Search Results (5,778)

Background and Objectives: In-hospital cardiac arrest (IHCA) in critically ill patients with COVID-19 is among the most severe clinical outcomes, associated with high mortality and a significant risk to healthcare workers during cardiopulmonary resuscitation (CPR). The aim of this study was to evaluate the incidence, characteristics, associated factors, and outcomes of IHCA among COVID-19 patients treated in the intensive care unit (ICU), with particular emphasis on resuscitation outcomes and survival. Materials and Methods: A retrospective cohort study was conducted including critically ill patients with confirmed SARS-CoV-2 infection treated in the ICU of the Clinical-Hospital Center (KBC) in Kosovska Mitrovica between March 2020 and December 2022. Patients were categorized into two groups: (1) CA group—patients who experienced CA in the ICU, and (2) non-CA group—patients who did not experience CA during ICU treatment. Results: A total of 222 patients were analyzed, of whom 114 (51.4%) experienced IHCA. Patients with IHCA were significantly older, more frequently obese, and had a higher burden of comorbidities. They also exhibited more pronounced hematological and inflammatory abnormalities, including lower erythrocyte and hemoglobin levels, thrombocytopenia, and elevated leukocyte counts, fibrinogen, C-reactive protein, and procalcitonin levels. In addition, higher lactate and D-dimer concentrations were observed, along with a more frequent occurrence of hyperkalemia and hypernatremia. The predominant cause of IHCA was respiratory failure, most commonly associated with severe hypoxemia (59.6%), while non-shockable initial rhythms (asystole and pulseless electrical activity (PEA)) were most common (76.3%). Among patients with IHCA, return of spontaneous circulation (ROSC) was achieved in 11 patients (9.6%), and 3 patients (2.6%) survived to hospital discharge. Conclusions: Despite rapid response and CPR in the ICU setting, outcomes remained poor. More favorable outcomes were observed mainly in cases with potentially reversible etiologies (such as myocardial infarction and pulmonary embolism (PE)), in contrast to hypoxia-mediated CA. Full article

Background/Objectives: Incretin-based pharmacotherapies are the most effective non-surgical treatments for obesity to date, yet 85% of patients discontinue within the second year of real-world use. No established framework exists for managing this post-cessation transition. This narrative review evaluates the evidence for structured exercise to mitigate physiological rebound and support long-term weight management following discontinuation. Methods: A narrative review was conducted per Assessment of Narrative Review Articles (SANRA) guidelines using PubMed, Scopus, and Web of Science from January 2005 through to June 2026. Results: Post-cessation weight regain averages 5.6 kg within one year and is observationally associated with dose-dependent cardiometabolic worsening. Lean mass losses averaging 6–7 kg and reductions in bone mineral density are seen during active treatment, creating a metabolically unfavorable state at cessation compounded by fat-preferential regain. Exercise and pharmacotherapy generate fundamentally different body composition outcomes. Exercise preserves lean mass, bone density, cardiorespiratory fitness, and insulin sensitivity, while pharmacotherapy alone does not, with downstream implications for resting metabolic rate and post-cessation rebound. Controlled trial data show exercise initiated during incretin treatment is associated with significantly less weight regain, greater sustained weight loss, and maintained physical activity levels one year after medication and supervised program end. This evidence derives from a single liraglutide-based trial and may not generalize directly to semaglutide, tirzepatide, or next-generation agents. Real-world data associate exercise counseling with durable weight loss after discontinuation. Conclusions: No randomized controlled trial has directly evaluated exercise at pharmacotherapy cessation; conclusions are based on post-treatment extension, real-world observational, and mechanistic evidence. Combined aerobic and resistance training is a biologically plausible, low-risk adjunct to incretin-based pharmacotherapies. Resistance training, adequate dietary protein, and individualized clinical screening are likely important components pending direct evidence from post-cessation trials. Full article

