Journal of Obesity最新文献

Background: Obesity is a complex multifactorial disease that has been associated with higher morbidity and mortality. Objectives: This study aimed to compare changes in body mass index (BMI) and obesity prevalence between two cross-sectional samples of Brazilian women. Furthermore, retrospective assessments of lifetime body weight changes were explored. Methods: Two independent population-based cross-sectional surveys were conducted in 2003 (first survey) and 2015 (second survey) with women living in the urban area city in southern Brazil. Both surveys had a similar design and included 981 women aged 20-60 years. Mean BMI and the presence of obesity (BMI ≥ 30 kg/m²) were estimated. Additionally, lifetime body weight change was obtained for the retrospective longitudinal assessment. Results: After 12 years, there was a significant increase from 25.9 ± 5.3 kg/m² to 28.1 ± 6.2 kg/m² in mean BMI. Between 2003 and 2015, the prevalence of obesity increased by 73% (18.0%; 95% CI: 15.8-20.6 vs. 31.2%; 95% CI: 28.3-34.1; p < 0.001). The means of estimated cumulative body weight gain from 15 to 50 years were 15.2 kg (95% CI: 13.3-17.1) and 17.2 kg (95% CI: 15.5-18.9) in 2003 and 2015, respectively; the greater cumulative difference between the two periods was observed at 40 years of age (3.3 kg). Conclusions: There was a significant increase in the mean BMI and prevalence of obesity between 2003 and 2015. Moreover, women experienced higher body weight gain during their lives in both survey periods, mainly in early adulthood.

Overweight and obesity are linked to the severity of infections and the development of chronic conditions among children and adolescents in Ghana. Hence, estimating the current prevalence and its determinants is imperative to guide public health interventions. This review mapped evidence on the prevalence and determinants of overweight and obesity among in-school children and adolescents (aged 5-19 years) in Ghana. Three main databases (PubMed, Central, and JSTOR) were searched for studies conducted in Ghana. Also, the study included only studies published online between 2010 and 2022. The search produced 1214 records, with an additional 23 identified through a search conducted in Google, Google Scholar, the WHO library, HINARI, and institutional repositories. After a thorough screening, 24 records were synthesized. The prevalence of overweight/obesity among the 23,663 in-school children and adolescents in Ghana was 0.5%-47.06%. Females have higher odds of being overweight than males. In addition, lack of nutrition and physical activity (PA) knowledge and low participation in school sports and physical activities exposed in-school children and adolescents in Ghana to overweight and obesity. Consumption of unhealthy foods, late bed, smoking, loneliness, watching television, and playing computer games exposed schoolchildren and adolescents in Ghana to overweight and obesity. There are relatively high levels of overweight and obesity among school-going children and adolescents in Ghana. Addressing sex gaps in PA, ensuring healthy eating, and limiting sedentary lifestyles is the surest way to promote healthy weight among in-school children and adolescents in Ghana.

Objective: Genetic variability significantly impacts metabolism, weight gain, and feeding behaviors, predisposing individuals to obesity. This study explored how variations in key genes related to obesity-FOXO3A (forkhead box O3), AMPK (protein kinase AMP-activated), and POMC (proopiomelanocortin)-are associated with extreme obesity (EOB). Methods: We conducted a case-control study with 251 EOB patients and 212 healthy controls with a body mass index (BMI) of less than 25 kg/m². We genotyped 10 single nucleotide variants (SNVs) using TaqMan-based assays. Results: Four SNVs-rs1536057 in FOXO3A, rs103685 in AMPK, rs934778, and rs6545975 in POMC-were associated with an increased risk of EOB. The strongest association was observed with rs934778 (POMC), which had a maximum odds ratio (OR) of 5.26 (95% CI: 2.86-9.09). While these genetic variations are closely linked to EOB, they do not affect serum glucose, triglycerides, HDL, LDL, BMI, or waist circumference. Conclusions: These findings indicate that factors beyond traditional metabolic pathways, potentially related to feeding behavior or hormonal regulation, may also link these genetic variations to obesity. Further research in a larger sample is essential to validate these findings and explore their potential to guide clinical interventions and public health strategies.

Background: Visceral adipose tissue (VAT) abnormalities are directly associated with obesity-associated disorders. The underlying mechanisms that confer increased pathological risk to VAT in obesity have not been fully described. Methods: A case-control study was conducted that included 10 women with obesity (36.80 ± 7.39 years, BMI ≥ 30 kg/m²) and 10 women of normal weight (32.70 ± 9.45 years, BMI < 24.9 kg/m²). RNA was extracted from greater omentum biopsies, and, using a DNA microarray, differential transcriptomic expression of VAT in women with obesity was evaluated taking as a reference that of women with normal weight. The differentially expressed genes (DEGs) were classified into functional biological processes and signaling pathways; moreover, the protein-protein interaction (PPI) networks were integrated for a deeper analysis of the pathways and genes involved in the central obesity-associated disorders. The expression of TNF-α, MAPK, and AKT proteins was also quantified in VAT. Results: The VAT of women with obesity had 3808 DEGs, mainly associated with the cellular process of inflammation and carbohydrates and lipid metabolism. Overexpressed genes were associated with inflammatory, metabolic, hormonal, neuroendocrine, carcinogenic, and infectious pathways. Cellular processes related to addictive behaviors were notable. MAPK and PI3K-AKT pathways were overexpressed, and Mapk1 and Akt3 genes were common crossing points among obesity-associated disorders' pathways. The increased expression of MAPK, AKT, and TNF proteins was confirmed in the VAT of women with obesity. Conclusion: VAT confers a complex and blended pathogenic transcriptomic profile in obese patients, where abnormal processes are mainly controlled by activating intracellular signaling pathways that exhibit a high degree of redundancy. Identifying shared cross points between those pathways could allow specific targeting treatments to exert a widespread effect over multiple pathogenic processes.

