Physiological research最新文献

Sarcopenic obesity (SO) is a complex pathological condition characterized by the simultaneous presence of excessive adipose tissue and the loss of muscle mass and strength. This combination leads to an increased risk of metabolic, cardiovascular, and functional complications. In recent years, there has been growing interest in the use of microRNAs (miRNA) as biomarkers capable of detecting early changes in body composition and predicting the progression of SO. MiRNAs are small noncoding RNA molecules that play a key role in regulating gene expression and cellular pathways related to inflammation, metabolism, and muscle trophism. This article summarizes current knowledge about miRNAs expression in patients with sarcopenic obesity, their regulatory functions, and their potential use in diagnostics and therapy. Key words microRNA " Sarcopenic obesity " miRNA " Biomarkers " Muscle atrophy " Inflammation.

This review provides a comprehensive synthesis of validated prediction equations for body composition assessment using single- and multi-frequency bioelectrical impedance analysis (BIA), covering studies published between 2000 and April 2025. While traditional models for estimating compartments such as total body water (TBW) and fat-free mass (FFM) have long been established, they often fail to reflect current populations and technologies. The review includes 43 studies that developed 98 unique equations for TBW, FFM, extracellular water (ECW), intracellular water (ICW), body cell mass (BCM), and bone mineral content (BMC), derived using reference methods such as deuterium dilution, DXA, or multi-component models. Most equations targeted FFM and TBW, with a noticeable lack of models for ECW, ICW, and BMC. The review identifies a geographic and demographic imbalance in study populations and emphasizes the need for updated, population-specific models. It also highlights the growing use of multi-frequency BIA devices to improve estimation accuracy. The findings support the continued refinement of BIA-based prediction models for broader clinical applicability and underscore the importance of external validation across diverse populations and health conditions. Key words Bioelectrical impedance analysis " Body composition " Prediction equations " Total body water " Fat-free mass.

The role of M4 muscarinic receptors in locomotor activity regulation remains controversial, with conflicting findings hampering our understanding of movement disorders. This uncertainty is further complicated by the unexplored relationship between M4 receptors and biological rhythms, as well as potential sex-specific effects that may explain previous inconsistent results. Through systematic investigation of locomotor functions in biological rhythm paradigms, we discovered that M4 muscarinic receptors significantly modulate locomotor activity rhythms via brain pacemaker mechanisms. Notably, this regulatory effect displayed marked sexual dimorphism, being present exclusively in females, suggesting crucial interactions with sex hormones. Our research identified the striatum as the key structure directing these locomotor biological rhythms. These findings provide critical insights into the sex-specific nature of M4 receptor function and establish a new framework for understanding hyperactivity disorders, particularly those exhibiting sex-based differences in prevalence or manifestation. Key words M4 muscarinic receptors " M1 muscarinic receptors " Biological rhythm " Locomotor activity " Striatum.

Bariatric surgery is the most effective way to treat obesity and improves obesity-related comorbidities. Laparoscopic sleeve gastrectomy (LSG) is one of several standard procedures, laparoscopic greater curvature plication (LGCP) is a relatively alternative bariatric technique, and Roux-en-Y gastric bypass (RYGB) is the gold standard of bariatric surgical procedures. The study included 95 patients who underwent three types of bariatric surgery. 48 of the subjects (28 women, 20 men) underwent LSG, 35 of the patients (21 women, 14 men) underwent LGCP and 12 of the subjects (8 women, 4 men) underwent RYGB. Anthropometry and biochemical parameters (glucose, glycated hemoglobin, cholesterol, HDL and LDL cholesterol, triglycerides, adiponectin, leptin, ANGPTL3, ANGPTL4, ApoD, ApoE, FGF19, and FGF21) were determined before and after 3, 6, 12 and 18 months of surgeries. All types of bariatric surgeries markedly decreased body weight, BMI, and percentage of body fat. The surgical procedures resulted in a decrease in mean fasting glucose, triglycerides, glycated hemoglobin concentrations and leptin concentrations in blood serum. On the other hand, plasma concentrations of adiponectin increased significantly. Different results were observed in serum ANGPTL3, ANGPTL4, ApoD, ApoE, FGF19, and FGF21 levels after all surgeries. All three types of bariatric surgery resulted in significant weight loss and changes in the levels of the measured parameters. Key words Bariatric surgery " Adipokines " FGF19 " FGF21 " ANGPTL.

