To address the major public health problems of increased body weight and obesity, causing conditions such as hypertension and diabetes. Early obesity in childhood and adolescence has more severe long-term health consequences. The Developmental Origins of Health and Disease (DOHaD) concept examines how early overfeeding and other factors affect health throughout life. This study hypothesized that a short-term metformin treatment during puberty could reduce metabolic dysfunction caused by neonatal overfeeding. We investigated whether the same intervention would have a similar effect on metabolic programming in adulthood. Male Wistar rats raised in small (SL, three pups per mother) and normal (NL, 9 pups per mother) litters were used as models of early overfeeding. Some of the SL and NL animals received intraperitoneal injections of metformin (NL-M and SL-M), whereas the controls received saline (NL-C and SL-C) from days 35-42 (puberty) or 70-81 (adulthood). Two months after the intervention, at both puberty and adulthood, the SL animals exhibited metabolic dysfunction, and were significantly heavier with greater tissue fat accumulation than the NL animals (p <0.0001). SL-M animals treated during puberty exhibited significant reductions in white adipose tissue and liver weight, as well as lower weight gain (p <0.05). In contrast, metformin treatment in adulthood did not alter metabolism. These findings suggest that short-term metformin treatment in rats during puberty can mitigate adult metabolic dysfunction induced by neonatal overnutrition. However, this intervention in adulthood did not result in long-term metabolic changes, which confirms the DOHaD concept.

Observational evidence suggests ultra-processed food (UPF) may contribute to obesity, but some people who consume a larger amount of UPF remain at normal weight. This study examined whether childhood UPF consumption was associated with obesity in early adulthood and whether the association was modified by genetic susceptibility to body mass index (BMI). This prospective cohort study included data from 3061 participants of the Avon Longitudinal Study of Parents and Children (ALSPAC) in England with follow-up from 7 to 24years. UPF consumption was calculated from food diaries based on the NOVA classification. LDpred2 was used to construct a polygenic score (PGS) for body mass index (BMI). Linear regression models were used to estimate the association between UPF intake at 7years and BMI at 24years. The PGS-UPF interaction was examined to see whether genetic susceptibility modifies the association between childhood UPF consumption and early adulthood BMI. Each 10% increase in the proportion of total energy intake coming from UPF at 7 was associated with 0.21 (95% CI 0.05-0.37) kg/m2 higher BMI at 24, after adjusting for BMI at 7, age, sex, ethnicity, physical activity, socioeconomic position, and total energy intake. There is evidence for PGS-BMI interaction (0.19; 95% CI 0.02-0.36), and the UPF-BMI association was only retained in children with the highest genetic predisposition to higher BMI (0.74, 95% CI 0.07-1.42) in the subgroup analysis. UPF consumption in childhood is only associated with early adulthood obesity among children more genetically predisposed to higher BMI.

Despite limitations in using BMI to assess obesity, little is known about central obesity's role in pregnancy and postpartum cardiometabolic conditions. We investigated associations of central obesity with perinatal cardiometabolic conditions, independently and jointly with BMI. We examined associations of early pregnancy central obesity measures (waist circumference, waist-to-hip ratio, waist-to-height ratio, and body roundness index) with gestational diabetes mellitus, hypertensive disorders of pregnancy, postpartum prediabetes/diabetes, and postpartum chronic hypertension using modified Poisson (prenatal outcomes) and Cox (postpartum outcomes) regression. Among the 3,055 individuals in the study, there was a dose-response relationship between increasing central obesity and all outcomes, even after adjusting for BMI. Among individuals with healthy prepregnancy BMI, central obesity was associated with a higher risk of gestational diabetes mellitus (relative risks 1.92-2.42), postpartum prediabetes/diabetes (hazard ratios [HRs] 1.50-2.16), and postpartum chronic hypertension (HRs 2.04-3.63). Early pregnancy central obesity measures may enhance perinatal cardiometabolic risk assessment, helping identify at-risk individuals who could be missed using BMI alone.

