Real-world effectiveness of oral semaglutide on body weight, composition, and metabolic parameters in patients with obesity without diabetes.

Assessing the accuracy of bioelectrical impedance analysis for fat-free mass estimation in growing pigs using dual-energy X-ray absorptiometry as a reference method.

Sarcopenia and recurrence risk in high-risk non-muscle-invasive bladder cancer: a nonlinear modeling approach.

Sleep duration, body composition and mortality: a prospective study of 156,565 Mexican adults.

COVID-19 may be associated with unfavourable body composition changes. This includes increased fat mass and decreased muscle mass, which can lead to sarcopenia and sarcopenic obesity (SO), conditions associated with impaired physical performance and reduced quality of life, among other adverse outcomes. This study investigated the prevalence of sarcopenia and SO in individuals who recovered from the first COVID-19 wave and their association with functional outcomes. Clinical characteristics, body composition (bioelectrical impedance analysis), functional status (handgrip strength [HGS], 6-min walk test [6MWT]), and lung function (spirometry) were collected. 37 individuals (89.2 % Caucasians, 64.9 % females, median age 48 years [IQR: 40; 60], 10.8 % > 65y) were assessed after a median of 189 days (IQR: 169; 201) post-COVID-19 infection. The combined prevalence of sarcopenia/SO was 40.5 %, was identified in 37.8 %, while a single case (2.7 %) of sarcopenia without obesity was found. The sarcopenia/SO group had lower 6MWT and phase angle, and higher prevalence of hypertension. Sarcopenia/SO was negatively associated with 6MWT performance (β: -115.35, 95 % CI: -161.57 to -69.12), COVID-19 symptoms, disease severity, and duration were not associated with sarcopenia/SO diagnosis. A high presence of sarcopenia/SO was identified and was negatively associated with health outcomes in individuals post-COVID-19. Thus, it is important to assess and address conditions associated with abnormal body composition after infectious diseases to better inform strategies for improving long-term outcomes.

The association between cancer history and long-term body composition based on a 10-year follow-up.

Mitigating loss of lean muscle in GLP-1 and dual GLP-1/GIP agonists: Pipeline opportunities and limitations.

Cardiovascular diseases (CVDs) remain the leading cause of morbidity and mortality worldwide, and excess adiposity is a major contributor to cardiovascular (CV) risk. However, obesity is a heterogeneous condition, and body mass index (BMI) alone fails to capture important differences in fat distribution and lean mass that substantially influence CV outcomes. Growing clinical and epidemiological evidence indicates that body composition, rather than body weight per se, provides a more accurate and biologically meaningful framework for CV risk assessment. This narrative review summarizes clinical evidence linking key components of body composition, including total and regional adiposity, skeletal muscle mass, and ectopic fat depots, to CV risk and prognosis. Central and visceral adiposity are consistently shown to be more strongly associated with cardiometabolic dysfunction, atherosclerosis, and CV events than generalized obesity. In parallel, reduced lean mass and sarcopenia emerge as independent predictors of adverse CV outcomes, particularly in older adults and patients with established CVD. Ectopic fat depots, such as epicardial and hepatic fat, further contribute to CV pathology through local and systemic mechanisms. Collectively, these findings highlight the limitations of BMI-centered approaches and support the integration of body composition measures into CV risk stratification. Emphasizing body recomposition, with reduction of harmful fat depots and preservation of skeletal muscle, may enable more precise, individualized strategies for CV prevention and management.

Handgrip strength and body composition in children and adolescents with acute lymphoblastic leukemia: A cross-section study.