Postoperative atrial fibrillation (POAF) remains a significant complication following minimally invasive thoracoscopic mitral valve surgery (MITMVS), yet current risk prediction models inadequately capture the underlying metabolic determinants of arrhythmogenesis. We investigated whether computed tomography (CT)-derived body composition parameters, as markers of metabolic status, could predict POAF risk in patients undergoing mitral valve repair. We retrospectively studied 104 consecutive MITMVS patients (2014-2023). Preoperative CT scans quantified skeletal muscle index, muscle density, and visceral/subcutaneous adipose tissue. Patients were grouped by preexisting atrial fibrillation (AF) with concurrent Maze (n=48) vs. no AF history (n=56). The primary outcome was POAF development. Higher visceral (VAT) and subcutaneous (SAT) adipose tissue density showed associations with increased POAF odds in multivariable analysis (VAT: OR 1.075, 95 % CI: 1.010;1.149, p=0.026; SAT: OR 1.073, 95 % CI: 1.011;1.146, p=0.025). Quartile analysis revealed a striking 5.5-fold increased POAF risk in the highest VAT density quartile compared to the lowest (42.3 % vs. 7.7 %). Notably, the relationship between intramuscular adipose tissue (IMAT) density and POAF differed between groups (interaction p=0.029), with a positive association in patients without prior AF (OR 1.167, 95 % CI: 1.011;1.377, p=0.047), but no significant relationship in those with preexisting AF (p=0.175). CT-derived tissue quality parameters, particularly VAT density, demonstrate robust associations with POAF risk following MITMVS. These findings establish preoperative CT-based metabolic assessment as a promising tool for perioperative risk stratification without additional testing burden. Key words Postoperative atrial fibrillation " Body composition " Computed tomography " Mitral valve surgery " Metabolic risk factors.

SARS-CoV-2 engages ACE2 for cell entry, perturbing the counter-regulatory ACE2/Ang-(1-7)/Mas axis and shifting the renin angiotensin system toward ACE/Ang II/AT1 signaling, with a concomitant reduction in nitric oxide (NO) bioavailability. NO sits at the crossroads of these pathways, acting both as an antiviral modulator of spike-ACE2 interactions and as a downstream mediator of Mas-dependent endothelial protection. This review summarizes evidence on NO across three layers: (i) viral entry (S nitrosylation of spike/ACE2, protease modulation), (ii) cardiovascular comorbidities (hypertension, obesity, diabetes) where ACE2 downregulation impairs endothelial NO synthase (eNOS)-dependent NO production and promotes thrombosis and microvascular dysfunction, and (iii) neurovascular/ neurodegenerative sequelae, in which renin-angiotensin-aldosterone system (RAAS) dysregulation along with imbalance between protective eNOS/nNOS and inflammatory iNOS fosters blood-brain barrier disruption, microthrombosis, and cognitive impairment. Shared mechanisms - endotheliitis, microvascular dysfunction, and neuroinflammation may explain convergent risks for cardiac injury and cognitive decline in long COVID-19. Putative therapeutic strategies may include restoring physiological NO (via Mas agonism, Ang-(1-7), inhibition of Ang 1-7 degradation and recombinant ACE2), pulmonary-selective inhaled NO, hybrid S nitrosylated agents, and selective attenuation of iNOS/peroxynitrite alongside endothelial support. Targeted modulation - enhancing eNOS/nNOS while constraining iNOS offers a unified framework to mitigate both cardiovascular and neurodegenerative consequences of COVID-19.

This study investigated how non-hepatic surgery and subsequent acute stress affect iron distribution, redox state, antioxidant defence, and inflammation-related gene expressions and iron metabolism in the liver of borderline hypertensive rats. We used air-jet stress as a model of acute psychological stress (3 sessions of 5 sec. air-jet) applied approximately 22 hours post-surgery (carotid artery and jugular vein cannulation). Both the surgery (Su) and post-surgical stress (Su+Str) increased corticosterone and reduced iron concentrations in plasma, while increasing remanent magnetisation (Mr) and coercivity (Hc) in whole blood. In the liver, Su and Su+Str reduced mRNA expressions of genes encoding NFR2 and GPX4 proteins (Nfe2l2 and Gpx4, respectively), and induced a significant increase in hepatic conjugated dienes, proinflammatory factors (Il1b) and iron-regulating genes mRNA (Hmox1, Fpn1, Fth1, Hamp, Tfr1), despite elevated Hmox1 and Sod1 mRNA expressions. In addition, hepatic Mr and Hc after Su and Su+Str were elevated, suggesting a qualitative change of iron-containing substances in circulation and liver tissue. In addition, in the Su+Str group, the elevated saturation magnetisation (Ms) is indicative of elevated total iron content. These findings suggest that a mild non-hepatic surgery may reduce hepatic mRNA expression of NRF2 and GPX4, which was associated with oxidative tissue damage accompanied by qualitative alterations in cellular iron, indicating a pro-ferroptotic state that, together with enhanced inflammation, may contribute to post-surgical liver injury. Additionally, the combination of surgery and acute post-surgical stress led to tissue iron accumulation, which may contribute to liver damage.

