Acta Physiologica最新文献

{"title":"Lipocalin-2 Restores Soluble Guanylyl Cyclase-Dependent Dilation of the Afferent Arteriole After Renal Transplantation or Ex Vivo Hypoxia/Reoxygenation in Mice","authors":"Liang Zhao,&nbsp;Minze Xu,&nbsp;Anna Maria Pfefferkorn,&nbsp;Cem Erdogan,&nbsp;Hubert Schwelberger,&nbsp;Pinchao Wang,&nbsp;Pratik Hemant Khedkar,&nbsp;Marc Eigen,&nbsp;Falk-Bach Lichtenberger,&nbsp;Rusan Catar,&nbsp;En Yin Lai,&nbsp;Felix Aigner,&nbsp;Pontus B. Persson,&nbsp;Igor Maximilian Sauer,&nbsp;Andreas Patzak,&nbsp;Muhammad Imtiaz Ashraf","doi":"10.1111/apha.70077","DOIUrl":"https://doi.org/10.1111/apha.70077","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>Dilatory microvascular function is impaired in ischemia/reperfusion injury in the kidney. Nitric oxide independent activators of soluble guanylyl cyclase (sGC) provide renal protection by dilating microvessels and preserving perfusion, but their efficacy declines after severe hypoxia. This study explores whether lipocalin-2 (Lcn2), a key iron-transporting protein, can restore the sGC-mediated dilation in mouse afferent arterioles (AAs) after hypoxia/reoxygenation (<i>H</i>/<i>R</i>) and kidney transplantation.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Dilation of isolated, angiotensin II (Ang II) pre-constricted, AAs was induced by application of sGC activator cinaciguat after pre-constriction with Ang II following <i>H</i>/<i>R</i> (<i>H</i>: 30 min, <i>R</i>: 10 min ± holo-rLcn2, apo-rLcn2, deferoxamine) and syngeneic kidney transplantation (cold ischemia: 30 min or 5.5 h, reperfusion: 20 h ± holo-rLcn2) in C57BL/6 mice. To corroborate the dilatory function at the organ level, vascular relaxation was assessed using an isolated mouse kidney perfusion system.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Dilation of AAs was impaired following <i>H</i>/<i>R</i>. Pretreatment with holo-rLcn2 (iron-bound) preserved dilation, whereas apo-rLcn2 (iron-free) had no effect. The reversal of holo-rLcn2's effect by deferoxamine confirmed the role of iron. AAs from kidney transplants showed reduced dilation compared to sham-operated controls, with greater impairment following prolonged ischemia. Treatment with holo-rLcn2 significantly improved dilatory function after extended cold ischemia (5.5 h), restoring it to levels seen with shorter ischemia (30 min). Ex vivo perfusion of the isolated mouse kidney with holo-rLcn2 enhanced cinaciguat-induced vascular relaxation, confirming its beneficial effect at the organ level.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>This study identifies a novel role for holo-rLcn2 in preserving renal vascular function post-<i>H</i>/<i>R</i> and kidney transplantation, apparently by upholding iron levels in vascular cells.</p>\u0000 </section>\u0000 </div>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"241 8","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apha.70077","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144551124","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reversal of Diabesity Through Modulating Sympathetic Inputs to Adipose Tissue Following Carotid Body Resection","authors":"Bernardete F. Melo,&nbsp;Joana F. Sacramento,&nbsp;Julien Lavergne,&nbsp;Fátima O. Martins,&nbsp;Daniela Rosendo-Silva,&nbsp;Clara Panzolini,&nbsp;Cláudia S. Prego,&nbsp;Aidan Falvey,&nbsp;Elena Olea,&nbsp;Paulo Matafome,&nbsp;Asuncion Rocher,&nbsp;Jesus Prieto-Lloret,&nbsp;Miguel C. Correia,&nbsp;Phillipe Blancou,&nbsp;Silvia V. Conde","doi":"10.1111/apha.70074","DOIUrl":"https://doi.org/10.1111/apha.70074","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background and Aims</h3>\u0000 \u0000 <p>The development of innovative strategies to treat diabesity and its comorbidities is of major societal importance. The carotid bodies (CB), classically defined as O₂ sensors, are also metabolic sensors whose dysfunction contributes to the genesis and progression of metabolic disturbances. Here, we tested the hypothesis that the CBs are key players in the neural hypothalamic-sympathetic circuit controlling glucose and energy homeostasis. Moreover, we investigated if abolishment of CB activity has an anti-diabesity effect in Wistar rats and C75BL/6J mice, associated with increased visceral white and brown adipose tissue (AT) metabolism and the restoration of sympathetic activity within these tissues.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>We demonstrate that resection of the carotid sinus nerve, the CB-sensitive nerve, promotes weight loss and restores metabolic function in obese rats and mice by enhancing tyrosine hydroxylase expression at the paraventricular nucleus of the hypothalamus and its efferent sympathetic neurons to the AT. Moreover, we found that CSN resection increases sympathetic integration and catecholaminergic action in the AT in a manner that restores or even increases AT metabolism.