Journal of Obesity & Metabolic Syndrome最新文献

Obesity is a major global health concern, with diet playing a crucial role in its development and treatment. Ultra-processed foods (UPFs) have become prevalent in diets due to changes in the food environment. These foods are energy-dense; high in fat, sugars, or salt; and low in fiber, protein, vitamins, and minerals, raising concerns about their effects on health. In addition to traditional research focused on nutrients, food, and dietary quality, growing evidence has linked UPF consumption to obesity. Therefore, this study provides a comprehensive review of the levels and trends of UPF consumption, current epidemiological evidence on the association between UPF consumption and obesity, and UPFs' potential role in the etiology of obesity and weight gain. Additionally, this study reviews strategies for reducing UPF consumption and outlines future studies of the link between UPF consumption and obesity.

Background: Pediatric obesity is a global public health concern. South Korea is witnessing a notable increase in obesity rates among children and adolescents, despite various governmental interventions. Parents play a crucial role in preventing and managing pediatric obesity, as they are typically the primary observers of their child's weight and daily habits.

Methods: This study involved 10 parents of overweight or obese children and adolescents in South Korea, identified from a 2023 Student Health Examination. Focus group interviews were conducted to explore participants' experiences, followed by a rigorous qualitative content analysis of the data.

Results: The analysis revealed one main theme, parental roles and challenges in managing pediatric obesity, that encompassed five categories: parental awareness and perception of pediatric obesity; causes of pediatric obesity; parental strategies for managing obesity; barriers to management; and support systems and resources. Parental recognition of their child's obesity was predominantly initiated through student health examinations at school, and the cause of obesity was multifactorial. Parents use various strategies, such as dietary changes and exercise promotion, but face barriers, including stigma and resource constraints. Parents demand comprehensive support from schools, healthcare providers, and community programs to effectively manage obesity.

Conclusion: These findings highlight the need for tailored interventions to address parents' specific obstacles in managing pediatric obesity. Enhancing parental awareness, providing clear information, and strengthening support systems are essential for preventing and managing pediatric obesity in South Korea.

Mendelian randomization (MR) is a statistical method that uses genetic variants as instrumental variables to estimate the causal effect of exposure on an outcome in the presence of unmeasured confounding. In this review, we argue that it is crucial to acknowledge the instrumental variable assumptions in MR analysis. We describe widely used MR methods, using an example from obesity-related metabolic disorders. We describe situations in which instrumental variable assumptions are violated and explain how to evaluate these violations and employ robust methods for accommodating such violations.

The worldwide prevalence of obesity is a key factor involved in the epidemic proportions reached by chronic societal diseases. A revolution in the study of obesity has been the development of imaging techniques for the measurement of its regional distribution. These imaging studies have consistently reported that individuals with an excess of visceral adipose tissue (VAT) were those characterized by the highest cardiometabolic risk. Excess VAT has also been found to be accompanied by ectopic fat deposition. It is proposed that subcutaneous versus visceral obesity can be considered as two extremes of a continuum of adiposity phenotypes with cardiometabolic risk ranging from low to high. The heterogeneity of obesity phenotypes represents a clinical challenge to the evaluation of cardiometabolic risk associated with a given body mass index (BMI). Simple tools can be used to better appreciate its heterogeneity. Measuring waist circumference is a relevant step to characterize fat distribution. Another important modulator of cardiometabolic risk is cardiorespiratory fitness. Individuals with a high level of cardiorespiratory fitness are characterized by a lower accumulation of VAT compared to those with poor fitness. Diet quality and level of physical activity are also key behaviors that substantially modulate cardiometabolic risk. It is proposed that it is no longer acceptable to assess the health risk of obesity using the BMI alone. In the context of personalized medicine, precision lifestyle medicine should be applied to the field of obesity, which should rather be referred to as 'obesities.'

Background: Whether there is a causal relationship between childhood obesity and increased risk of chronic kidney disease (CKD) remains controversial. This study sought to explore how body size in childhood and adulthood independently affects CKD risk in later life using a Mendelian randomization (MR) approach.

Methods: Univariate and multivariate MR was used to estimate total and independent effects of body size exposures. Genetic associations with early-life and adult body size were obtained from a genome-wide association study of 453,169 participants in the U.K. Biobank, and genetic associations with CKD were obtained from the CKDGen and FinnGen consortia.

Results: A larger genetically predicted early-life body size was associated with an increased risk of CKD (odds ratio [OR], 1.27; 95% confidence interval [CI], 1.14 to 1.41; P=1.70E-05) and increased blood urea nitrogen (BUN) levels (β=0.010; 95% CI, 0.005 to 0.021; P=0.001). However, the association between the impact of early-life body size on CKD (OR, 1.12; 95% CI, 0.95 to 1.31; P=0.173) and BUN level (β=0.001; 95% CI, -0.010 to 0.012; P=0.853) did not remain statistically significant after adjustment for adult body size. Larger genetically predicted adult body size was associated with an increased risk of CKD (OR, 1.37; 95% CI, 1.21 to 1.54; P=4.60E-07), decreased estimated glomerular filtration rate (β=-0.011; 95% CI, -0.017 to -0.006; P=5.79E-05), and increased BUN level (β=0.010; 95% CI, 0.002 to 0.019; P=0.018).

Conclusion: Our research indicates that the significant correlation between early-life body size and CKD risk is likely due to maintaining a large body size into adulthood.