Stroke survivors frequently present with impaired trunk control, which is a key determinant of mobility, balance, and independence in activities of daily living (ADL). Reliable clinical tools are therefore needed to evaluate postural stability, particularly in patients unable to stand. This randomized controlled study assessed the applicability of the Trunk Impairment Scale (TIS) and Stroke Impact Scale (SIS) in post-stroke patients after completion of a complementary sensory intervention targeting sitting postural stability. Forty inpatients in the subacute stage after stroke were randomized into an Experimental group receiving daily postural training with visual biofeedback in addition to standard physiotherapy, and a Control group receiving standard physiotherapy only. Assessments included TIS and SIS at baseline and post-intervention. Both groups demonstrated significant improvements in trunk control, mobility, strength and ADL over time, as reflected by higher TIS and SIS scores. However, the Experimental group achieved greater gains, with the most pronounced effects observed in TIS, as well as SIS Mobility, and SIS ADL domains. Mobility improvements were strongly associated with enhanced ADL performance, underscoring the relevance of trunk control rehabilitation. These findings confirm the clinical sensitivity of TIS and SIS in capturing meaningful postural changes associated with functional recovery after stroke. This study demonstrates that targeted trunk-focused interventions with complementary sensory input can significantly enhance both motor and functional outcomes in stroke survivors. Combining TIS and SIS provides a comprehensive evaluation of clinical performance and patient-reported outcomes, offering valuable insight for rehabilitation strategies aimed at improving independence and quality of life.

Type 2 diabetes (T2D) associated with obesity is accompanied not only by metabolic but also cardiovascular disorders, including impaired vascular function. In addition to nitric oxide (NO), another gaseous transmitter, hydrogen sulfide (H2S), plays a key role in vascular homeostasis, but its function under pathological conditions is not fully understood. Escalated metabolic disorder associated with T2D could disrupt sulfide signaling and shift the balance between its pathological and compensatory action. The aim of the study was to investigate the role of H2S and NO signaling in the vascular function of obese Zucker diabetic fatty (ZDF) rats and to evaluate the impact of chronic treatment with zofenopril, an ACE inhibitor containing a sulfhydryl group. Cardiometabolic and biochemical parameters, as well as reactivity of the isolated thoracic aorta after 4 weeks of treatment, were assessed. Obese rats exhibited increased systolic blood pressure (SBP), cardiac and renal hypertrophy, increased adiposity, dyslipidemia, and impaired glucose tolerance compared with controls. Endothelium-dependent relaxation was reduced, with loss of H2S-derived relaxant component and dysregulation of NO signaling. Zofenopril significantly reduced SBP, attenuated cardiac and renal hypertrophy, and restored endothelial and contractile function. At the molecular level, it increased the expression of H2S-synthesizing enzymes, restored H2S-dependent vasorelaxation, and normalized NOS activity with a predominance of eNOS. In conclusion, zofenopril restored the balance of H2S and NO signaling in obese ZDF rats, thereby providing cardiovascular protection independent of improvements in glycemia or lipid profile. This dual mechanism may represent a promising therapeutic approach in preventing complications of obesity-induced T2D.

Combined renin-angiotensin system (RAS) inhibition can enhance blood pressure control but has not improved clinical outcomes, underscoring the importance of complex changes in angiotensin peptide profiles in combined RAS blockade. We investigated hemodynamics and circulating and tissue angiotensin peptide profile in spontaneously hypertensive rats (SHR) treated with lisinopril, olmesartan and aliskiren and their dual combinations. SHR exhibited hypertension and left ventricular hypertrophy along with reduced circulating Ang I, Ang II, and Ang 1-7. Lisinopril produced the most pronounced antihypertensive effects, with additional reduction when combined with olmesartan or aliskiren. In contrast, aliskiren - either alone or in combination - had only modest effects in this low-RAS setting. The morphological changes of the myocardium largely mirrored the blood pressure responses across treatment groups, reinforcing the hemodynamic basis of structural remodeling in SHR. Lisinopril and olmesartan markedly increased Ang I and Ang 1-7, but lisinopril suppressed Ang II while olmesartan increased Ang II. Aliskiren further reduced Ang II and Ang 1-7. Across treatment strategies, dual RAS blockade frequently decreased both renal and circulating Ang 1-7 despite greater hemodynamic efficacy. Tissue analyses revealed minimal intrinsic Ang II synthesis in the left ventricle, consistent with AT?-dependent uptake of circulating Ang II, while renal peptide profiles indicated some local enzymatic activity with differential reliance on ACE and neprilysin. Our results advocate a cautious, mechanism-aware approach to combination RAS blockade and support therapeutic strategies that balance blood pressure lowering with preservation of the Ang 1-7 axis.