Clinical presentation of inactivating PTH/PTHrP signaling disorders (iPPSDs, historically pseudohypoparathyroidism (PHP)) exhibits pronounced age-dependence. Indeed, main features, including PTH resistance and brachydactyly, develop during late childhood, whilst other features (ectopic ossifications, obesity and hypothyroidism) are the most prevalent in toddlers. The latter are included among minor diagnostic criteria; therefore, a significant diagnostic delay has been reported. Aim of this work is to describe the early natural history of a large cohort of iPPSD/PHP patients, in order to improve the diagnosis, with the final goal of proposing new diagnostic criteria for early infancy and reducing the diagnostic delay. We included 117 patients regularly followed up in two European Endocrinology tertiary centres and we retrospectively collected data on the age of onset of main clinical and hormonal features. In our cohort the median age at diagnosis was 5.9 years. Age of onset of PTH resistance and brachydactyly, major criteria for diagnosis, was significantly different from that of both TSH resistance and obesity (median age 6.1, 5.8, 1.85 and 2 years, respectively). Minor diagnostic criteria were more represented than major criteria in children before 2 years (p=0.002). Indeed, in 64% of patients before 2 years none of the major criteria were observed, conversely 71% had already developed at least one minor criterion; in particular, 20% had developed TSH resistance and obesity. Clinical picture of iPPSD/PHP in early infancy differs from that of mid-late infancy and adults, thus current diagnostic criteria may not be appropriate for children. We suggest that the combination of early onset obesity and elevated TSH should raise the suspicion and trigger genetic screening before 2 years of age.

Weight trajectories and obesity onset between 17 and 60 years of age, and cause-specific mortality: the Obesity and Disease Development Sweden (ODDS) pooled cohort study.

Abdominal obesity and related cardiometabolic risk (CMR) factors frequently begin in adolescence and contribute to long‑term health burden, yet longitudinal trajectories in U.S. youth are poorly characterized. This study quantifies the prevalence and 2‑ and 4‑year incidence of emerging CMR, with emphasis on excess adiposity, in a diverse adolescent cohort. We analyzed longitudinal data from the Adolescent Brain Cognitive Development Study, collected at three time points: 2018-2020 (mean age, 12.1 years), 2020-2022 (mean age, 14.2 years), and 2022-2024 (mean age, 16.1 years). Adolescents (n = 4788 to 3313) with anthropometric and laboratory data were included. Abdominal obesity was defined as a waist-to-height ratio > 0.5. Additional CMR factors included elevated total cholesterol (≥ 145mg/dL), glycated hemoglobin (HbA1c ≥ 5.7%), and high blood pressure (≥ 95th percentile for age, sex, and height). Weighted prevalence and 2- and 4-year incidence were calculated. At baseline, abdominal obesity affected 38.4% (95% CI: 36.4%-40.4%), followed by elevated cholesterol (17.6%), HbA1c (8.7%), and blood pressure (3.0%). Over a four-year period, new-onset abdominal obesity occurred in 10.5% of individuals, compared with 15.4% for cholesterol, 4.7% for HbA1c, and 3.1% for blood pressure. The steepest CMR progression was observed for lipid and adiposity markers. Abdominal obesity is highly prevalent by early adolescence, and new cardiometabolic risk develops rapidly, particularly for adiposity and dyslipidemia. These results highlight the need for early obesity screening and interventions to mitigate long‑term cardiometabolic risk in youth.

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.

This study analyzed non-communicable disease screening in Indonesia, focusing on pre-elderly efforts to prevent the burden on the elderly. This study uses a descriptive quantitative design with frequency and percentage analysis. The authors collected secondary data from the Indonesian health profile for the year 2023. The results indicate that West Nusa Tenggara has the highest percentage for priority screening of sensory disorders, cervical cancer, and breast cancer. Smoke-free areas are well implemented. Gorontalo, West Nusa Tenggara, and Jakarta have the highest percentages of early obesity detection and Highland Papua has the lowest percentage.

Acceptance of weight loss medication in patients with atypical hyperplasia or carcinoma of the endometrium as part of the fertility preservation treatment: A qualitative study

Plenty of epidemiological studies have focused on obesity and allergic diseases, less is known about the interaction of the comorbidity. The present study was conducted to identify the relationship between obesity and allergy and to clarify the potential regulatory roles of gut microbiota in the development of comorbidity. Four-week-old male BALB/c mice were used to establish the comorbidity model. The high-fat diet was used to induce obese mice, and ovalbumin was used to induce allergic mice. The post-obesity allergy mice and post-allergy obesity mice (n = 12/group) were used to clarify the effects of obesity on allergic reactions and those of allergy on metabolic function. Changes in gut microbiota, short-chain fatty acids (SCFAs), bile acids (BAs), the expression of the SCFAs and the BAs receptors were also detected. In the post-obesity allergy study, the serum Immunoglobulin E and the splenic CD4+CD25+FOXP3+ T cells (Tregs) in post-obesity allergic mice were higher than that in allergic mice. Post-obesity allergic mice had higher abundance of Alistipes, Parabacteroides, Rikenellaceae_RC9_gut_group, Colidextribacter, Muribaculum, Lachnospiraceae_NK4A136_group, and Erysipelatoclostridium but lower levels of SCFAs and expressions of GPR41 and 43. In the post-allergy obesity study, OVA-induced allergy alleviated fat accumulation and glycolipid metabolism disorder in obese mice. However, there was no significant difference in the gut microbiota and the SCFAs receptors between post-allergy obese mice and obese mice, except for BAs. The post-obesity allergy model suggested that early obesity impaired allergic reaction and immune function, which aggravated the development of allergy via altering the composition of the gut microbiota and the contents and function of SCFAs. The post-allergy obesity study suggested that early allergy did not promote metabolic disorder, instead of alleviating the development of obesity, and BAs may contribute to this alleviation.