Background: Although the presence of both obesity and reduced muscle mass presents a dual metabolic burden and additively has a negative effect on a variety of cardiometabolic parameters, data regarding the associations between their combined effects and left ventricular diastolic function are limited. This study investigated the association between the ratio of skeletal muscle mass to visceral fat area (SVR) and left ventricular diastolic dysfunction (LVDD) in patients with preserved ejection fraction using random forest machine learning.

Methods: In total, 1,070 participants with preserved left ventricular ejection fraction who underwent comprehensive health examinations, including transthoracic echocardiography and bioimpedance body composition analysis, were enrolled. SVR was calculated as an index of sarcopenic obesity by dividing the appendicular skeletal muscle mass by the visceral fat area.

Results: In the random forest model, age and SVR were the most powerful predictors of LVDD. Multivariate logistic regression analysis demonstrated that older age (adjusted odds ratio [OR], 1.11; 95% confidence interval [CI], 1.07 to 1.15) and lower SVR (adjusted OR, 0.08; 95% CI, 0.01 to 0.57) were independent risk factors for LVDD. SVR showed a significant improvement in predictive performance and fair predictability for LVDD, with the highest area under the curve noted in both men and women, with statistical significance. In non-obese and metabolically healthy individuals, the lowest SVR tertile was associated with a greater risk of LVDD compared to the highest SVR tertile.

Conclusion: Decreased muscle mass and increased visceral fat were significantly associated with LVDD compared to obesity, body fat composition, and body muscle composition indices.

Background: Although an appropriate weight management strategy is essential for obese individuals, weight loss can have adverse effects on bone mineral density (BMD). We conducted a systematic review of randomized controlled trials to evaluate changes in BMD after the implementation of various weight loss strategies.

Methods: The PubMed, Embase, Web of Science, and Cochrane Library databases were searched to find articles published from database inception until June 2023. Randomized controlled trials of various treatments for obese patients that reported changes in BMD were selected. The primary outcome was BMD of the whole body, lumbar spine, and total hip, measured using dual X-ray absorptiometry.

Results: Eighteen randomized controlled trials involving 2,510 participants with obesity were included in the analysis. At follow-up examination, the BMD of the lumbar spine decreased significantly after metabolic surgery (mean difference [MD]=-0.40 g/cm²; 95% confidence interval [CI], -0.73 to -0.07; I²=0%); lifestyle and pharmacological interventions did not result in a significant decrease in BMD at any location. Metabolic surgery also produced the most substantial difference in weight, with an MD of -3.14 (95% CI, -3.82 to -2.47).

Conclusion: This meta-analysis is the first to examine the effects of all categories of anti-obesity strategies, including the use of anti-obesity medications, on BMD. Bariatric metabolic surgery can have adverse effects on BMD. Moreover, medications can be used as a treatment for weight loss without compromising bone quality.

Diseases affecting adipose tissue (AT) function include obesity, lipodystrophy, and lipedema, among others. Both a lack of and excess AT are associated with increased risk for developing diseases including type 2 diabetes mellitus, hypertension, obstructive sleep apnea, and some types of cancer. However, individual risk of developing cardiometabolic and other 'obesity-related' diseases is not entirely determined by fat mass. Rather than excess fat accumulation, AT dysfunction may represent the mechanistic link between obesity and comorbid diseases. There are people who remain metabolically healthy despite obesity, whereas people with normal weight or very low subcutaneous AT mass may develop typically obesity-related diseases. AT dysfunction is characterized by adipocyte hypertrophy, impaired subcutaneous AT expandability (ectopic fat deposition), hypoxia, a variety of stress, inflammatory processes, and the release of proinflammatory, diabetogenic, and atherogenic signals. Genetic and environmental factors might contribute to AT heterogeneity either alone or via interaction with intrinsic biological factors. However, many questions remain regarding the mechanisms of AT dysfunction initiation and whether and how it could be reversed. Do AT signatures define clinically relevant subtypes of obesity? Is the cellular composition of AT associated with variation in obesity phenotypes? What roles do environmental compounds play in the manifestation of AT dysfunction? Answers to these and other questions may explain AT disease mechanisms and help to define strategies for improving AT health. This review focuses on recent advances in our understanding of AT biology.

While inflammation is a crucial response in injury repair and tissue regeneration, chronic inflammation is a prevalent feature in various chronic, non-communicable diseases such as obesity, diabetes, and cancer and in cardiovascular and neurodegenerative diseases. Long-term inflammation considerably affects disease prevalence, quality of life, and longevity. Our research indicates that the growth hormone/insulin-like growth factor 1 (GH/IGF-1) axis is a pivotal regulator of inflammation in some tissues, including the hypothalamus, which is a key player in systemic metabolism regulation. Moreover, the GH/IGF-1 axis is strongly linked to longevity, as GH- or GH receptor-deficient mice live approximately twice as long as wild-type animals and exhibit protection against aging-induced inflammation. Conversely, GH excess leads to increased neuroinflammation and reduced longevity. Our review studies the associations between the GH/IGF-1 axis, inflammation, and aging, with a particular focus on evidence suggesting that GH receptor signaling directly induces hypothalamic inflammation. This finding underscores the significant impact of changes in the GH axis on metabolism and on the predisposition to chronic, non-communicable diseases.