Journal of Obesity & Metabolic Syndrome最新文献

The global obesity epidemic underscores the urgent need to elucidate the mechanisms underlying metabolic disorders. Although excessive caloric intake and sedentary lifestyles have traditionally been viewed as primary contributors, recent evidence highlights significant roles for genetic, environmental, and immunological factors. Notably, dysfunction within the central nervous system (CNS), particularly the hypothalamus, has emerged as a crucial regulator of metabolic homeostasis through CNS-peripheral interactions. Hypothalamic inflammation is primarily mediated by microgliosis, which disrupts systemic homeostasis. This review discusses the detrimental effects of hypothalamic microgliosis on energy metabolism and highlights emerging evidence suggesting paradoxically beneficial roles of hypothalamic microgliosis in metabolic regulation. Within adipose tissue, immune cells, including adipose tissue macrophages (ATMs), T cells, and B cells, exert significant influence over systemic metabolism. Short-term activation of the sympathetic nervous system (SNS) promotes the anti-inflammatory polarization of ATMs and enhances the induction of regulatory T cells; thereby, improving insulin sensitivity. In contrast, chronic SNS activation may exacerbate inflammation due to β-adrenergic receptor desensitization and catecholamine resistance. Parasympathetic acetylcholine signaling is also known to suppress inflammation through activation of α7 nicotinic receptors on macrophages; however, parasympathetic innervation within white adipose tissue is considerably limited. Despite the critical role of the nervous system in systemic metabolism, comprehensive insight into neuro-immune interactions remains lacking. In-depth studies using advanced technologies are needed to deepen knowledge in this field and to cover novel therapeutic targets for obesity and related metabolic disorders.

The arcuate nucleus of the hypothalamus is arguably the most important nucleus for regulating energy homeostasis and metabolism. Since its initial description in the human brain, its function in metabolic regulation has been studied extensively. Key neuronal populations such as agouti-related peptide and pro-opiomelanocortin neurons have been discovered to play critical roles in feeding and body weight regulation. Recent studies have started to reveal the functional significance of other neuronal populations, especially those that promote feeding (orexigenic neurons). In this review, we discuss the history and key findings of the arcuate nucleus, with a focus on orexigenic neurons. We also highlight current challenges and knowledge gaps that remain to be addressed in future studies.

Background: To assess cardiorespiratory efficiency in obese adults, two exercise test treadmill protocols with 2- or 3-minute stages were compared.

Methods: Thirty-six obese adult subjects were involved in this study. Sixteen men (age 51.5±10.5 years; body mass index [BMI] 36.7±4.8 kg/m²) and 20 women (age 42.4±12.4 years; BMI 36.5±4.7 kg/m²) performed submaximal incremental graded tests on treadmills with 2- or 3-minute stages on different days. During each testing session, heart rate (HR), oxygen uptake (VO₂ mL/min/kg), rate of perceived exertion (RPE), fat oxidation (FO) at maximal fat oxidation (MFO), and maximal fat oxidation zone (Fatmax zone) were measured.

Results: No differences were found for HR, VO₂, and RPE at MFO between the two protocols. Significant differences (2-minute vs. 3-minute) were found for FO (576.3±162.9 mg/min vs. 506.0±148.1 mg/min respectively; P<0.05) at MFO between the two protocols. No differences were found for VO₂ and HR in high and low Fat_max zone borders. Moreover, a difference was found for FO at the low and high borders.

Conclusion: Exercise intensity at which the MFO and Fat_max zone occur is not influenced by the duration of stage-to-stage increments. The two exercise testing protocols could be considered interchangeable to assess HR, VO₂, and RPE at MFO.

Background: This study examined the association of soy foods consumption with obesity in Korean adults.

Methods: Data on 131,477 adults (47,828 men and 83,649 women) were selected from the Korean Genome and Epidemiology Study-Health Examinees study. Consumption of soy foods was estimated using a food frequency questionnaire based on classes of non-fermented soy foods or fermented soy paste. General obesity was defined as a body mass index ≥25 kg/m² and abdominal obesity as a waist circumference ≥90 cm in men and ≥85 cm in women. The association of soy foods consumption with obesity was examined using multiple logistic regression.

Results: Greater consumption of non-fermented soy foods was inversely associated with abdominal obesity in both men and women (≥7 servings/week vs. non-consumers: odds ratio [OR], 0.71; 95% confidence interval [CI], 0.57 to 0.87; P for trend=0.001 in men; OR, 0.82; 95% CI, 0.70 to 0.94; P for trend <0.001 in women). Among non-fermented soy foods, higher consumption of legumes was inversely associated with general and abdominal obesity in women. Consumption of tofu or soymilk was inversely associated with obesity in both men and women. Higher consumption of fermented soy paste was associated with a reduced OR for general obesity in men and increased OR for abdominal obesity in women. The inverse association between non-fermented soy foods consumption and obesity was more prominent in postmenopausal women.