Pediatric obstructive sleep apnea (OSA) is a common disorder associated with significant neurocognitive, behavioral, cardiovascular, and metabolic consequences. Although adenotonsillectomy remains first-line therapy for many children, residual OSA is common, particularly among those with obesity, craniofacial abnormalities, genetic syndromes, neuromuscular disease, or other forms of medical complexity. Continuous positive airway pressure (CPAP) is the standard non-surgical treatment; however, long-term effectiveness is frequently limited by poor tolerance and adherence. Heated high-flow nasal cannula (HFNC) therapy has emerged as a potential alternative for selected children with sleep-disordered breathing, particularly those who are unable to tolerate conventional positive airway pressure therapy. Unlike CPAP, HFNC delivers heated, humidified gas through an open nasal interface and may improve sleep-disordered breathing through a combination of flow-dependent positive airway pressure generation, dead-space washout, improved ventilatory efficiency, enhanced gas conditioning, and reductions in inspiratory resistance. However, the relative contribution of these mechanisms during sleep remains incompletely understood. Current clinical evidence consists primarily of physiological studies, retrospective cohorts, case series, and a limited number of prospective comparative studies. Collectively, these data suggest that HFNC can reduce obstructive respiratory events and improve oxygenation in selected pediatric populations, including children with persistent OSA, CPAP intolerance, medical complexity, and syndromic conditions. Nevertheless, important uncertainties remain regarding optimal patient selection, titration strategies, patient monitoring, long-term adherence and comparative effectiveness relative to CPAP. This review summarizes the physiological basis of HFNC therapy, critically appraises the current clinical evidence, discusses practical considerations related to adherence and implementation, and highlights key knowledge gaps and future research priorities. Overall, HFNC should be viewed as an alternative for selected children who cannot tolerate CPAP, rather than as a universal substitute for pressure-based therapy. Full article

Background: Contemporary antidiabetic therapy has evolved from a glucose-centered approach toward integrated cardiometabolic risk reduction. However, real-world evidence regarding treatment patterns and their association with glycemic and cardiovascular–renal profiles remain limited. Methods: This retrospective observational study included 250 adults with type 2 diabetes mellitus receiving non-insulin glucose-lowering therapy in routine specialist clinical practice. Demographic, clinical, biochemical, and pharmacological data were extracted from medical records. Glycemic control was assessed using HbA1c levels and HbA1c variation, while cardiovascular–renal parameters included estimated glomerular filtration rate (eGFR), C-reactive protein (CRP), lipid profile, blood pressure, and heart failure prevalence. Comparative analyses and multivariate logistic regression were performed. Results: The cohort had a mean age of 61.8 ± 11.3 years, and all patients had type 2 diabetes mellitus (100.0%). Obesity, metabolic syndrome, hypertension, ischemic heart disease, and chronic kidney disease were highly prevalent. Metformin was the most frequently prescribed therapy (58.8%), followed by GLP-1 receptor agonists (28.8%) and SGLT-2 inhibitors (27.6%). Patients receiving GLP-1 receptor agonists or SGLT-2 inhibitors showed numerically lower HbA1c values and greater HbA1c reductions compared with conventional therapies. However, differences in HbA1c, CRP, and eGFR were not statistically significant after correction for multiple comparisons. Longer diabetes duration independently predicted poor glycemic control, whereas increasing age was associated with a lower probability of HbA1c > 7%. Conclusions: Contemporary antidiabetic therapies were associated with favorable numerical cardiometabolic trends, although these associations did not remain statistically significant after multiple-comparison correction. The findings should therefore be considered exploratory and hypothesis-generating. Full article