Growing attention has been directed toward the long-term consequences of critical illness, particularly the physical, cognitive, and psychological impairments following intensive care unit (ICU) discharge. At the core of the physical domain lies ICU-acquired weakness (ICU-AW). ICU-AW is driven by systemic inflammation, prolonged catabolism, malnutrition, and immobility. The resultant sustained muscle loss significantly impairs recovery and causes loss of independence, reduced quality of life, and increased mortality. Malnutrition-either preexisting or acquired in the ICU-is a major determinant of recovery, yet nutrition management remains challenging because of the risks of both overfeeding and underfeeding. Compounding this is the lack of robust biomarkers to guide individualized nutrition strategies. Current evidence supports illness phase-specific, personalized nutrition, starting with hypocaloric feeding during the acute phase of critical illness and progressing to higher-energy, protein-rich support during recovery. Recent studies caution against excessive early protein provision, which may suppress autophagy and induce metabolic stress. Monitoring tools such as indirect calorimetry and body composition analysis may guide tailored interventions. Additionally, immunonutrients, anabolic agents, and early rehabilitation show promise as adjunctive strategies, although further high-quality trials are needed to define their role and risk-to-benefit ratio. This narrative review examines the pathophysiology of muscle wasting during critical illness; reviews recent data addressing the central role of nutrition in modulating outcomes, including post-intensive care syndrome; and reviews recent developments that are improving our understanding of nutrition, biomarkers, and individualized nutrition and nutrition adjuncts.

Osteoporosis poses a health risk to post-menopausal females. The menopause transition is associated with hormone fluctuations (e.g., follicle-stimulating hormone (FSH), estrogen), and other biochemical and physiological changes that contribute a decline in bone mineral density (BMD). This will investigate the relationship between biochemical and physiological markers of BMD across the menopause transition. Fifty-six middle-aged females who completed their menopause transition were included in this longitudinal sub-analysis. Participants were recruited from the Ottawa/Gatineau region. Menopause status was classified using menstrual history and FSH plasma levels. BMD and body composition were assessed using dual-energy x-ray absorptiometry (DXA). Additional measures included BMI, cardiorespiratory fitness (VO2max), diet calcium and Vitamin D, and biochemical markers (i.e., FSH, cortisol, calcium). Statistical analysis included repeated measures analysis of variance, linear mixed modeling, and group-based trajectory modeling to identify distinct FSH trajectory groups and their associations with BMD changes over time. Serum calcium was negatively associated with BMD at the lumbar spine [β: -0.0799, 95% confidence interval (CI): -0.139; -0.020, p=0.009]. Further, the high FSH trajectory group experienced a greater decrease in BMD across the 5-year period, at the femur neck [β: 0.067, CI: 0.050; 0.084 vs. β: 0.035, CI: 0.021; 0.048; p=0.003] and total body [β: 0.045, CI: 0.035; 0.055 vs. β: 0.028, CI: 0.020; 0.036; p=0.007] than the low FSH trajectory group. Associations between serum calcium and lumbar spine BMD, and a greater BMD decline in individuals with high FSH levels were revealed. This information suggests that serum calcium and FSH should be monitored throughout the menopause transition to protect BMD.

The effects of short-term dietary calorie restriction combined with aerobic exercise on systemic inflammation in overweight or obese individuals with knee osteoarthritis: a randomised controlled trial.

Promoting healthy aging: A systematic review of the transformative effects of nutritional interventions in elderly population.

Association between sarcopenic obesity and cognitive impairment among taiwanese older adults with type 2 diabetes mellitus: A cross-sectional study.

Effects of two postbiotics (yeast culture and complex probiotics) on growth performance, body composition, liver and intestinal health, and fillet quality of rice field eel (Monopterus albus)

Effects of exercise on the efficacy and adverse effects of immunosuppressants: a systematic review and meta-analysis.

Experimental studies have suggested that the autocrine/paracrine effects of bone-derived Fibroblast Growth Factor 23 (FGF23) inhibit adipogenesis and promote osteoblastic differentiation of bone marrow stroma cells. To examine whether there is relationship between circulating levels of FGF23 and bone marrow adiposity assessed by MRI. This cross-sectional study included 199 postmenopausal women without apparent disorders in phosphate homeostasis. University Hospital of Lille, France. C-terminal FGF23 (cFGF23, relative units (RU)/ml) and intact FGF23 (iFGF23, pg/ml). The Proton Density Fat Fraction (PDFF) of the lumbar spine and the proximal femur was assessed using MRI with chemical shift-based water-fat separation (WFI) and DXA of the hip and spine. Our main goal was to explore the relationships between PDFF, cFGF23, and iFGF23 levels in women who are postmenopausal. The relationships between cFG23, iFGF23, and body composition metrics were subsequently analyzed. A significant positive correlation was observed between cFGF23 and iFGF23 (R=0.534, p<0.0001). Significant inverse associations were found between cFGF23, iFGF23, and femoral neck PDFF (reciprocally, coefficient β (95%CI), -1.35 (-2.49 to -0.21), p=0.020 and-1.66 (-3.00 to -0.32), p=0.016) after adjustment for age, recent fragility fracture, BMI, eGFR, and BMD. Conversely, there were no notable associations identified between cFGF23, iFGF23, and lumbar spine PDFF, regardless of whether adjustment models were applied. No significant associations were found between cFGF23, iFGF23, and body composition parameters (total body fat and visceral adipose tissue). An inverse association was found between cFGF23, iFGF23, and proximal femur PDFF (particularly femoral neck PDFF), but not with lumbar spine PDFF. Moreover, cFGF23 and iFGF23 levels were not associated with other adipose deposits.