Conclusion: Greater consumption of non-fermented soy foods is inversely associated with obesity in Korean adults. Further cohort studies are needed to confirm the relationship between soy foods consumption and obesity.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is a prevalent liver disorder globally, including in Asia-Pacific countries. In addition to contributing to severe liver disorders, MASLD increases the risk of various complications. Currently, resmetirom is the only U.S. Food and Drug Administration-approved treatment for MASLD-related fibrosis in the United States. Therefore, lifestyle modifications, particularly regular exercise, remain a crucial approach in managing MASLD. Exercise is generally classified into two types: aerobic and resistance. The two forms offer benefits for individuals with MASLD, despite the difference between their effects and underlying mechanisms. Aerobic exercise is accessible, low cost, and promotes high energy expenditure, improving several MASLD-related clinical parameters. However, associated fatigue and discomfort can reduce long-term adherence. Resistance exercise, referring to muscle contractions performed to counteract external resistance, enhances muscle strength, muscle mass, and bone mineral density while also helping to correct metabolic derangement. It is especially suitable for subjects with MASLD who cannot conduct aerobic exercise or have poor cardiorespiratory function. Mechanistically, aerobic exercise enhances insulin sensitivity, while resistance exercise improves metabolic flexibility through adenosine monophosphate-activated protein kinase activation, muscle fiber adaptation, and muscle-liver cross-talk. In terms of aerobic training, traditional moderate-intensity continuous training (MICT) and high-intensity interval training (HIIT) have shown comparable benefits. This review is designed to offer refreshed perspectives on the advantages of exercise, compare the effects and mechanisms of aerobic and resistance exercise, and evaluate the advantages and disadvantages of MICT and HIIT, with emphasis on their impact on hepatic steatosis in subjects with MASLD.

Background: Obesity causes metabolic dysregulation and contributes to diseases, and autophagy plays a pivotal role in that process. In mice, autophagy, a cellular recycling mechanism, is influenced by factors beyond obesity, including caloric restriction (CR) and CR combined with voluntary wheel running (CR+Ex). However, the regulation of autophagy in skeletal muscle during obesity, CR, and CR+Ex remains poorly understood.

Methods: Mice (n=42) were randomly divided into six groups: normal diet, normal diet CR, normal diet CR+Ex, high-fat diet, high-fat diet CR, and high-fat diet CR+Ex. All mice were fed ad libitum with either a normal or high-fat diet for the first 4 months, followed by the respective interventions for the subsequent 4 months. Body composition, motor function, and autophagy signaling were assessed.

Results: Obesity resulted in increased total mass, lean mass, fat mass, and fat percentage in tissue and decreased grip strength and endurance capacity. Notably, CR+Ex reduced total mass, lean mass, and fat mass in obese mice. In both the normal and obese conditions, the expression of the autophagy markers p62, light chain 3B (LC3B)-I, and LC3B-II was significantly higher in red muscle than white muscle. Obesity led to a reduction in cathepsin L expression, and CR further increased LC3B-I expression in red muscle.

Conclusion: CR+Ex was an effective strategy for counteracting the adverse changes in body composition associated with obesity. Compared with red muscle, white muscle exhibits lower autophagy-related protein levels and might require elevated cathepsin L expression to mitigate the negative effects of obesity.

Metabolic dysfunction-associated steatotic liver disease (MASLD), previously known as non-alcoholic fatty liver disease, is one of the most common causes of liver dysfunction worldwide, posing a significant economic burden. However, our understanding of the cellular and molecular mechanisms underlying the pathogenesis of MASLD is in its early stages. Over the last two decades, epigenetic mechanisms and autophagy have emerged as two independent phenomena that control cellular and molecular processes in health and disease. Epigenetic events and defects in autophagy have been linked with the pathogenesis of MASLD and metabolic dysfunction-associated steatohepatitis (MASH) in cellular studies, mouse models, and human research. However, the connection between epigenetic mechanisms and autophagy regulation in MASLD and MASH pathogenesis remains unclear. This review highlights the importance of epigenetic modifications and their regulatory switches in controlling downstream pathways that significantly impact metabolic disease pathogenesis. We also review the need to identify key epigenetic factors regulating autophagy in MASLD and MASH pathogenesis. Such insights could aid the development of novel strategies to restore autophagy and improve disease outcomes.