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>We provide groundbreaking and innovative data showing a new circuit involving the CB-hypothalamus-sympathetic efferents and the AT in controlling glucose and energy homeostasis and so a novel pathway for managing diabesity.</p>\u0000 </section>\u0000 </div>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"241 7","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apha.70074","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144367602","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of Dietary BCAAs Intake on the Blood Pressure in Dahl Salt-Sensitive Rats","authors":"Meng Chen,&nbsp;Li Zeng,&nbsp;Xiangbo Chen,&nbsp;Lan Chen,&nbsp;Di Gao,&nbsp;Zhe Yang,&nbsp;Zhongmin Tian","doi":"10.1111/apha.70070","DOIUrl":"https://doi.org/10.1111/apha.70070","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>Circulating branched-chain amino acids (BCAAs) have been widely found to be associated with the risk of hypertension, but mechanisms remain unclear. In this study, we hypothesized that BCAAs could alleviate the development of salt-induced hypertension in Dahl salt-sensitive (SS) rats. The objective was to explore whether long-term high-salt diets (a major dietary risk for high blood pressure) alter BCAAs levels in SS rats and how dietary BCAAs influence salt-induced hypertension.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>SS rats received an 11-week dietary intervention to investigate the effects of dietary BCAAs on SS hypertension. Metabolic changes were studied using GC–MS and LC–MS/MS, as well as selected enzyme activity measurements. Western blotting was used to measure the protein levels of p-BCKDHA/BCKDHA and AQP. HUVECs and HK-2 cells were treated with 2 mM BCAAs for 24 h before measuring metabolites and enzyme activities.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>An 11-week high-salt diet increased blood pressure in SS rats, which was accompanied by reduced circulating BCAAs levels. Dietary BCAAs attenuated salt-induced hypertension, restored circulating BCAAs levels, and enhanced BCAAs metabolic activity. It also decreased aquaporin-1 (AQP1) levels in the renal cortex, promoting water and sodium excretion and improving renal function in SS rats. Additionally, metabolomic analysis demonstrated that dietary BCAAs enhanced arginine-NO metabolism in the kidneys and thoracic aorta of SS rats, promoting NOS-mediated NO synthesis and improving vasodilation. The promotion of NO synthesis by BCAAs was confirmed at the cellular level.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Long-term BCAAs intake promoted water and sodium excretion, enhanced NO synthesis in kidneys and thoracic aortas, and lowered blood pressure in SS rats on a high-salt diet, suggesting BCAAs may improve SS hypertension rather than exacerbate it.</p>\u0000 </section>\u0000 </div>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"241 7","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144339559","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cardiolipin Remodeling in Cardiovascular Diseases: Implication for Mitochondrial Dysfunction","authors":"Huijie Zhang,&nbsp;Fengzhi Yu,&nbsp;Zhenjun Tian,&nbsp;Dandan Jia","doi":"10.1111/apha.70073","DOIUrl":"https://doi.org/10.1111/apha.70073","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>Mitochondrial dysfunction is pivotal in both the development and progression of cardiovascular diseases (CVDs), though its exact mechanisms remain unclear. Cardiolipin (CL), a key mitochondrial phospholipid, is involved in various mitochondrial functions, including dynamics, membrane integrity, oxidative phosphorylation, mitochondrial DNA maintenance, and mitophagy. Due to enzyme limitations in the CL biosynthesis pathway, premature CL undergoes remodeling to acquire the proper acyl content for its function. Disruption in CL composition leads to mitochondrial dysfunction, contributing significantly to CVDs. The purpose of this review is to explore the role of CL remodeling in the mechanism of mitochondrial dysfunction that occurs in CVDs.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This review examines CL’s critical role in mitochondrial function, the consequences of CL deficiencies in CVDs, and the impact of mutations or deficiencies in CL remodeling enzymes-tafazzin (TAZ), Acyl-CoA:lysocardiolipin acyltransferase-1 (ALCAT1), and Monolysocardiolipin acyltransferase (MLCLAT1)-on CL homeostasis, mitochondrial function, and CVDs pathogenesis. Emerging CL-targeted therapies are also reviewed.