BackgroundAccurate tracking of skeletal muscle mass (SMM) and fat mass percent (FM%) is central to evaluating obesity treatment. The InBody H20N bioelectrical impedance analysis (BIA) device could offer a scalable, lower-cost alternative. However, its accuracy compared to dual-energy X-ray absorptiometry (DXA) and research-grade BIA in adults with obesity is unknown.MethodsBaseline SMM and FM% was measured in 55 participants with obesity (62.6±7.6 y, 67.3% female, BMI: 37.6±5.7 kg/m2) enrolled in a behavioral weight-loss program using three modalities: the InBody H20N, InBody S10, and DXA. Agreement was assessed using intraclass correlation coefficients (ICC) analyses with two-way mixed-effects and absolute-agreement, Bland-Altman plots with limits of agreement, and Lin's concordance correlation coefficients.ResultsFor SMM, agreement was good between H20N and DXA (ICC 0.78; 95% CI -0.15-0.94) and excellent between H20N and S10 (ICC 0.93; 95% CI 0.87-0.96). For FM%, agreement was excellent between H20N and DXA (ICC 0.93; 95% CI 0.79-0.97) and good between H20N and S10 (ICC 0.81; 95% CI 0.66-0.89). All ICCs were statistically significant (p<0.001).ConclusionResults indicate that the H20N provides clinically useful estimates of body composition relative to DXA and research-grade BIA, supporting its potential in resource-constrained environments.

[This corrects the article DOI: 10.3389/fcvm.2021.752640.].

Obesity, a global epidemic, is closely linked to metabolic complications like insulin resistance and type 2 diabetes. Pancreatic dysfunction (impaired islet secretion and local inflammation) is central to this deterioration, yet the underlying mechanisms remain unclear. Pancreatic macrophages regulate tissue inflammation and metabolic homeostasis, but their context-specific polarization in obesity is undefined. This review discusses the role of triggering receptor expressed on myeloid cells 2 (TREM2) in modulating pancreatic macrophage behavior in the context of obesity, based on findings from diet-induced obese mouse models and ex vivo pancreatic analyses. Emerging evidence indicates that TREM2 expression is markedly upregulated in pancreatic macrophages of obese subjects, where TREM2-driven macrophage activation promotes pro-inflammatory cytokine release and disrupts macrophage-islet β-cell crosstalk. Transcriptomic profiling reveals that TREM2 signaling reshapes macrophage transcriptional landscapes, enhancing pro-inflammatory phenotypes while impairing islet-supporting capacity. Notably, macrophage-specific TREM2 ablation has been shown to ameliorate pancreatic inflammation, restore islet insulin secretion, and alleviate systemic metabolic disorders in obese mice. Collectively, these findings identify TREM2 as a pivotal molecular switch governing pancreatic macrophage-mediated metabolic dysfunction in obesity, highlighting TREM2+ pancreatic macrophages as a potential therapeutic target. These findings advance the understanding of immune-metabolic crosstalk in the pancreas, laying a foundation for developing novel immunometabolic interventions.

Phytosterols are plant-derived sterols structurally similar to cholesterol and present in vegetable oils, seeds, legumes, and whole grains. Their best-established health effect is lowering circulating low-density lipoprotein cholesterol, mainly through inhibition of intestinal cholesterol absorption. Beyond this classical role, recent studies suggest that phytosterols may influence biological processes relevant to human health. Proposed mechanisms include changes in membrane lipid organization, modulation of nuclear receptors such as liver X receptors and peroxisome proliferator-activated receptors, activation of AMP-activated protein kinase, and regulation of metabolic and inflammatory signaling pathways. Experimental and human evidence indicates possible effects on adipose tissue function, hepatic lipid accumulation, insulin sensitivity, inflammation, oxidative stress, and immune responses. These findings have increased interest in the relevance of phytosterols to obesity, metabolic dysfunction-associated steatotic liver disease, type 2 diabetes, and immune-mediated disorders such as rheumatoid arthritis. Interactions with the gut microbiota and bile acid metabolism may provide additional pathways linking phytosterol intake with systemic effects, although human evidence remains limited. Antioxidant and anti-inflammatory actions have also been linked to neuroprotective and anticancer effects, but current support is mainly from preclinical studies. This review critically summarizes mechanistic and translational evidence, with emphasis on bioavailability, interindividual variability, safety, and remaining research gaps.