The mechanisms linking early environmental risk (EER) and obesity via the interplay of mental health and lifestyle factors in the early life stage remain unclear. To examine whether EER was associated with later mental health, lifestyle factors and obesity and to identify the mediating roles of mental health and lifestyle in these relationships. Using data from the Millennium Cohort Study (valid n=5401), we longitudinally assessed the relationship between EER (prenatal risks, neonatal risks, low socioeconomic status, maternal psychological problems and harsh parenting; 9 months to age 3 years), mental health problems in childhood (internalising and externalising problems; age 7 years), lifestyle factors in early adolescence (diet, exercise, smoking and drinking; age 11 years) and obesity in late adolescence (age 14-17 years). Structural equation modelling was used to test proposed pathways. The proposed model showed an acceptable fit (Comparative Fit Index=0.926, Tucker-Lewis Index=0.875, root mean square error of approximation=0.034, standardised root mean square residual=0.046). EER was significantly associated with later mental health problems, lifestyle factors (ie, diet, exercise, smoking) and obesity. Higher EER was modestly associated with higher obesity risk via the interplay of externalising problems and drinking (β=0.01, p=0.036). The sex-stratified model results indicated differences between males and females. By highlighting the importance of EER and the mediating role of lifestyle factors in mental health and later obesity risk, our findings provide evidence of shared risk mechanisms linking mental and physical health. These findings suggest that integrating mental health assessment (especially externalising symptoms) with routine screening for adolescent alcohol use and other risk factors could inform more targeted obesity prevention in clinical and public health settings.

ABSTRACT Objectives To assess the prevalence and determinants of early pregnancy obesity (EPO) and its effects on the preterm cardiometabolic profile. Materials and Methods This study was conducted at the antenatal care unit of the Dschang district hospital. Apparently healthy Cameroonian pregnant women in the third trimester of their pregnancy were included in the study. Participants were assessed on sociodemographic, lifestyle parameters, and dietary habits using standardised and structured questionnaires. Early pregnancy weight was collected from medical records. Anthropometric parameters, blood pressure, and biochemical markers were measured using standard procedures. Results The study included 195 pregnant women. The prevalence of EPO was 31.28% (95%CI: 24.85–38.30) associated with age (OR: 1.17; 95%CI: 1.07–1.27; p = 0.0002) and dietary habits including regular consumption of raw vegetables at least 1 day a week (OR: 0.25; 95%CI: 0.10–0.62; p = 0.003). EPO significantly affects the blood level of HDL cholesterol in participants, with a significantly lower ( p = 0.039) concentration in participants with EPO (42.42 ± 25.30 mg/dL) than in normal weight (58.22 ± 43.97 mg/dL) or overweight (55.88 ± 38.64 mg/dL) participants. Simple linear models show a decrease of 1.18 mg/dL in HDL cholesterol concentration with an increase of 1 kg/m 2 in Early Pregnancy Body Mass Index (EPB): ( b = −1.18; p = 0.02) and a decrease in the overall weight gain with EPB ( b = −0.16; p = 0.01). Conclusion The prevalence of EPO was 31.28% (95%CI: 24.85–38.30), associated with age and dietary habits. It significantly affects the concentration of HDL cholesterol and the weight gain during the preterm period.