Background: The adverse cardiometabolic outcomes that have been associated with early menopause include obesity, insulin resistance, and metabolic syndrome. Other studies have also linked metabolic dysfunction with vitamin D deficiency. However, the independent association of serum 25-hydroxyvitamin D [25(OH)D] concentrations with metabolic syndrome and type of menopause is unclear. Thus, the present study was designed to assess the association between vitamin D status and metabolic syndrome in women with early menopause compared with those with natural menopause. Methods: A total of 301 postmenopausal women were enrolled. Metabolic syndrome was assessed independently according to the NCEP-ATP III and IDF diagnostic definitions. They were classified into two groups: early menopause (EM, n = 79) and physiological menopause (PHYSM, n = 222). Demographic, anthropometric, biochemical, and lifestyle characteristics were recorded. The criteria for diagnosing metabolic syndrome were those of the National Cholesterol Education Program Adult Treatment Panel III (NCEP-ATP III) and the International Diabetes Federation (IDF). Serum 25(OH)D was also categorized as deficiency, insufficiency, or sufficiency. Multivariable logistic regression analyses were used to determine independent predictors of metabolic syndrome. Multivariable linear regression analyses were used to determine the association between serum 25(OH)D and individual metabolic parameters. Results: Women with early menopause had a higher body mass index than those with physiological menopause, whereas current smoking was more prevalent among women with physiological menopause. No significant differences were observed between the groups in the prevalence of metabolic syndrome, 25(OH)D concentrations, lipid profile, blood pressure, glycaemic indices, or other biochemical parameters. In multivariable analyses, menopausal status was not independently associated with metabolic syndrome according to either the NCEP-ATP III or IDF criteria. Body mass index was the only independent predictor of metabolic syndrome in the adjusted IDF model (OR 1.2, 95% CI 1.0–1.4; p = 0.047). Serum 25(OH)D concentrations were independently associated only with lower fasting glucose levels and were not independently associated with metabolic syndrome or its other components. Although vitamin D categories showed significant associations with metabolic syndrome in unadjusted analyses, these associations were attenuated after adjustment for demographic, anthropometric, menopausal, and lifestyle-related factors. Conclusions: Menopausal type was not independently associated with the prevalence of metabolic syndrome or vitamin D status. Although metabolic syndrome prevalence differed across vitamin D categories in unadjusted analyses, these associations were attenuated after adjustment for demographic, anthropometric, menopausal, and lifestyle-related factors. Obesity appeared to be the strongest independent predictor of metabolic syndrome within this cohort. Given the retrospective observational design, these findings should be interpreted cautiously, and prospective longitudinal studies are warranted to confirm these associations. Full article

Gut lactic acid bacteria are emerging as potential targets for modulating host purine metabolism and alleviating hyperuricemia-related disorders. This study aimed to isolate purine-degrading lactic acid bacterial strains from porcine intestine and systematically evaluate their probiotic potential through both in vitro and in vivo approaches. A strain designated Pedio6-1 was isolated and identified as Pediococcus acidilactici based on 16S rRNA sequencing. In vitro assays demonstrated that P. acidilactici Pedio6-1 exhibited nearly complete adenine clearance (approaching 100%) and a total purine clearance rate of 30.73%, along with strong tolerance to acidic conditions, bile salts, and gastrointestinal enzymes. To further assess its in vivo efficacy, a high-fat diet-induced obese mouse model was employed. After 8 weeks of intervention, Pedio6-1 supplementation significantly reduced the final body weight and liver index, and markedly decreased hepatic guanine levels (p < 0.05), with a trend toward lower total purine content compared to the obese control group. Mechanistically, Pedio6-1 treatment significantly downregulated the hepatic mRNA expression of pro-inflammatory cytokines IL-1β and TLR4 (p < 0.05). Serum untargeted metabolomics revealed that Pedio6-1 treatment shifted the metabolic profile toward that of normal diet-fed mice, with differential pathways predominantly enriched in porphyrin metabolism and amino acid biosynthesis and metabolism. Notably, key metabolites with antioxidant and metabolic regulatory functions, including bilirubin, biliverdin, glutathione, citrate, L-cystathionine, and 4-pyridoxic acid, were significantly elevated following treatment, while N-acetylornithine and methylmalonate ester were decreased, indicating coordinated remodeling of oxidative stress defense, vitamin B6 homeostasis, and energy metabolism. Collectively, these findings indicate that Pedio6-1 not only possesses direct purine-degrading activity in vitro, but also ameliorates purine metabolic disturbances, inflammation, and oxidative stress in obese mice, likely through the modulation of porphyrin and amino acid metabolic pathways, highlighting its promise as a functional probiotic candidate for managing obesity-associated purine metabolic disorders. Full article