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Proper CL function is crucial for mitochondrial health and cardioprotection. Pathological CL remodeling due to mutations or deficiencies in TAZ, ALCAT1, or MLCLAT1, drives mitochondrial dysfunction and accelerates CVDs progression. Based on these insights, current CL-based therapeutic strategies are also summarized, including precision medicine/gene therapy, targeted pharmacotherapy, and dietary interventions.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Targeting CL may represent a promising clinical therapeutic strategy for CVDs.</p>\u0000 </section>\u0000 </div>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"241 7","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144308706","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fatty Acid Taste Quality Information via GPR40 and CD36 in the Posterior Tongue of Mice","authors":"Yumiko Nagai,&nbsp;Kenichi Tokita,&nbsp;Keiko Yasumatsu","doi":"10.1111/apha.70071","DOIUrl":"https://doi.org/10.1111/apha.70071","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>Taste cells expressing GPR120 and connected chorda tympani nerve (CT) fibers are necessary for obtaining specific information on long-chain fatty acids (FA) in mice. However, the functions of GPR40, GPR120, and CD36 in the posterior part of the tongue remain unclear. Therefore, the present study has examined the neuron types coding for FA information in the glossopharyngeal (GL) nerve and their functions.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We performed single-fiber recordings in the GL nerve from GPR120-knockout (KO) and wild-type (WT) mice and behavioral preference tests based on five-minute intake using WT mice after the CT (and greater petrosal) nerves were sectioned bilaterally.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Single fibers were classified into FA-(F), S-, M-, electrolyte-(E), Q-type, and N-best groups, based on their maximal responses to oleic acid (OA), sucrose, monopotassium glutamate, HCl, quinine hydrochloride, and NaCl. Among the GL fibers, 3.8% of GPR120-KO and 11.8% of WT mice were F-type. Furthermore, 81.8% or more of the S- and M-type fibers showed responses to FAs in both mouse genotypes. Residual responses to FAs were substantially suppressed by GPR40 and CD36 antagonists in GPR120-KO mice. Preference scores for OA decreased significantly with the addition of CD36 or GPR40 antagonists. Additionally, the preference scores for monopotassium glutamate and sucrose decreased when the mice were conditioned to avoid OA.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>These results suggest that GPR120 contributes only to the existence of F-type fibers and that CD36 and GPR40 mediate the palatable umami or sweet taste of FAs via the activation of S- and M-type fibers in the GL nerve.</p>\u0000 </section>\u0000 </div>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"241 7","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144273245","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular Dynamics Simulations of a Putative Novel Mechanism for UCP1-Assisted FA Anion Transport","authors":"Sanja Vojvodić,&nbsp;Giorgia Roticiani,&nbsp;Mario Vazdar,&nbsp;Elena E. Pohl","doi":"10.1111/apha.70068","DOIUrl":"https://doi.org/10.1111/apha.70068","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Mitochondrial energy can be stored as ATP or released as heat by uncoupling protein 1 (UCP1) during non-shivering thermogenesis in brown adipose tissue. UCP1, located in the inner mitochondrial membrane, reduces the proton gradient in the presence of long-chain fatty acids (FA). FA act as weak, protein-independent uncouplers, with the transport of the FA anion across the membrane being the rate-limiting step. According to the fatty acid cycling hypothesis, UCP1 catalyzes this step through an as-yet-undefined mechanism.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We used computational and experimental techniques, including all-atom molecular dynamics (MD) simulations, membrane conductance measurements, and site-directed mutagenesis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>We identified two novel pathways for fatty acid anion translocation (sliding) at the UCP1 protein–lipid interface, ending at key arginine residues R84 and R183 in a nucleotide-binding region. This region forms a stable complex with fatty acid anion, which is crucial for anion transport. Mutations of these two arginines reduced membrane conductance, consistent with the MD simulation prediction that the arachidonic acid anion slides between helices H2–H3 and H4–H5, terminating at R84 and R183. Protonation of the arachidonic acid anion predicts its release from the protein–lipid interface, allowing it to move to either cytosolic or matrix leaflets of the membrane.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>We provide a novel, detailed mechanism by which UCP1 facilitates fatty acid anion transport, as part of the fatty acid cycling process originally proposed by Skulachev. The residues involved in this transport are conserved in other SLC25 proteins, suggesting the mechanism may extend beyond UCP1 to other members of the superfamily.