Obesity presents significant challenges in anesthetic management because physiologic and body composition changes can substantially alter drug pharmacokinetics (PK) and pharmacodynamics (PD). Propofol is one of the most commonly used intravenous anesthetic agents for procedural sedation and general anesthesia; however, optimal dosing strategies in patients with obesity remain controversial. Conventional dosing based on total body weight (TBW) may increase the risk of adverse events, whereas alternative weight scalars and model-informed approaches have been proposed. This systematic review aimed to evaluate the impact of obesity on propofol dosing and propofol-associated anesthetic outcomes, with particular emphasis on hypnotic adequacy, hemodynamic stability, respiratory safety, recovery characteristics, and PK/PD considerations. This systematic review was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) 2020 guidelines. A comprehensive literature search was performed using PubMed, BioMed Central, and ClinicalTrials.gov. Eligible studies included randomized controlled trials, prospective and retrospective observational studies, and PK/PD investigations evaluating propofol administration in adults with obesity. Primary outcomes were hypnotic adequacy and hemodynamic stability. Secondary outcomes included respiratory and airway events, recovery characteristics, and PK/PD parameters. Risk of bias was assessed using the Joanna Briggs Institute Critical Appraisal Tools. Owing to substantial heterogeneity in study design, patient populations, dosing strategies, and outcome reporting, findings were synthesized using a structured narrative approach. Sixteen studies met the eligibility criteria and were included in the qualitative synthesis. The included studies demonstrated that obesity significantly influences propofol pharmacology and clinical response. Across studies, TBW-based dosing was frequently associated with greater hemodynamic depression, including hypotension and bradycardia, without consistently improving hypnotic adequacy. Respiratory and airway complications, particularly hypoxemia and the need for airway interventions, occurred more frequently in patients with higher body mass indexes during procedural sedation. PK/PD investigations consistently reported alterations in volume of distribution, clearance, and concentration-effect relationships in obese patients, supporting the use of lean body weight-based or model-informed dosing approaches. Recovery outcomes were less frequently reported, but when reported, generally indicated improved recovery profiles with reduced propofol requirements through individualized dosing strategies or adjunctive agents. Current evidence indicates that obesity substantially alters propofol's PK, PD, and clinical anesthetic outcomes. TBW-based dosing may increase the risk of hemodynamic and respiratory adverse events without reliably improving anesthetic effectiveness. The available evidence supports considering alternative weight-scaling factors, individualized dose titration, and physiologic monitoring to optimize propofol administration in adults with obesity. Further prospective studies are needed to establish standardized dosing strategies and validate clinically applicable model-informed approaches.

Type 1 diabetes mellitus (T1DM) is the most common form of diabetes in young people, and the prevalence of type 2 diabetes mellitus (T2DM) is increasing due to obesity. Latent autoimmune diabetes in adults (LADA) typically presents after age 30, and these patients do not require insulin during the first 6 months after diagnosis. A similar clinical profile presenting before age 30 is known as latent autoimmune diabetes in young (LADY). Maturity-onset diabetes in young (MODY) is a monogenic form of diabetes classified into 14 subtypes based on the pathogenic gene variant and systemic manifestations. We present a 22-year-old woman who was incidentally found to have diabetes at age 18 and had a positive glutamic acid decarboxylase (GAD) antibody. She received oral hypoglycemic agents for the first 4 years and recently started insulin due to poor glycemic control. Whole exome sequencing revealed a heterozygous single-base pair deletion in exon 11 of the carboxyl ester lipase (CEL) gene (chr9:g.133071542del; c.2040del; p.Val681CysfsTer23), suggestive of CEL-MODY, also known as MODY 8. Our report highlights the unusual occurrence of double diabetes (LADY and MODY) in a young woman.