Acta Physiologica最新文献

{"title":"Exercise modifies fatty acid perception and metabolism","authors":"Deepankumar Shanmugamprema,&nbsp;Karthi Muthuswamy,&nbsp;Vinithra Ponnusamy,&nbsp;Gowtham Subramanian,&nbsp;Keerthana Vasanthakumar,&nbsp;Vasanth Krishnan,&nbsp;Selvakumar Subramaniam","doi":"10.1111/apha.13968","DOIUrl":"https://doi.org/10.1111/apha.13968","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>Obesity is a major public health issue, which is associated with several chronic diseases. In rodents, voluntary wheel running (VWR) is a type of exercise that influences ingestive behavior. This study aims to investigate the possible function of VWR activity in the perception of fat taste and if it mitigates the immediate effects of fatty acid (FA) ingestion.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Male C57BL/6 mice were arbitrarily assigned to either a sedentary (SED) lifestyle or free access to a running wheel after 5 weeks of dietary regimen. Later these mice groups were used in the investigations on fat preference, metabolic tolerance, and electrophysiology. Diet-induced alterations in CD36 and GPR120 expression that are related to fat perception and the capacitative calcium signaling caused by FA in taste bud cells (TBCs) were also examined.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>In obese groups, VWR temporarily reduced body weight, demonstrated improvement in preference scores for FA, and recovered from a deterioration in glucose homeostasis. In CD36-positive TBCs, electrophysiological investigations showed alterations in [Ca²⁺]i caused by FA. Further, in the TBCs of circumvallate papillae, there are differences in the expression of the genes CD36 and GPR120 between the active and SED controls. Obese mice also show lower incentive salience for long-chain fatty acids (LCFA) and adapted to the reward system of VWR which may lead to improved incentive salience accredited to wheel running.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>In conclusion, this study provides the first evidence that VWR causes orosensory adaptations to fat and appears to alter taste preference for LCFAs.</p>\u0000 </section>\u0000 </div>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"238 4","pages":""},"PeriodicalIF":6.3,"publicationDate":"2023-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"5742225","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":"Translation: Bench to bedside—And back","authors":"Pontus B. Persson,&nbsp;Philipp Hillmeister,&nbsp;Anja B. Persson","doi":"10.1111/apha.13965","DOIUrl":"https://doi.org/10.1111/apha.13965","url":null,"abstract":"","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"238 1","pages":""},"PeriodicalIF":6.3,"publicationDate":"2023-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"5792149","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":"Sleep and circadian rhythms in α-synucleinopathies—Perspectives for disease modification","authors":"Dieter Kunz,&nbsp;Henrik Oster,&nbsp;Oliver Rawashdeh,&nbsp;Wolf-Julian Neumann,&nbsp;Thomas Münte,&nbsp;Daniela Berg","doi":"10.1111/apha.13966","DOIUrl":"https://doi.org/10.1111/apha.13966","url":null,"abstract":"<p>The global north is facing an unprecedented rise in the prevalence of neurodegenerative diseases. The increasing incidence of Parkinson's disease is being referred to as a pandemic. The reason for the enormous increase is only partly understood. Lifestyle factors are known to play a role, but they alone cannot account for the surge. One factor that—although being recognized as important—has not been explored in detail so far is the influence of circadian rhythms. Sleep and circadian rhythm disruption are known as key factors in neurodegeneration, and their occurrence during early disease stages suggests a causal role in the pathogenesis. Isolated rapid eye movement (REM) sleep behavior disorder (iRBD) has been identified as a prodromal state of α-synucleinopathies, such as Parkinson's disease, Lewy body dementia, and multiple system atrophy offering a window for insights into the early development of these diseases. Even though REM sleep is the sleep state most pronounced, driven and modulated by the circadian timing system, specific circadian abnormalities have not been described in iRBD. Novel experimental and clinical approaches exploiting the molecular circuitry underlying circadian timekeeping hold promise to disentangle some of the pathophysiologic mechanisms of α-synucleinopathies. In this review, we summarize current knowledge on sleep and circadian rhythm disruptions in α-synucleinopathies with an emphasis on molecular aspects and therapeutic potentials. These insights might contribute to our understanding of the pathogenesis of neurodegenerative diseases and may allow therapeutic interventions addressing the disturbed circadian system at the early stage of disease.