To investigate differences in body composition among female college students with varying BF% using DEXA, and to explore its potential implications for early obesity risk identification and targeted clinical intervention. A total 80 participants were divided into three groups according to BF% degrees: mild obesity group (BF% 30%-35%, N = 14), moderate obesity group (BF% 35%-40%, N = 38), and severe obesity group (BF% > 40%, N = 28). DEXA was used to assess body composition distribution in female college students with differing degrees of obesity. Within the cohort of female college students. With mild, moderate, and severe obesity groups, significant differences were observed in TFM, A/G, Android %fat, Gynoid %fat, AFM, GFM, VFA, VFM, VFV, SFA, SFM, and SFV (P < 0.05). These indicators showed an increasing trend from the mild obesity group to the moderate obesity group to the severe obesity group (P < 0.05). No significant changes were seen in TLM among the groups (P > 0.05). This study shows that BF% is a reliable and accurate measure for evaluating and classifying female obesity. As BF% degrees rise (mild, moderate, and severe obesity group), fat accumulation in specific areas significantly increases, while lean tissue shows no significant changes. The characteristics of alterations in body composition may adversely affect the general health of female college students.

The relationship between adipokine meteorin-like protein (Metrnl) and postprandial hypertriglyceridemia (PHTG) in overweight and obese populations remains unclear. This study examined the association between serum Metrnl and PHTG with normal fasting lipid profiles, using a standardized oral fat tolerance test (OFTT) to classify fat tolerance. The aim was to explore potential therapeutic targets for early obesity intervention. We enrolled 105 adults with normal fasting lipid profiles who met Chinese lipid management criteria for low-risk atherosclerotic cardiovascular disease (ASCVD) prevention. Participants were grouped as control (CON), overweight (OW), or obese (OB). All underwent an OFTT, with venous blood collected fasting serum Metrnl, total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), fasting insulin (FINS). Venous blood samples were collected at 1, 2, 3, and 4 hours postprandially to quantitatively analyze the dynamic changes in serum lipid profiles. Serum Metrnl showed a significant negative correlation with PHTG (r = -0.473, P < 0.001), fasting TG (r = -0.370, P < 0.001), FINS (r = -0.261, P = 0.007). Multivariate regression identified fasting TG as a risk factor for PHTG. Each 0.1 mmol/L increment in fasting triglycerides was significantly associated with a 76.9% higher risk of PHTG. Metrnl was identified as protective (OR = 0.211, P<0.001), the protective cutoff for Metrnl was 2.11ng/ml. A combined model of fasting TG and Metrnl improved PHTG prediction over fasting TG or Metrnl alone, with ROC analysis showing an AUC of 0.908, sensitivity of 82.7%, and specificity of 90.6%. Overweight and obese adults with normal fasting lipid profiles are at high risk of PHTG. Low serum Metrnl is closely associated with early lipid abnormalities and insulin resistance. Combining Metrnl with TG enhances diagnostic accuracy for PHTG.

Obesity is a multifactorial condition and represents a major public health issue. In 5% of cases, obesity is monogenic, secondary to an abnormality in a gene of the leptin-melanocortin signaling pathway. The aim of our retro-prospective descriptive study is to reclassify heterozygous variants of unknown significance (VUS) and to describe the clinical and biological phenotypes of the patients carrying these variants. Our study population included adult and pediatric patients followed in the Hospices Civils de Lyon for severe obesity, with a heterozygous probably pathogenic variant or a variant of unknown significance on a specific gene of interest identified by genetic analysis between January 2018 and December 2022. Reclassification of variants was based on family segregation and the recent literature data. The data concerning medical history, phenotypic characteristics, and biological results were extracted from medical files. Twenty-six patients underwent family segregation analysis: 10 patients were identified as carriers of a heterozygous probably pathogenic variant or VUS with a positive segregation. All patients had early-onset obesity at a mean age of 2.8 years. Our study highlights the clinical relevance of family segregation in reclassifying VUS within the leptin-melanocortin pathway and underscores the diagnostic value of early obesity onset in identifying potential monogenic forms.

Gut microbiota composition and derived enterotypes are associated with ponderal status in preschool children. Childhood obesity risk assessment longitudinal study (CORALS) cohort.

Radish sprouts (Raphanus sativus L.) are rich in dietary fibers and phytochemicals with antioxidant and anti-inflammatory activities. However, their whole-food effects on the gut-brain axis remain poorly defined. This study examined the preventive potential of whole-food red radish sprout (RS) powder against high-fat diet (HFD)-induced obesity and cognitive decline in mice, focusing on its effects on barrier integrity, inflammation, oxidative stress, and gut microbiota. Male C57BL/6 mice were fed an HFD for 16weeks with or without RS powder (low or high dose). Assessments included body and tissue indices, oral glucose tolerance, serum leptin, cognitive performance, oxidative stress in brain, gene expression of tight junction and inflammatory markers in colon and brain, and fecal microbiota profiling using 16S rRNA sequencing. RS supplementation attenuated HFD-induced weight gain, improved glucose tolerance, and reduced leptin levels, with stronger effects at the higher dose. Cognitive deficits were rescued by RS, accompanied by alleviation of brain oxidative stress and reduced expression of neuroinflammatory genes (Tnf, Il6, Il1b, Aif1, Gfap). RS restored tight-junction genes (Tjp1, Ocln, Cldn1, Jam2, Cdh5) while simultaneously decreasing Cldn2 and pro-inflammatory transcripts, and upregulating Il10. Although alpha diversity was unchanged, beta diversity differed significantly; RS reduced the Firmicutes/Bacteroidota ratio, enriched Akkermansia and Lactobacillus, and suppressed Oscillibacter and Desulfovibrio. Whole-food RS powder prevents HFD-induced obesity and cognitive decline by reinforcing barrier integrity, reducing inflammation and oxidative stress, and reshaping gut microbiota. These findings support RS as a practical functional food for early obesity intervention via gut-brain axis regulation.