Consumers' risky eating behaviours aided by the current food environment have led to an increase in diet-related metabolic disorders. Metabolic (dysfunction)-associated fatty liver disease origin represents a major global health burden that is increasing at an alarming rate on an annual basis. Modifying the timing of calorie consumption, dietary composition, or caloric intake offers a promising therapeutic approach for the management of this condition. The aim of this review was to provide a concise analysis of the impact of intermittent fasting on the regulation of glucocorticoid levels and diet-induced metabolic disorders with a focus on non-alcoholic fatty liver diseases. We found that intermittent fasting primarily regulates hepatic autophagy via nutritional and hormonal pathways, aiding in the maintenance of energy equilibrium, enhancement of mitochondrial function, regulation of liver quality, preservation of cellular homeostasis, protection of cells from harmful factors, mitigation of liver metabolic disorders, and improvement of liver inflammation. Also, the physiological changes induced by intermittent fasting and their metabolic consequences arise through multiple mechanisms, including alterations in hepatic metabolism, hepatic autophagy, inflammatory responses, liver functional enzymes, hepatic steatosis, fibroblast growth factor signalling, White adipoe tissue browning, adipokines, circadian rhythms, lipid profiles, body composition, the adipose tissue-gut microbiome axis, skeletal muscle, and the autophagy process. Interestingly, we identified the complex interplay among glucocorticoids, intermittent fasting, and non-alcoholic fatty liver diseases highlighting the hepatic macrophage glucocorticoid receptor as a pivotal mediator of fasting-induced reprogramming of the macrophage secretome, including fasting-suppressed cytokines. In conclusion, existing data indicates that intermittent fasting in patients with non-alcoholic fatty liver diseases is a viable, safe, and successful strategy for weight reduction, demonstrating notable trends in the amelioration of dyslipidaemia and non-alcoholic fatty liver diseases.

The effects of beta-hydroxy-beta-methylbutyrate on sarcopenia in stable decompensated cirrhosis: A pilot randomized controlled trial.

Growth differentiation factor 15 (GDF15) is a protein that is produced by senescent cells during the aging process. Its level in blood increases with age and is associated with an increased risk of several age-related diseases and mortality. We measured GDF15 level in serum archived 1174 men and women aged between 70 and 79yr in the Health Aging and Body Composition study who had measurements of BMD of the hip, markers of bone turnover (PINP and CTX) and tested for several physical functions (6m gait speed, standing balance and grip strength, BMI, and appendicular lean mass) and falls, and were followed-up for incident fracture. Cox proportional hazard models were used to estimate hip fracture risk by increasing GDF15 quartiles. The mean GDF15 was significantly higher in men than in women (p < .0001) and the level significantly increased with age, slower gait speed, lower standing balance test time, and lower handgrip strength. During 11.5 (SD 4.5)yr of follow-up, 93 (8%) of the participants suffered a hip fracture and the risk was higher among women (p < .015), associated with older age, lower BMI, lower FN and TH BMD, lower appendicular lean mass, and weaker grip strength. In the unadjusted hazard model participants in the highest quartile of GDF15 had a 2-fold increased hip fracture risk (HR 2.12, p < .014) that remained significant after adjustment for age and sex (p < .037). However, the association was no longer statistically significant after adjusting for grip strength (HR 1.8, 95% CI: 0.97-3.34; p < .06). In conclusion, increased GDF15 is a predictor of hip fractures. This relationship might be partially mediated by muscle function and low lean mass but not BMD.