests), and persistent inflammation, including a peritoneal macrophage pro-inflammatory profile and adipose tissue infiltration. We define this phenomenon as “obesogenic inflammatory memory”, highlighting that obesity leaves an immunological imprint that sustains inflammation even after normalization of weight and metabolic parameters. These findings demonstrate that weight cycling is associated with chronic macrophage-mediated inflammatory states, linked to long-term behavioral and neurological manifestations, and opening new avenues for future investigation and therapeutic approaches. Full article

Background: The increasing prevalence of low-birth-weight (LBW) offspring from obese mothers underscores the need for dietary strategies to mitigate the transgenerational propagation of metabolic diseases. Objectives: We determined whether dietary protein restriction under obesogenic conditions altered maternal energy balance and led to LBW offspring and whether branched-chain amino acid (BCAA) supplementation improved maternal energy balance and mitigated weight and craniofacial skeletal deficits in offspring. Methods: High-fat-fed obese pregnant Sprague Dawley rats (~8–10 weeks of age, n = 8–11/group) were randomized in study 1 to control high-fat diet (20% protein; HFD), low-protein diet (LP; 5% protein), and LP + BCAA diet (100% BCAA requirements) and in study 2 to control HFD (20% protein), LP (10% protein), and LP + 2BCAA diet (200% BCAA requirements). Post-weaning offspring were fed HFD until 8 weeks of age. Results: Protein restriction promoted hyperphagia and energy expenditure, whereas BCAA supplementation attenuated such hyperphagic effects in pregnancy but not in lactation. Protein restriction reduced maternal body weight in lactation, and although BCAA supplementation did not reverse the weight loss, it enhanced insulin sensitivity and paradoxically reduced offspring survival. Maternal protein restriction reduced offspring body weight and craniofacial bone growth that persisted into adulthood, but BCAA supplementation did not rescue such deficits. Conclusions: Maternal protein restriction in obese dams enhanced maternal energy expenditure but impaired offspring growth and development. Although BCAA supplementation improved maternal energy balance, it was insufficient to reverse the adverse effects of maternal protein restriction on offspring growth under obesogenic conditions. Full article

Obesity is among the top contributing factors for non-communicable chronic disease development and has attained menacing global proportions, affecting approximately one of eight adults. Phytochemicals that support energy metabolism and prevent obesity development have been the subject of intense research endeavors over the past several decades. Cycloastragenol is a natural triterpenoid compound and aglycon of astragaloside IV, known for activating telomerase and mitigating cellular aging. Here, we aim to characterize the effect of cycloastragenol on lipid metabolism in a glucose-induced obesity model in Caenorhabditis elegans. We assessed the changes in the body length, width, and area in C. elegans maintained under elevated glucose through automated WormLab system. Lipid accumulation in the presence of either cycloastragenol (100 μM) or orlistat (12 μM), used as a positive anti-obesity control drug, was quantified through Nile Red fluorescent staining. Furthermore, we evaluated the changes in key energy metabolism molecular players in GFP-reporter transgenic strains. Our results revealed that cycloastragenol treatment decreased mean body area and reduced lipid accumulation in the C. elegans glucose-induced model. The mechanistic data indicated that cycloastragenol suppresses the nuclear hormone receptor family member NHR-49 and the delta(9)-fatty-acid desaturase 7 (FAT-7) enzyme, and activates the 5′-AMP-activated protein kinase catalytic subunit alpha-2 (AAK-2) and the protein skinhead 1 (SKN-1) signaling. Collectively, our findings highlight that cycloastragenol reprograms lipid metabolism by down-regulating the insulin-like receptor (daf-2)/phosphatidylinositol 3-kinase (age-1)/NHR-49 signaling while simultaneously enhancing the activity of the AAK-2/NAD-dependent protein deacetylase (SIR-2.1) pathway. The anti-obesogenic potential of cycloastragenol rationalizes further validation in the context of metabolic diseases and obesity management. Full article