</p>\u0000 </section>\u0000 </div>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"241 7","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apha.70068","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144256036","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aquaporin-4-Mediated Water Permeability Rescues Aquaporin-3 Deficiency Caused Nephrogenic Diabetes Insipidus","authors":"Yi Ying,&nbsp;Zhiwei Qiu,&nbsp;Jihan Liu,&nbsp;Yazhu Quan,&nbsp;Yongpan An,&nbsp;Feng Lu,&nbsp;Keying Wang,&nbsp;Min Li,&nbsp;Hong Zhou,&nbsp;Baoxue Yang","doi":"10.1111/apha.70072","DOIUrl":"https://doi.org/10.1111/apha.70072","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>The aim of this study was to determine whether water or solute transport plays a critical role in AQP3-mediated urine concentrating ability, using AQP3 knockout (AQP3-KO) mice and a novel mouse model in which the AQP3 gene coding region is replaced with AQP4 cDNA (AQP4-KI).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>AQP3-KO and AQP4-KI mice were characterized using Western blot and immunofluorescence to confirm the absence of AQP3 and the in situ replacement of AQP4. Urinary output, osmolality and urea concentration were measured in mouse models under various conditions, including water deprivation, acute urea loading and high protein intake.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>AQP3-KO mice exhibited a significantly increased daily urine output (6 times that in wild-type mice) and reduced urinary osmolality (&lt; 1000 mOsm/kg), with a marked inability to concentrate urea and osmolality in response to water deprivation, urea loading or high protein intake. In contrast, AQP4-KI mice showed restoration of urine output, urinary osmolality and urea concentration, approaching wild-type levels.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>In situ replacement of AQP3 with AQP4 restores AQP3-mediated water permeability in the renal collecting duct, rescuing the nephrogenic diabetes insipidus (NDI) phenotype in AQP3-deficient mice. This study provides evidence that AQP3-mediated water permeability plays a crucial role in the renal urine concentrating mechanism.</p>\u0000 </section>\u0000 </div>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"241 7","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144256035","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multi-Wearable Approach for Monitoring Diurnal Light Exposure and Body Rhythms in Nightshift Workers","authors":"Steffen L. Hartmeyer,&nbsp;Nicholas E. Phillips,&nbsp;Friedrich C. Jassil,&nbsp;Céline Joris,&nbsp;Charna Dibner,&nbsp;Tinh-Hai Collet,&nbsp;Marilyne Andersen","doi":"10.1111/apha.70069","DOIUrl":"https://doi.org/10.1111/apha.70069","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>As our understanding of light's impact on human health grows, studies examining light exposure and related health outcomes in everyday settings are increasingly important, particularly in high-risk groups like nightshift workers.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>In this observational study, we monitored personal light exposure and physiological functions in a large cohort of healthcare nightshift workers using a spectrally resolved light dosimeter and wearable body temperature, actigraphy, and electrocardiography sensors.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Our findings revealed a common occurrence of unfavorable light conditions during both shift types. During nightshift work, participants frequently experienced exposure to biologically potent cool-white LED lighting. On dayshifts, melanopic light levels often failed to meet recommended guidelines, with daylight as the primary source of bright light levels. Sleep duration, but not quality, significantly varied between shifts, with longer sleep before the first nightshift but shorter sleep on subsequent nights. Daytime and nighttime napping helped compensate for reduced sleep on nightshifts. Limited associations between light exposure and sleep were found, partially contradicting existing knowledge. Diurnal physiological and activity rhythms followed the change from day-active to night-active schedules; however, the change in physiological rhythms appeared partly dissociated from that of activity, suggesting a circadian modulation. Moreover, physiological functions exhibited bi-directional phase-shifts across consecutive nightshifts, which may have been mediated by differences in daytime light exposure before the first nightshift.