Purpose of Review: Obesity is a growing global health challenge, with severe obesity projected to affect up to 25% of individuals with obesity by 2030. Bariatric surgery remains the most effective treatment, yet the molecular mechanisms underlying its metabolic benefits are not fully understood. This review summarizes current evidence on the role of microRNAs in bariatric/metabolic surgery and evaluates their potential as biomarkers and therapeutic targets. Recent Findings: Bariatric surgery induces significant alterations in circulating and tissue-specific miRNA profiles, particularly those involved in glucose metabolism, inflammation, and adipose tissue remodeling. Among the most frequently reported candidates, miR-122, miR-221, miR-27a, miR-126, miR-144, miR-222, miR-223, miR-375, miR-92a, and miR-155 have been associated with weight loss, improved insulin sensitivity, and diabetes remission. Emerging data suggest that these miRNAs may act not only as biomarkers of metabolic recovery but also as regulators of insulin signaling, inflammatory pathways, and adipocyte function. Summary: Current evidence supports a role for miRNAs in the metabolic adaptations observed after bariatric surgery. Although further validation is required, miRNAs show promise as minimally invasive biomarkers for predicting and monitoring treatment response and may provide insight into the molecular mechanisms underlying obesity remission and improvement of obesity-related comorbidities. Full article

Background/Objectives: Obesity is increasingly recognised as a clinically relevant comorbidity in patients with inflammatory bowel disease (IBD), with potential effects on inflammatory burden, treatment response, surgical risk, nutritional status, and quality of life. Endoscopic bariatric therapies (EBTs), including intragastric balloons and endoscopic sleeve gastroplasty, offer minimally invasive weight-loss options between pharmacotherapy and bariatric surgery. However, their role in IBD remains poorly defined. This narrative review examines patient selection, nutritional risk, periprocedural management, and future research priorities for EBTs in IBD. Methods: A narrative review was performed, focusing on obesity in IBD, bariatric endoscopy, bariatric surgery, nutritional deficiencies, sarcopenic obesity, biologic therapy, and periprocedural risk. Evidence from general bariatric endoscopy studies, IBD-specific obesity literature, clinical guidelines, and expert consensus documents was synthesised. Results: Direct evidence evaluating EBTs in patients with IBD is very limited. Most practical considerations must therefore be extrapolated from general bariatric endoscopy studies and bariatric surgery data in IBD. Patients with sustained clinical and preferably endoscopic remission, stable nutritional status, and uncomplicated disease phenotypes may represent the most suitable candidates. Active upper gastrointestinal Crohn’s disease, stricturing or penetrating disease, recent surgery, severe malnutrition, sarcopenia, and high-dose corticosteroid exposure should prompt caution or avoidance. Structured follow-up is needed to monitor nutritional deficiencies, body composition, procedural symptoms, and possible IBD activity. Conclusions: EBTs may represent a promising option for selected patients with IBD and obesity, but current evidence remains insufficient for firm recommendations. Prospective registries, phenotype-stratified cohort studies, and comparative trials are needed. Full article