Background/Objectives: The increasing prevalence of obesity among children and adolescents is alarming, and the obesogenic environment is considered a major contributing factor to this public health concern. Nevertheless, individuals exposed to the same obesogenic environment exhibit considerable variability in their body weight and eating behaviors. Therefore, this study investigated the relationships between eating behaviors, sensory processing profiles, and peripheral biomarkers in the context of adolescent obesity. Methods: A total of 99 adolescents aged 11–18 years (51 in the obese group and 48 in the control group) were enrolled in the study. Blood and saliva samples were obtained from participants. All participants also completed a Sociodemographic Information Form, the Adolescent/Adult Sensory Profile (A/ASP), and the Dutch Eating Behavior Questionnaire (DEBQ). Results: No statistically significant differences were found between the groups in any of the sensory processing quadrants (p > 0.05). A moderate positive correlation was observed between Sensory Sensitivity (A/ASP) and Emotional Eating (DEBQ) (r = 0.442, p < 0.001), whereas no other associations between A/ASP quadrants and DEBQ subscales reached statistical significance after adjustment for multiple comparisons. After controlling for the effects of sex, BMI and physical activity, plasma leptin, ghrelin, and salivary cortisol levels were not significantly associated with restrained, emotional, or external eating behaviors (p > 0.05). Conclusions: Obese and control group adolescents exhibited similar sensory processing profiles, yet higher sensory sensitivity scores were associated with greater emotional eating. These findings suggest that sensory sensitivity may be relevant for understanding emotional eating in adolescence; however, longitudinal research is required to determine whether this association is causal and to clarify the processes underlying it. Full article

This study investigated the anti-obesogenic effects of 3D-printed snacks—developed from indigenous composite inks of cowpea, sorghum, and orange-fleshed sweet potato—in male and female Wistar rats fed a high-fat diet (HFD). Four experimental diets (TD1–TD4) were formulated from snacks using two blend ratios (33.33%:33.33%:33.33%) and 50%:10%:40%) and two processing states (raw and bioprocessed). Following a five-week HFD-induction period, the rats were supplemented for an additional five weeks with diets containing 20% of these snacks, Orlistat, or HFD alone. Physiological assessments included body weight, fasting glucose, insulin, homeostatic model assessment for insulin resistance (HOMA-IR), serum lipids, sex hormones, angiotensin-converting enzyme (ACE) activity, and histological evaluation of cardiac tissue. HFD feeding induced hyperglycemia, dyslipidemia, and insulin resistance. Supplementation with the 3D-printed snacks improved glycemic control, with the TD4 (bioprocessed blend; 50:10:40%) restoring glucose levels close to baseline. TD1 and TD2 (raw blends) improved lipid and hormonal profiles in females, whereas TD3 (bioprocessed blend; 33.33%:33.33%:33.33%) significantly reduced triglycerides and elevated HDL in males. Importantly, only TD1 (raw blend; 33.33%:33.33%:33.33%) significantly reduced ACE activity in males, providing a unique cardioprotective mechanism not observed with other snack formulations. Histological analyses revealed inflammatory infiltration and fibroplasia in HFD and Orlistat groups, whereas all 3D-printed snacks preserved normal myocardial architecture without necrosis or fibrosis. Collectively, these findings demonstrate that 3D-printed snacks derived from indigenous composite inks improved metabolic dysfunctions associated with diet-induced obesity. The optimal formulation appears application-specific: TD4 for glycemic control, TD3 for lipid management in males, and TD1/TD2 for metabolic improvements in females. Full article

Background/Objectives: Insufficient dietary fiber intake contributes to gut microbiota dysbiosis, systemic inflammation, and the onset of obesity-related metabolic disorders. Agro-industrial by-products have emerged as sustainable sources to restore microbial and metabolic balance. This study aimed to evaluate the effects of a mango bagasse- and peel-based confectionery (MC) on gut microbiota composition, short-chain fatty acids (SCFAs), and hepatic gene expression in Wistar rats fed either a standard diet (STD) or a high-fat diet (HFD). Methods: Twenty-four rats were randomly assigned to four groups (STD, MC-STD, HFD, MC-HFD) and treated for 11 weeks. Eating behavior, body composition, microbiota composition, SCFAs, and hepatic transcriptomics were evaluated. Results: MC supplementation did not significantly alter weight gain or SCFA levels but shifted clustering patterns in principal component analysis, indicating a distinct dietary response. Microbiota analysis revealed a trend toward lower relative abundances of obesogenic species such as Phascolarctobacterium faecium and Ruminococcus torques, while Intestimonas butyriciproducens and Anaerostipes hadrus were modulated according to diet type. Transcriptomic profiling demonstrated consistent downregulation of lipid metabolism–related genes (Cyp4a14, Hmgcs1, Cyp51, Fads1), linked to PPAR signaling pathways. Conclusions: MC supplementation may beneficially modulate the gut–liver axis and highlights the nutritional potential of fruit by-products as functional ingredients to promote metabolic health under high-fat dietary conditions. Full article