Objective: The importance of early microbial dysbiosis in later development of obesity and metabolic disorders has been a subject of debate. Here we tested cause and effect in mice.

Methods: Germ-free male Swiss Webster mice were colonized in a specific-pathogen-free (SPF) facility at 1 week (1W) and 3 weeks (3W) of age. They were challenged with a high-fat diet and their responses were compared with SPF mice. Gut microbiota was analyzed by 16S rRNA gene sequencing. Moreover, RNA sequencing of the liver was performed on additional 3W and SPF mice on a regular chow diet.

Results: There were no significant differences in weight, food consumption, epididymal fat weight, HbA1c levels, and serum insulin and leptin, whereas the early germ-free period resulted in mice with impaired glucose tolerance. Both the 1W and 3W group peaked 56% (p < 0.05) and 66% (p < 0.01) higher in blood glucose than the SPF control group, respectively. This was accompanied by a 45% reduction in the level of the anti-inflammatory cytokine IL-10 in the 1W mice (p < 0.05). There were no differences in the gut microbiota between the groups, indicating that all mice colonized fully after the germ-free period. Marked effects on hepatic gene expression (728 differentially expressed genes with adjusted p < 0.05 and a fold change ± 1.5) suggested a potential predisposition to a higher risk of developing insulin resistance in the 3W group.

Conclusions: Lack of microbes early in life had no impact on adiposity but led to insulin resistance and altered liver gene expression related to glucose metabolism in mice. The study strongly supports the notion that microbial signaling to the liver in the beginning of life can alter the host's risk of developing metabolic disorder later in life.

Objective: Obesity, chronic inflammation, and oxidative stress can influence mitochondrial DNA (mtDNA) content. Our objective was to evaluate the oxidation level and content of mtDNA and its relationship with metabolic parameters in metabolically healthy obese (MHO) compared to metabolically unhealthy obese (MUO) and normal weight (NW) controls.

Materials and methods: We studied 94 NW, 95 MHO, and 97 MUO individuals between 18 and 80 years old. Relative mtDNA content and mtDNA oxidation level (8-oxoguanine, 8-OxoG) were determined in peripheral blood leukocytes by the SYBR Green method of real-time PCR. One-way ANOVA and Tukey test were used to compare biochemical, clinical, and anthropometric characteristics, as well as mtDNA content and 8-OxoG.

Results: A progressive decrease in mtDNA content was observed between NW, MHO, and MUO with significant differences in MUO vs. NW (p: 0.04). An increase in 8-OxoG was observed in MUO patients compared to the other groups (MUO vs. MHO p: 0.01; MUO vs. NW p: 0.04). mtDNA content was directly correlated with HDL-c (p < 0.01) and inversely with waist circumference (p: 0.01) and LDL-c (p: 0.05). mtDNA content decreased, and the oxidation level increased concomitantly with the presence of obesity, the number of MS components, higher coronary risk, and insulin resistance parameters.

Conclusion: MHO presented a similar mtDNA oxidation level to NW and mtDNA content to the MUO, placing the MHO individuals as having an intermediate phenotype. Changes in mtDNA content and oxidation were correlated to the lipid profile related to obesity and/or MS presence, probably associated with oxidative stress and chronic low-grade inflammation.

Obesity is a complex chronic disease characterized by excess body fat (adipose) that is harmful to health and has been a major global health problem. It may be associated with several diseases, such as nonalcoholic fatty liver disease (NAFLD). Polyunsaturated fatty acids (PUFA) are lipid mediators that have anti-inflammatory characteristics and can be found in animals and plants, with capybara oil (CO) being a promising source. So, we intend to evaluate the hepatic pathophysiological alterations in C57Bl/6 mice with NAFLD, caused by obesity, and the possible beneficial effects of OC in the treatment of this disease. Eighteen 3-month-old male C57Bl/6 mice received a control or high-fat diet for 18 weeks. From the 15th to the 18th week, the animals received treatment-through orogastric gavage-with placebo or free capybara oil (5 g/kg). Parameters inherent to body mass, glucose tolerance, evaluation of liver enzymes, percentage of hepatic steatosis, oxidative stress, the process of cell death with the apoptotic biomarkers (Bax, Bcl2, and Cytochrome C), and the ultrastructure of hepatocytes were analyzed. Even though the treatment with CO was not able to disassemble the effects on the physiological parameters, it proved to be beneficial in reversing the morphological and ultrastructural damage present in the hepatocytes. Thus, demonstrating that CO has beneficial effects in reducing steatosis and the apoptotic pathway, it is a promising treatment for NAFLD.