Metabolic syndrome (MetS) is a complex cluster of interconnected metabolic abnormalities, including central obesity, insulin resistance, dyslipidemia, hypertension, chronic inflammation, and impaired glucose metabolism, which collectively increase the risk of type 2 diabetes and cardiovascular diseases. Although current therapeutic strategies, including lifestyle interventions and pharmacological treatments, can be effective in managing specific MetS components, the multifactorial nature of this condition continues to encourage the search for complementary approaches and novel bioactive compounds. Salt-tolerant plants (STPs), particularly halophytes, survive under adverse saline and oxidative stress conditions through specialized physiological and biochemical adaptations, including the production of diverse secondary metabolites such as phenolic acids, flavonoids, sterols, terpenoids and polysaccharides. Several of these compounds have been associated with health-promoting properties, including antioxidant, anti-inflammatory, antidiabetic, antihypertensive, lipid-modulating and cardioprotective effects. This review provides an integrated and critical overview of the ethnomedicinal uses, phytochemistry and bioactivities of STPs with potential relevance to MetS and its associated conditions, namely chronic inflammation, diabetes, hypertension, cardiovascular disorders, dyslipidemia and obesity. The review first introduces the main features of MetS and the relevance of STPs as bioresources, followed by a synthesis of ethnomedicinal uses related to MetS-associated disorders. It then discusses in vitro and in vivo evidence for selected species, extracts and compounds, including reported bioactive metabolites and proposed mechanisms of action when available. Finally, the most promising species, extracts and metabolites are highlighted, together with current limitations and future research needs regarding efficacy, safety, bioavailability, standardization and clinical relevance. Full article

Knee osteoarthritis (KOA) is a degenerative joint disease characterized by inflammatory reactions and bone lesions within the joint, which is mainly caused by the degeneration of articular cartilage. This disease primarily affects middle-aged and elderly populations, especially those over 50 years old; however, a distinct trend of younger onset has been observed in recent years, which is closely associated with factors such as sports-related injuries and obesity. Astaxanthin (AST), a ketone carotenoid belonging to the xanthophyll family, exhibits extremely strong antioxidant and broad-spectrum anti-inflammatory activities with no obvious toxic and side effects due to its unique molecular structure, thus showing great potential in the prevention and treatment of KOA. This article reviews the research evidence and action mechanisms of AST in the prevention and treatment of KOA from multiple aspects, including alleviating joint pain, reducing cartilage structural damage, resisting oxidative stress, inhibiting inflammatory responses, and regulating cartilage metabolism and functional disorders, while exploring the key factors and signaling pathways involved. On this basis, a strategy combining AST with exercise intervention for the prevention and treatment of KOA is proposed, which provides a certain reference for the clinical treatment and scientific research of KOA. Full article

Background: Glucagon-like peptide-1 receptor agonists and dual glucose-dependent insulinotropic polypeptide/glucagon-like peptide-1 (GIP/GLP-1) receptor agonists have substantially improved the management of obesity and cardiometabolic disease, providing significant benefits on weight reduction, glycemic control, and cardiovascular outcomes. Despite these advances, gastrointestinal (GI) adverse events remain a major cause of dose reduction, treatment interruption, and poor long-term adherence. Increasing evidence suggests that interactions between incretin-based therapies and the intestinal microenvironment may contribute to GI tolerability and influence treatment persistence. Methods: We conducted a narrative review of the literature examining the relationship between incretin-based therapies, gut microbiota, intestinal barrier function, and microbial metabolites. Evidence from randomized clinical trials, observational studies, systematic reviews, and mechanistic investigations was evaluated to explore potential gut-directed supportive strategies during incretin-based treatment. Results: Preclinical and mechanistic evidence suggests possible bidirectional interactions between incretin pharmacology and the intestinal microenvironment, whereas direct human evidence remains limited and inconsistent. Alterations in gastrointestinal motility induced by GLP-1 receptor agonists could theoretically influence microbial composition and fermentation dynamics, although human studies have not consistently demonstrated significant microbiota changes. Based on these observations, we propose the Incretin–Microbiota Tolerance Axis (IMTA) as a conceptual framework linking gut homeostasis, GI tolerability, and treatment adherence. Among potential supportive interventions, partially hydrolyzed guar gum (PHGG) may promote SCFA-producing microbiota and improve bowel function, whereas simethicone may provide symptomatic relief of gas-related discomfort during dose escalation. SCFA-supportive nutritional approaches may further contribute to maintenance of intestinal homeostasis. Conclusions: Optimization of the intestinal microenvironment may represent a complementary strategy to improve GI tolerability and support long-term adherence during incretin-based therapy. Although the IMTA framework is supported by biological plausibility and emerging evidence, prospective clinical studies are required to determine whether microbiota-targeted interventions improve treatment persistence and cardiometabolic outcomes in patients receiving GLP-1 receptor agonists or dual GIP/GLP-1 receptor agonists. Full article