Background: Obesity is a risk factor for several non-communicable diseases and premature death. The Western-type diet, rich in calories and diverse in tastes, smells, and textures, promotes the onset and progression of obesity. We compared the effects of two Western-style palatable obesogenic diets—the cafeteria (CAF) diet, which allows for self-selection of calorie-dense food items consumed by humans, and the fast-food diet (FFD)—composed of a fixed combination of cheeseburgers and fries—on the manifestation of obesity-related complications. Methods: 3-month-old female rats consumed either the control (CTRL), FFD, or CAF diet for 12 months. Body weight was monitored weekly. At the end of the experiment, rats underwent metabolic and behavioral testing. Cardiometabolic markers and those characterizing glycoxidative and carbonyl stress, inflammatory status, and tryptophan metabolism were determined. Results: The CAF rats gain most weight (CTRL: +111 ± 40 g; FFD: +211 ± 77 g; CAF: 316 ± 87 g). CAF feeding produced a classical metabolic syndrome–like profile with severe obesity, insulin resistance, dyslipidemia, and liver steatosis, whereas the FFD model led to moderate obesity with preserved insulin sensitivity but elevated blood pressure and hepatic cholesterol accumulation. Thus, the CAF group developed a severe metabolic syndrome-like pathology assessed as continuous metabolic syndrome z-core (CTRL: −2.3 ± 1.0; FFD: −0.4 ± 1.9; CAF: 3.0 ± 2.4). Despite these differences, both diets promoted neuroinflammation and social deficits, likely mediated through gut microbiota–derived metabolites such as 5-HIAA and indoxyl sulfate. Conclusions: In female rats, self-selected CAF diet drives more severe and distinct pattern of metabolic syndrome-like pathology than a fixed FFD. Full article

An unhealthy prepubertal diet can have long-lasting effects throughout life. This study investigated hair concentrations of adrenal and sex steroids, in an in vivo mouse model of juvenile obesity subjected to control (CTRL), obesogenic (HFHC) diet, or nutraceutical supplementation (silymarin or coconut oil) diets. 87 3-week-old C57BL/6 mice (42 females, 45 males) were fed CTRL or HFHC diets for 8 weeks. Afterward, the CTRL group continued on CTRL diet while the HFHC diet group was divided into five groups: HFHC, HFHC→CTRL, HFHC→CTRL + silymarin (SIL), HFHC→HFHC + SIL and HFHC→HFHC + Coconut oil. At 4 weeks, the HFHC group showed increased cortisol/dehydroepiandrosterone (DHEA) ratio compared to CTRL group. At 20 weeks, the HFHC→HFHC group showed higher levels of progesterone (P4) and dehydroepiandrosterone sulfate (DHEA-S) and lower levels of estradiol (E2) compared to the CTRL→CTRL group. The switch from HFHC→CTRL was the optimal therapy because the body weight and almost all the hormones were close to those observed for the CTRL diet group. Supplement with SIL or Coconut oil reduced DHEA-S and increased in E2 compared with the endocrine setting seen with the HFHC diet. These interventions should be considered as supportive measures rather than substitutes for dietary correction. Full article

Obesity is a chronic, multifactorial metabolic disease associated with various factors such as insulin resistance, increased adipogenesis, induction of gluconeogenesis, epigenetic mechanisms, chronic inflammatory state, and oxidative stress. Anti-obesity drugs such as Semaglutide and Tirzepatide are currently used in therapies for obese patients and exert remarkable anti-obesogenic effects, determining weight loss and inhibition of insulin resistance. The impairment of the adipogenesis process and the inhibition of the differentiation of human bone marrow mesenchymal stem cells into adipocytes should also be considered to improve the therapeutic strategies for obesity. Notably, the ability of several flavonoids to inhibit adipogenesis has been described. Flavonoids are the most abundant polyphenols in the human diet and exhibit a wide range of biological properties, including antioxidant and anti-inflammatory effects. Furthermore, many flavonoids can modulate the activity of enzymes involved in epigenetic mechanisms, which play a crucial role in obesity development. The purpose of this review is the identification of those flavonoids able to exert anti-adipogenic and anti-obesity effects in both in vitro and in vivo experimental models, with the aim of combining these natural molecules, as adjuvants, with anti-obesogenic drugs to develop innovative therapeutic approaches for the treatment of obesity pathology. Full article