Obesity Reviews最新文献

Healthy food retail (HFR) interventions utilize marketing strategies (e.g., product availability, placement, pricing, and promotion) to create food outlet (e.g., grocery store, food service) environments that support consumers in making healthier food purchases. To ensure ongoing population health benefits, these strategies must be sustained over time. This systematic review aimed to explore the determinants of sustained HFR environment changes (e.g., sociopolitical context, retailer-related factors). Six databases were searched up to September 12, 2024. Eligible articles followed up on HFR environment changes for at least 2 years and identified factors influencing sustained HFR changes. Articles were thematically synthesized using the Integrated Sustainability Framework, and the findings for each construct were presented as frequency counts. Risk of bias was assessed using the Mixed Methods Appraisal Tool. Fifteen articles met the inclusion criteria, with studies undertaken in grocery stores or small stores (n = 8), school canteens (n = 3), healthcare settings (n = 2), and other settings (n = 2). The most common domains identified were “processes” (e.g., “fidelity, monitoring, and enforcement”) and “interorganizational factors” (e.g., “external partners, support, and resources”). Sustainment-related findings were often reported as secondary outcomes in study results, limiting the comprehensiveness of the review and highlighting the need for more long-term evaluation of HFR interventions.

Obesity is a primary driver of obstructive sleep apnea and contributes substantially to its associated cardiovascular morbidity and mortality. Although continuous positive airway pressure remains the standard treatment, its efficacy is often limited by suboptimal patient adherence and its impact on cardiovascular outcomes has yet to be consistently established in major clinical trials. Treatments aimed at the underlying problem, excess adiposity, are therefore needed. Weight loss, whether achieved through lifestyle interventions or bariatric surgery is well-known to improve obstructive sleep apnea. The recent introduction of highly effective weight loss medications, most notably incretin-based agents, now offers a pharmacological approach to accomplish the same result. Recent randomized controlled trials in patients with obesity demonstrated that these medications significantly decrease the apnea-hypopnea index and enhance oxygen saturation, with a significant proportion of disease remission. In light of these findings, we propose a therapeutic algorithm stratifying treatment according to symptoms and body mass index. For asymptomatic patients with obesity and obstructive sleep apnea, we suggest incretin-based therapy as a first-line option to concurrently address excessive weight and obstructive sleep apnea. Conversely, in individuals with impaired sleep-related quality of life combining continuous positive airway pressure and incretin therapy may be more appropriate, pairing immediate symptom control with longer-term weight loss. This integrated strategy, prioritizing weight management alongside symptom relief, may offer a comprehensive approach to treat obesity-related obstructive sleep apnea and decrease its associated cardiovascular risks.

A resurgence in glucagon research has repositioned this pancreatic hormone as a promising target in the treatment of obesity and related metabolic disorders. Glucagon is classically known for contributing to glucose homeostasis, but emerging evidence points to a much wider role in metabolism, including energy balance and liver health. These findings are fueling attempts to understand how to leverage glucagon signaling to treat obesity and metabolic dysfunction-associated steatohepatitis (MASH). Due to potential hyperglycemic effects of glucagon signaling, most investigational compounds are dual agonists of both the glucagon and glucagon-like peptide-1 (GLP-1) receptors to harness the antihyperglycemic and anorectic effects of the latter hormone, analogs of which such as semaglutide are already proven to be potent obesity medications. Glucagon receptor/GLP-1 receptor dual agonists reduce food intake, decrease hepatic fat, and increase energy expenditure in animal models of obesity and MASH. In early clinical trials, some dual agonists substantially reduced body weight, hepatic steatosis, and hepatic fibrosis. Whether they are more effective than GLP-1 receptor mono-agonists remains to be established in definitive head-to-head studies. The precise balance between glucagon and GLP-1 signaling within individual compounds appears important for overall therapeutic effects-including glycemic control, which worsened with some dual agonists. However, the two most clinically advanced compounds-mazdutide (approved for chronic weight management and type 2 diabetes in China) and survodutide (ongoing global phase 3 trials)-had potent weight-loss and antihyperglycemic effects in people with obesity, with survodutide also improving liver health in people with MASH. Therefore, the research into glucagon physiology that led to glucagon receptor/GLP-1 receptor dual agonists is translating to advantageous new therapies for the highly prevalent diseases of obesity and MASH.

Metabolic and bariatric surgery (MBS) is the most effective treatment for severe obesity, yet it remains profoundly underutilized. Patients seeking MBS face pretreatment requirements, including mandatory psychological evaluation, documented failed diet attempts, and months of lifestyle interventions that are substantially more extensive than those required for most common gastrointestinal procedures. These requirements were initially developed with patient safety in mind, but evidence has accumulated that many lack outcome-specific support and have become barriers to care, particularly as third-party payers have increasingly used them to restrict access. Meanwhile, potent obesity management medications (OMMs) are prescribed with relatively limited oversight, often to individuals with preclinical disease, at costs that raise questions about economic sustainability. The Lancet Diabetes & Endocrinology Commission's distinction between preclinical obesity (excess adiposity with preserved organ function) and clinical obesity (a systemic illness characterized by objective organ dysfunction or substantial limitations of daily activities) provides a framework for evaluating current treatment access patterns. A critical implication of this framework, which warrants further exploration, is that it may narrow the population for whom medical treatment is considered necessary: for individuals with preclinical obesity, excess adiposity represents a risk state requiring monitoring and evidence-based counseling, not generally an ongoing illness requiring pharmacotherapy or surgery. This paper examines whether the current pattern, relatively low barriers to expensive, chronic pharmacotherapy for preclinical or early-stage disease; relatively high barriers to durable, cost-effective surgery for established clinical obesity, represents a departure from severity-matched care that warrants systematic reconsideration.