Background/Objectives: In obesity-associated type 2 diabetes (T2DM), therapeutic benefit increasingly requires assessment of not only HbA1c and total body weight, but also the composition and functional quality of weight change. We evaluated a myoprotective fat-loss phenotype, defined as a reduction in adiposity accompanied by preservation of lean mass and handgrip strength. Methods: This secondary patient-level analysis included 166 adults with T2DM who completed 12 months of follow-up without changing treatment in a real-world tertiary diabetes cohort. Patients received metformin alone or metformin combined with a sulfonylurea, a DPP-4 inhibitor, an SGLT2 inhibitor, a GLP-1 receptor agonist, or insulin. Body composition was assessed by bioimpedance and muscle function by handgrip dynamometry. The primary phenotype required a reduction in fat mass ≥5%, a loss of lean mass <3%, and a decrease in handgrip ≤1 kg. Phenotype distributions were compared between treatment groups; patient-level associations and adjusted contrasts were explored using correlation analyses and baseline-adjusted regression models with robust HC3 standard errors. Results: Fat-mass reduction ≥5% occurred in 58/166 patients (34.9%), lean-mass preservation in 129/166 (77.7%), and handgrip preservation in 143/166 (86.1%). The complete myoprotective phenotype was present in 35/166 patients (21.1%) and differed significantly across treatment groups (χ² = 131.58; permutation p < 0.0001). It was most frequent in the GLP-1 receptor agonist group (13/23; 56.5%) and the SGLT2 inhibitor group (12/25; 48.0%), less frequent with metformin monotherapy (9/46; 19.6%) and DPP-4 inhibitors (1/17; 5.9%), and absent in the sulfonylurea and insulin groups. GLP-1 receptor agonists showed the greatest crude fat-mass loss, whereas lean-mass loss, skeletal-muscle-mass change, and handgrip change did not differ significantly across groups after false-discovery-rate correction. Conclusions: Myoprotective fat-loss phenotypes can be identified in obesity-associated T2DM using body composition and handgrip measures. These observational findings support the assessment of the quality, not just the magnitude, of weight loss in diabetes care and require validation in larger prospective studies. Full article

Background: Knee osteoarthritis (KOA) in people with overweight or obesity is clinically heterogeneous, reflecting mechanical loading, synovial and systemic inflammation, metabolic dysfunction, structural severity, and pain-related factors. We evaluated multidomain outcomes after semaglutide initiation and characterized clinically relevant response patterns. Methods: This retrospective, self-controlled cohort included 93 adults treated in routine rheumatology care; 88 completed a six-month follow-up. There was no untreated concurrent comparator; within-patient changes and exposure–outcome associations were therefore interpreted as non-causal. Changes in pain, Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) function, anthropometry, inflammatory markers, glycated hemoglobin (HbA1c), lipids, dose exposure, and safety were evaluated. Joint multivariable models included percentage weight loss and maximum achieved dose. Exploratory K-means phenotyping integrated dose, weight loss, body mass index (BMI) decrease, visual analog scale (VAS) and WOMAC improvement, and C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), and HbA1c reductions, with candidate solutions and resampling stability examined. Results: At six months, mean weight decreased by 10.88 kg, VAS pain score by 2.47 points, WOMAC total by 22.50 points, CRP by 2.67 mg/L, ESR by 7.62 mm/h, and HbA1c by 0.51 percentage points (all p < 0.001). Weight loss remained independently associated with WOMAC improvement, while achieved dose retained positive adjusted associations with pain, function, inflammatory, and metabolic changes. Exploratory clustering identified five clinically interpretable patterns along a broader response-intensity gradient, including high-burden multidomain response, high-dose concordant response, dose-modified intermediate response, inflammation-preserved response despite moderate weight loss, and dose-limited graded response. These observational coefficients and clusters cannot distinguish treatment-related effects from residual confounding or co-interventions. Conclusions: Substantial within-patient improvements were observed, but the uncontrolled design precludes causal attribution. The exploratory patterns may be compatible with contributions from baseline disease burden, dose exposure, mechanical unloading, and residual inflammatory variation; they do not establish weight-independent pharmacologic effects or validated patient subtypes. Prospective controlled, multicenter validation is required. Full article