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>By employing a multi-wearable approach including recent sensors, we provide new insights into the lighting environments experienced by nightshift workers and the potential impact of nightshift work and light exposure on endogenous circadian rhythms.</p>\u0000 </section>\u0000 </div>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"241 7","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144244487","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Revisiting Concepts of Thermal Physiology: Understanding Feedback and Feedforward Control, and Local Temperature Regulation","authors":"Duncan Mitchell,&nbsp;Shane K. Maloney,&nbsp;Edward P. Snelling,&nbsp;Robyn S. Hetem,&nbsp;Andrea Fuller","doi":"10.1111/apha.70063","DOIUrl":"https://doi.org/10.1111/apha.70063","url":null,"abstract":"<p>Most experts agree that the dominant mechanism through which body temperature is regulated, under a thermal challenge, environmental or metabolic, is negative feedback control. However, some consider negative feedback to be too sluggish to account for the rapid speed of response. The impression of sluggishness is based on an assumption that the body temperature that is regulated is a core temperature, whereas we concur with those who have concluded that what is regulated is an integrated temperature compiled from inputs from multiple body parts, including the skin. Negative feedback control is supplemented, though, by feedforward control, which is initiated by cues about the predicted magnitude and timing of the thermal challenge. Feedforward control is anticipatory because it can excite thermo-effectors in advance of the thermal challenge impacting on body temperature. Feedforward control is improved by learning but always is supervised by feedback control. There is disagreement about whether the pro-active excitation of thermo-effectors by temperature receptors in the skin occurs by fast feedback control or by feedforward control. We show that skin temperature receptors can provide physiologically meaningful negative feedback within seconds. Both the feedback and the feedforward regulation of integrated body temperature can be modulated by regulation of the temperature of body parts that have special thermoregulatory needs, notably the scrotum.</p>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"241 7","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apha.70063","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144190664","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Branched-Chain Amino Acids and Di-Alanine Supplementation Attenuates Muscle Atrophy in a Murine Model of Cancer Cachexia","authors":"Mayra Colardo,&nbsp;Noemi Martella,&nbsp;Michela Varone,&nbsp;Daniele Pensabene,&nbsp;Giuseppina Caretti,&nbsp;Gianluca Bianchini,&nbsp;Andrea Aramini,&nbsp;Marco Segatto","doi":"10.1111/apha.70067","DOIUrl":"https://doi.org/10.1111/apha.70067","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>Cancer cachexia is a severe metabolic disorder leading to skeletal muscle atrophy. Muscle wasting is a major clinical problem in cachectic patients, as it limits the efficacy of chemotherapeutic treatments and worsens quality of life. Nutritional support based on branched-chain amino acids (BCAA) has been shown to be a promising approach to counteract cachexia-induced muscle atrophy, but its efficacy is still debated. Furthermore, the putative role of di-alanine (Di-Ala) supplementation has yet to be evaluated. The present study therefore sought to assess whether BCAA supplementation, alone or in combination with a Di-Ala peptide, could attenuate muscle wasting in a preclinical model of cancer cachexia.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>To this end, C26 tumor-bearing mice were administered BCAA supplementation, with or without Di-Ala. Body and muscle weights, as well as molecular, biochemical, and morphological analysis, were carried out to characterize prospective changes of markers involved in cachexia and muscle atrophy.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The main findings revealed that BCAA supplementation effectively prevented body weight loss and muscle atrophy. Of note, Di-Ala significantly amplified the effects of BCAA. These phenomena were found to be mediated by the suppression of pathways involved in protein catabolism.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Collectively, these results highlight that innovative formulations containing Di-Ala, capable of increasing BCAA bioavailability, may be efficacious in counteracting muscle atrophy, especially during mild-to-moderate cancer cachexia.</p>\u0000 </section>\u0000 </div>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"241 7","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apha.70067","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144179218","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}