Many investigations have indicated the significance of microRNAs (miRNAs) as potential biomarkers for early obesity in children. MiR-874-3p was revealed to be downregulated in overweight/obese children. However, the specific function and mechanism of miR-874-3p in the progression of childhood obesity remain unclear. Human Simpson-Golabi-Behmel syndrome (SGBS) adipocytes were stimulated with tumor necrosis factor α (TNF-α) to establish an in vitro cell model. CCK-8 assay and ELISA were used to assess cell viability and proinflammatory cytokine secretion, respectively. RT-qPCR was used for miR-874-3p expression analysis. Western blotting was utilized to evaluate protein levels of miR-874-3p downstream targets and nuclear factor kappa B (NF-κB) signaling-related markers. Luciferase reporter assay was conducted to verify the binding relation between miR-874-3p and nucleolin (NCL). MiR-874-3p overexpression attenuated TNF-α-induced inhibition of cell viability and promotion of proinflammatory cytokine production. Mechanistically, NCL served as a target of miR-874-3p, and overexpressing miR-874-3p inactivated NCL-mediated NF-κB signaling. Moreover, NCL upregulation reversed miR-874-3p overexpression-mediated effects on the viability and proinflammatory cytokines in SGBS adipocytes. MiR-874-3p alleviates TNF-α-induced inflammatory response in SGBS adipocytes by downregulating NCL and inactivating NF-κB signaling.

The global prevalence of obesity continues to rise, with gut microbiota implicated as a key environmental factor in its development. However, microbial heterogeneity across BMI categories and its potential as an early diagnostic marker remain poorly understood. Here, we systematically compared the gut microbiota of adults with normal weight, overweight, and obesity, and evaluated the diagnostic utility of integrated microbial and clinical indicators. In this study, a cohort of 214 participants was recruited and categorized into three groups based on BMI: normal weight (Nor, n = 85), overweight (Ow, n = 91), and obesity (Ob, n = 38). The gut microbiota was analyzed using 16S rRNA sequencing, which facilitated the assessment of α- and β-diversity, the identification of differentially abundant bacterial genera, and the evaluation of Spearman correlations with clinical indicators. Additionally, a diagnostic model was developed utilizing random forest, Least Absolute Shrinkage and Selection Operator (LASSO) regression and receiver operating characteristic (ROC) curve analysis. Clinical data showed no significant age differences among groups (p > 0.05), but the Ob group had markedly higher weight, BMI, total cholesterol, triglycerides, and uric acid levels (p < 0.001). Microbial analysis revealed reduced alpha diversity (Shannon index) in the Ob group and distinct microbial community structures among groups (PCoA, p < 0.001). LEfSe analysis showed enrichment of Escherichia-Shigella, Lactobacillus, and Parabacteroides in the Ob group, while Faecalibacterium, Enterobacter, and Agathobacter were predominant in the Nor group. The Ow group exhibited intermediate or specific enrichment, particularly in Ruminococcus gnavus group, Morganella, and Clostridium innocuum group. Correlation analysis indicated that bacteria abundant in the Nor group negatively correlated with BMI, TG, LDL-C, and positively with HDL-C, whereas those enriched in the Ow and Ob groups showed opposite trends. Four genera differentiated Ob from Ow individuals (AUC = 0.684), eight distinguished Ob from Nor (AUC = 0.787), and five separated Ow from Nor (AUC = 0.721). Integrating microbial and clinical data notably improved classification, with AUCs increasing to 0.908, 0.969, and 0.995, respectively. Intestinal microecological profiles vary significantly across BMI categories, and a model combining microbiota with metabolic markers shows strong potential for early obesity detection.

Using waist-to-height ratio to detect early central obesity in school-aged adolescents