</p>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"238 1","pages":""},"PeriodicalIF":6.3,"publicationDate":"2023-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apha.13966","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"5767503","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":"High-phosphate diet causes atrial remodeling and increases atrial fibrillation vulnerability via STAT3/NF-κB signaling and oxidative stress","authors":"Yu-Juei Hsu,&nbsp;Gwo-Jyh Chang,&nbsp;Ying-Ju Lai,&nbsp;Yi-Hsin Chan,&nbsp;Wei-Jan Chen,&nbsp;Chi-Tai Kuo,&nbsp;Yung-Hsin Yeh","doi":"10.1111/apha.13964","DOIUrl":"https://doi.org/10.1111/apha.13964","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>Hyperphosphatemia is associated with adverse cardiovascular outcomes in both the general population and patients with end-stage renal disease. We evaluated whether high inorganic phosphate (Pi) intake causes atrial remodeling and increased atrial fibrillation (AF) risk.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>The 5/6 nephrectomized chronic kidney disease (CKD) mice were fed a high-Pi (2%) diet for 10 weeks. AF vulnerability was evaluated through transesophageal burst atrial pacing. Phosphoproteomic, Western blotting, and immunohistochemistry were used to evaluate the effects of high Pi in atrial fibroblasts, atrial myocytes, and HL-1 myocytes.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>CKD and sham mice fed a high-Pi diet exhibited increased AF vulnerability, atrial fibrosis, and oxidative stress compared with mice fed a normal diet. Compared with normal (1 mM) Pi, high (2 mM) Pi significantly increased the activity of atrial fibroblasts and mitochondrial oxidative stress. Phosphoproteomic analysis revealed that compared with normal Pi, high Pi considerably increased the phosphorylation of intracellular proteins in atrial fibroblasts, including proteins related to NF-κB signaling and STAT3. Inhibition of NF-κB, STAT3, and Nox4 by small interfering RNA reduced the high-Pi-induced expression of collagen. In HL-1 myocytes, the high Pi induced the degradation of myofibril proteins and hyperphosphorylation of RyR2, which was abolished by Nox4 and CaMKII inhibition. Switching back to a normal-Pi diet improved the atrial abnormalities induced by high-Pi diet.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>High-Pi intake causes atrial structural and electrical remodeling and increases AF vulnerability, which is mediated through STAT3/NF-κB signaling and oxidative stress. High dietary Pi intake can exert detrimental effects on atria and may increase AF risk.</p>\u0000 </section>\u0000 </div>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"238 2","pages":""},"PeriodicalIF":6.3,"publicationDate":"2023-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"5904759","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":"Ventilatory responses to hypoxic and hypercapnic environments in naked mole-rats","authors":"Matthew E. Pamenter","doi":"10.1111/apha.13963","DOIUrl":"https://doi.org/10.1111/apha.13963","url":null,"abstract":"<p>Extreme environments are powerful drivers of physiological adaptation. Naked mole-rats offer an informative example of this relationship as they putatively encounter intermittent hypoxia and hypercapnia in their subterranean habitat. This has presumably driven the evolution of a suite of cellular and physiological adaptations that enable life in these conditions. Recently, my laboratory and others have begun to examine physiological responses to environmental hypoxia and hypercapnia in naked mole-rats, and the underlying cellular and molecular mechanisms that differentiate the responses of this species from those of other small mammals. Prominent among these adaptations are a robust hypoxic metabolic response and blunted ventilatory responses to hypoxia and hypercapnia. These responses are mediated in part by modifications to the central nervous system signaling pathways that sense and communicate changes in environmental gas levels and initiate and maintain downstream physiological responses. For example, naked mole-rats retain the signaling architecture necessary for “normal” ventilatory responses to hypoxia and hypercapnia; however, the underlying signaling pathways are muted, resulting in reduced, or even the absence of, sensitivity to otherwise powerful environmental stimuli. Herein, I discuss what we have learned about the manifestation and control of ventilatory and metabolic responses to hypoxia and hypercapnia in naked mole-rats. I also highlight areas where additional work is warranted and consider the implications of what we have learned for the ecophysiology of a species that thrives in conditions that are deleterious or lethal to most adult mammals.