Improving the health of skeletal muscle is an important component of obesity treatment. Apart from allowing for physical activity, skeletal muscle tissue is fundamental for the regulation of postprandial macronutrient metabolism, a time period that represents when metabolic derangements are most often observed in adults with obesity. In order for skeletal muscle to retain its capacity for physical activity and macronutrient metabolism, its protein quantity and composition must be maintained through the efficient degradation and resynthesis for proper tissue homeostasis. Life-style behaviors such as increasing physical activity and higher protein diets are front-line treatment strategies to enhance muscle protein remodeling by primarily stimulating protein synthesis rates. However, the muscle of individuals with obesity appears to be resistant to the anabolic action of targeted exercise regimes and protein ingestion when compared to normal-weight adults. This indicates impaired muscle protein remodeling in response to the main anabolic stimuli to human skeletal muscle tissue is contributing to poor muscle health with obesity. Deranged anabolic signaling related to insulin resistance, lipid accumulation, and/or systemic/muscle inflammation are likely at the root of the anabolic resistance of muscle protein synthesis rates with obesity. The purpose of this review is to discuss the impact of protein ingestion and exercise on muscle protein remodeling in people with obesity, and the potential mechanisms underlining anabolic resistance of their muscle.
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http://dx.doi.org/10.3389/fnut.2019.00087 | DOI Listing |
J Nephrol
January 2025
Department of Nephrology, Matsunami General Hospital, Gifu, Japan.
Background: The relationship between the psoas muscle gauge (PMG), a combined sarcopenia indicator obtained from psoas muscle index (PMI) and psoas muscle density (PMD), and adverse clinical outcomes in patients on hemodialysis remains unclear. We examined whether psoas muscle gauge could predict all-cause mortality and new cardiovascular events more accurately than psoas muscle index in these patients.
Methods: We retrospectively included 217 hemodialysis patients who underwent abdominal computed tomography.
Am J Physiol Heart Circ Physiol
January 2025
Vascular Biology Center and Department of Medicine, Medical College of Georgia at Augusta University, Augusta, GA USA.
The contribution of sex hormones to cardiovascular disease, including arterial stiffness, is established; however, the role of sex chromosome interaction with sex hormones, particularly in women, is lagging. Arterial structural stiffness depends on the intrinsic properties and transmural wall geometry that comprise a network of cells and extracellular matrix (ECM) proteins expressed in a sex-dependent manner. In this study, we used four-core genotype (FCG) mice to determine the relative contribution of sex hormones versus sex chromosomes or their interaction with arterial structural stiffness.
View Article and Find Full Text PDFUrol Res Pract
January 2025
Department of Pediatric Surgery, Zonguldak Bulent Ecevit University, Faculty of Medicine, Zonguldak, Türkiye.
Objective: Bladder tissue models have been developed using smooth muscle cells (SMCs) on various scaffolds to mimic bladder morphology and physiology. This study investigates the effects of co-culturing fetal and adult SMCs on growth properties and protein profiles to understand cellular interactions and population kinetics.
Methods: Bladder tissue samples from 10 adult and 10 fetal New Zealand rabbits were divided into 5 groups: adult SMCs (A), fetal SMCs (F), 50%A+50%F (A+F), 75%A+25%F (3A+F), and 25%A+75%F (A+3F).
Ann Med
December 2025
Central Laboratory, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Background: Despite surgical and intravesical chemotherapy interventions, non-muscle invasive bladder cancer (NMIBC) poses a high risk of recurrence, which significantly impacts patient survival. Traditional clinical characteristics alone are inadequate for accurately assessing the risk of NMIBC recurrence, necessitating the development of novel predictive tools.
Methods: We analyzed microarray data of NMIBC samples obtained from the ArrayExpress and GEO databases.
FEBS Lett
January 2025
Department of Microbiology and Immunology, Virginia Commonwealth University School of Medicine, Richmond, VA, USA.
Tissue fibrosis is a progressive pathological process with excessive deposition of extracellular matrix proteins (ECM). Myofibroblasts, identified by alpha-smooth muscle actin (αSMA) expression, play an important role in tissue fibrosis by producing ECM. Here, we found that the Wnt antagonist Dickkopf1 (DKK1) induced gene expressions associated with inflammation and fibrosis in lung fibroblasts.
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