Background: Type 2 diabetes mellitus is commonly associated with obesity, metabolic liver disease, and chronic low-grade inflammation. Semaglutide is known to improve glycaemic control and body weight, but its real-world associations with hepatic markers, fibrosis-related indices, and systemic inflammatory parameters remain incompletely characterized. This study evaluated changes in metabolic, hepatic, and inflammatory parameters during injectable semaglutide treatment and explored whether these changes differed according to baseline disease status. Methods: A retrospective observational study was conducted in patients with type 2 diabetes treated with injectable semaglutide 1 mg/week and followed for six months. Anthropometric, metabolic, hepatic, and inflammatory variables were collected at baseline and follow-up, including liver enzymes, the Fibrosis-4 (FIB-4) index, and the systemic immune–inflammation (SII) index. Analyses included correlation analyses and exploratory stratification according to baseline fibrosis risk and inflammatory status. Results: Semaglutide treatment was associated with significant reductions in body weight, body mass index, fasting glucose, HbA1c, and triglyceride levels. Alanine and aspartate aminotransferase levels decreased significantly, consistent with a reduction in liver enzyme abnormalities during follow-up. No significant overall changes were observed in FIB-4, an indirect fibrosis-related index, or in SII, an indirect hematological inflammatory index. However, exploratory stratified analyses suggested that patients with higher baseline FIB-4-estimated fibrosis risk or elevated SII values showed greater reductions in these indices, whereas those with low baseline risk showed no relevant changes. Conclusions: In routine clinical practice, six months of injectable semaglutide treatment was associated with favorable metabolic changes and reductions in liver transaminases in patients with type 2 diabetes mellitus. Findings related to FIB-4 and SII should be interpreted cautiously, as these are indirect indices and the baseline-dependent patterns observed were exploratory and hypothesis-generating. Full article

Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) and related incretin-based therapies are highly effective anti-obesity treatments, but weight loss may also include reductions in fat-free mass, raising concern for selected patients at risk of sarcopenia. This narrative review summarizes current evidence and practical, evidence-informed strategies to support muscle health during GLP-1 RA-based anti-obesity therapy. Particular emphasis is placed on identifying higher-risk patients, including older adults, frail individuals, patients with low baseline muscle mass or strength, sarcopenic obesity, chronic kidney disease, low physical activity, or rapid weight loss. Preventive strategies include baseline assessment of body composition and muscle function, individualized resistance and multicomponent exercise, adequate protein intake, attention to nutritional adequacy, and periodic monitoring of body composition, strength, and physical performance. Treatment pace and dose escalation may also be individualized in higher-risk patients when unfavorable changes in fat-free mass or function occur. Current evidence remains limited, and many recommendations are extrapolated from weight-loss, nutrition, exercise, and sarcopenia literature rather than GLP-1 RA-specific trials. Overall, a risk-stratified and multidisciplinary approach may help preserve muscle mass and function while maintaining the cardiometabolic benefits of GLP-1 RA-based therapy. Full article