</p>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"238 1","pages":""},"PeriodicalIF":6.3,"publicationDate":"2023-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apha.13963","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"6152834","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":"Circadian rhythm disruption in critically ill patients","authors":"Matthias Felten,&nbsp;Christof Dame,&nbsp;Gunnar Lachmann,&nbsp;Claudia Spies,&nbsp;Kerstin Rubarth,&nbsp;Felix Balzer,&nbsp;Achim Kramer,&nbsp;Martin Witzenrath","doi":"10.1111/apha.13962","DOIUrl":"https://doi.org/10.1111/apha.13962","url":null,"abstract":"<p>Patients admitted to the intensive care unit (ICU) are in need of continuous organ replacement strategies and specialized care, for example because of neurological dysfunction, cardio-pulmonary instability, liver or kidney failure, trauma, hemorrhagic or septic shock or even preterm birth. The 24-h nursing and care interventions provided to critically ill patients significantly limit resting and/or recovery phases. Consecutively, the patient's endogenous circadian rhythms are misaligned and disrupted, which in turn may interfere with their critical condition. A more thorough understanding of the complex interactions of circadian effectors and tissue-specific molecular clocks could therefore serve as potential means for enhancing personalized treatment in critically ill patients, conceivably restoring their circadian network and thus accelerating their physical and neurocognitive recovery. This review addresses the overarching issue of how circadian rhythms are affected and disturbed in critically ill newborns and adults in the ICU, and whether the conflicting external or environmental cues in the ICU environment further promote disruption and thus severity of illness. We direct special attention to the influence of cell-type specific molecular clocks on with severity of organ dysfunctions such as severity of brain dysfunction, pneumonia- or ventilator-associated lung inflammation, cardiovascular instability, liver and kidney failure, trauma, and septic shock. Finally, we address the potential of circadian rhythm stabilization to enhance and accelerate clinical recovery.</p>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"238 1","pages":""},"PeriodicalIF":6.3,"publicationDate":"2023-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apha.13962","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"6136480","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":"Have we got the guts to maintain target weight?","authors":"Nigel Irwin","doi":"10.1111/apha.13961","DOIUrl":"https://doi.org/10.1111/apha.13961","url":null,"abstract":"&lt;p&gt;With the obesity epidemic showing no signs of declining, understanding the mechanistic secrets behind losing body fat is highly relevant. In this issue of &lt;i&gt;Acta Physiologica&lt;/i&gt;, Gerstenberg, and co-workers&lt;span&gt;&lt;sup&gt;1&lt;/sup&gt;&lt;/span&gt; examine an increasingly important paradigm relating to lifestyle modifications that can induce and maintain body weight loss. Their studies cenetred on the secretion of appetite-regulating hormones from the gut of caloric-restricted rats fed a high-fat diet (HFD). In this setting, calorie restriction led to a 20% reduction in body weight in HFD rats at the time of experimentation. We are already aware that the secretion of appetite-inhibiting hormones is reduced in human obesity.&lt;span&gt;&lt;sup&gt;2&lt;/sup&gt;&lt;/span&gt; However, uncovering whether this effect is reversible following weight loss was the primary objective of Gerstenberg and colleagues.&lt;span&gt;&lt;sup&gt;1&lt;/sup&gt;&lt;/span&gt;&lt;/p&gt;&lt;p&gt;The chief experimental model employed by the investigators is the perfused rat small intestine.&lt;span&gt;&lt;sup&gt;3&lt;/sup&gt;&lt;/span&gt; The gut is the largest endocrine organ of the body and fundamental for the secretion of numerous appetite-regulating hormones. Earlier approaches to investigate gut hormone secretion predominantly involved primary or clonal cell lines as well as assessing hormone concentrations in plasma. The isolated intestinal perfusion model bridges the gap between these somewhat imperfect approaches, allowing for immediate assessment of dynamic hormone secretion under various stimuli in the absence of confounding factors.&lt;span&gt;&lt;sup&gt;3&lt;/sup&gt;&lt;/span&gt; Secretory concentrations of cholecystokinin (CCK), gastrin, glucose-dependent insulinotropic polypeptide (GIP), glucagon-like peptide-1 (GLP-1), neurotensin (NT), and somatostatin (SST), all gut-derived hormones known to suppress appetite, were measured using validated in-house radioimmunoassay's (RIAs).&lt;span&gt;&lt;sup&gt;1&lt;/sup&gt;&lt;/span&gt; To this end, the experimental tools employed here are the envy of physiology and biochemistry laboratories worldwide. That said, there were notable variations in baseline and stimulatory secretion profiles of some of the hormones studied, which may somewhat distort data interpretation. Whether this reflects model-specific issues, intra-assay variations of RIAs used, or simply the inherent unpredictability of gut hormone secretion remains to be elucidated. Indeed, gut hormone-secreting cells have a relatively rapid turnover rate and shown to possess the ability to switch hormone expression along the crypt-to-villus length.