Glucagon-like peptide-1 receptor agonists (GLP-1RAs) have emerged as pivotal agents in the treatment of type 2 diabetes (T2D) and obesity, with well-established metabolic and cardiovascular benefits that translate into improvement in quality of life and life expectancy. While a potential benefit may also be hypothesized in patients with metabolic disorders and malignancy, robust clinical evidence is still lacking. In recent years, attention has turned to their potential impact on cancer risk, although current evidence remains limited and, in some cases, conflicting. Several biological pathways, such as improvements in insulin sensitivity, reductions in chronic inflammation, modulation of cellular signaling, and changes in the tumor microenvironment, have been proposed as possible mechanisms through which GLP-1RAs might influence cancer development or progression. However, available data derive from preclinical or observational studies, and high-quality prospective clinical evidence is still lacking. While some reports suggest possible protective associations in specific cancer types, others raise concerns about potential risks, particularly in hormonally sensitive or receptor-expressing tissues. This position paper synthesizes available data on the oncologic safety and potential antitumor effects of GLP-1RAs, highlights key knowledge gaps, and discusses clinical implications, underscoring the need for further research to clarify their role in cancer prevention and treatment.

Introduction: The aim of this paper was to synthesize the evidence on the active components of behavioral weight reduction interventions delivered to individuals with overweight/obesity from vulnerable populations, including people with low socioeconomic position, ethnic minority status, older age, mental health issues, and rural residence.

Methods: A meta-review preregistered with the PROSPERO repository (number CRD42024532138) was conducted. Following the PRISMA guidelines for systematic reviews, seven electronic databases were searched, resulting in the inclusion of 37 reviews. The ROBIS tool was used to assess the risk of bias.

Results: Twelve behavior change techniques were identified as components of interventions that were effective in > 60% of trials targeting indicators of body weight reduction or physical activity improvements in vulnerable populations. For weight reduction-related indicators, goal setting, action planning, self-monitoring of behavior, self-monitoring of the outcome of behavior, instruction on how to perform the behavior, social comparison, prompts/cues, behavioral practice/rehearsal, and credible source were supported. For physical activity-related outcomes, social support (unspecified) and demonstration of the behavior were supported.

Conclusion: The results provide insights into behavior change techniques that may be prioritized in interventions aimed at weight reduction among adults from vulnerable populations.

Night shift workers are at higher risk of developing overweight and obesity. The disruption of the physiological circadian rhythm leads to metabolic alterations, such as decreased insulin sensitivity, increased adipogenesis, and inflammation, with effects on their health and leading, among other diseases, to obesity. Omics technologies represent novel investigation tools to understand in depth the biological mechanisms behind the circadian disruption and consequent effects on metabolism. The data obtained from the use of omics technologies in the field of transcriptomics, proteomics, metabolomics, and metagenomics reveal the involvement of molecular pathways in the circadian disruption due to shift work and give comprehensive insights into the most crucial molecules, such as clock genes, hormones, or microorganisms responsible for a downstream cascade effect. There is a clear need to further explore obesity risk in night shift workers through omics-based studies, particularly in human field studies. Many of the investigations so far have focused on animal models with simulated circadian disruption. Upcoming omics data can undoubtedly support the advancement toward a personalized approach that could protect the health of night shift workers. This review focuses on studies supported by omics technologies on circadian disruption and metabolic alterations leading to obesity or increasing its risk.

The distribution of adipose tissue is a key determinant of obesity-related disease risk. When the capacity of subcutaneous adipose tissue to safely store energy is exceeded, lipid overflow into visceral depots occurs, increasing free fatty acid flux, promoting insulin resistance, and triggering chronic low-grade inflammation. More than 80 years ago, the physician Jean Vague recognized the association between android (central) obesity and cardiometabolic disease; subsequent advances from imaging technologies have expanded this framework to include ectopic fat accumulation within non-adipose organs. Ectopic fat deposition in the liver, pancreas, heart, kidneys, skeletal muscle, and upper airway contributes to organ-specific dysfunction through mechanisms including lipotoxicity, adipokine dysregulation, oxidative stress, and local inflammatory signaling. This review summarizes the evidence linking visceral and ectopic fat to metabolic dysfunction-associated steatotic liver disease and steatohepatitis, type 2 diabetes, cardiovascular and renal disease, sarcopenic obesity, and obstructive sleep apnea. Importantly, visceral and ectopic fat depots are modifiable. Lifestyle-induced energy deficit, incretin-based pharmacotherapy, and metabolic bariatric surgery reduce visceral and ectopic fat and improve glycemic control, liver fat content, cardiovascular risk factors, physical function, and sleep-disordered breathing. Incorporating ectopic fat characterization into clinical practice may enhance risk stratification and support more personalized management of obesity phenotypes.