&lt;span&gt;&lt;sup&gt;4&lt;/sup&gt;&lt;/span&gt; In addition, the authors also examined gene expression of gut hormone nutrient transporters and markers of gut barrier integrity along the full length of the intestine.&lt;/p&gt;&lt;p&gt;The main finding from the study was that a 20% reduction of body weight in HFD rats did not affect the secretion of gut-derived CCK, gastrin, GIP, GLP-1, NT, and SST when compared to HFD control rats.&lt;span&gt;&lt;sup&gt;1&lt;/sup&gt;&lt;/span&gt; In addition, enteric gene expression was ","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"238 1","pages":""},"PeriodicalIF":6.3,"publicationDate":"2023-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apha.13961","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"5851478","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":"mTOR signaling in renal ion transport","authors":"Anastasia Adella,&nbsp;Jeroen H. F. de Baaij","doi":"10.1111/apha.13960","DOIUrl":"https://doi.org/10.1111/apha.13960","url":null,"abstract":"<p>The mammalian target of rapamycin (mTOR) signaling pathway is crucial in maintaining cell growth and metabolism. The mTOR protein kinase constitutes the catalytic subunit of two multimeric protein complexes called mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2). As such, this pathway is indispensable for many organs, including the kidney. Since its discovery, mTOR has been associated with major renal disorders such as acute kidney injury, chronic kidney disease, and polycystic kidney disease. On top of that, emerging studies using pharmacological interventions and genetic disease models have unveiled mTOR role in renal tubular ion handling. Along the tubule, mTORC1 and mTORC2 subunits are ubiquitously expressed at mRNA level. Nevertheless, at the protein level, current studies suggest that a tubular segment-specific balance between mTORC1 and mTORC2 exists. In the proximal tubule, mTORC1 regulates nutrients transports through various transporters located in this segment. On the other hand, in the thick ascending limb of the loop of Henle, both complexes play a role in regulating NKCC2 expression and activity. Lastly, in the principal cells of the collecting duct, mTORC2 determines Na⁺ reabsorption and K⁺ excretion by regulating of SGK1 activation. Altogether, these studies establish the relevance of the mTOR signaling pathway in the pathophysiology of tubular solute transport. Despite extensive studies on the effectors of mTOR, the upstream activators of mTOR signaling remain elusive in most nephron segments. Further understanding of the role of growth factor signaling and nutrient sensing is essential to establish the exact role of mTOR in kidney physiology.</p>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"238 1","pages":""},"PeriodicalIF":6.3,"publicationDate":"2023-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apha.13960","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"5827727","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":"Introducing a special series: Membrane proteins, epithelial transport, and kidney physiology","authors":"Henrik Dimke","doi":"10.1111/apha.13958","DOIUrl":"https://doi.org/10.1111/apha.13958","url":null,"abstract":"&lt;p&gt;Membrane proteins, facilitating transport across epithelia, are fundamental for a range of essential physiological processes throughout the organism. For instance, the regulation of epithelial transport is critically important for the homeostatic control of electrolyte and fluid balance, as well as many other solutes. Adjusting these epithelial transport mechanisms is at the core of a myriad of diverse physiological mechanisms, including the maintenance of blood pressure, glucose homeostasis, nutrient uptake, and the removal of waste products into urine. Knowledge of these epithelial transport mechanisms informs of their perturbations in pathophysiological conditions, as exemplified in cystic fibrosis, where the transmembrane conductance regulator anion channel disrupts epithelial chloride transport in airways and other organs,&lt;span&gt;&lt;sup&gt;1&lt;/sup&gt;&lt;/span&gt; or in familial hyperkalemia and hypertension where pathogenic variants in the with-no-lysine (WNK) protein kinases alter renal epithelial transport.&lt;span&gt;&lt;sup&gt;2&lt;/sup&gt;&lt;/span&gt; Understanding these epithelial transport processes open the door to targeted treatments.&lt;/p&gt;&lt;p&gt;Seminal discoveries of membrane proteins being essential components include the sodium-potassium ATPase by Jens Christian Skou&lt;span&gt;&lt;sup&gt;3&lt;/sup&gt;&lt;/span&gt; and aquaporin water channels by Peter Agre.&lt;span&gt;&lt;sup&gt;4&lt;/sup&gt;&lt;/span&gt; In recognition, both pioneers became Nobel laureates. Knowledge of the epithelial transport processes oftentimes precedes the identification of the responsible protein, while at other times the identification of a protein allows the identification of the transport process. These discoveries have shaped our understanding of epithelial transport physiology. None more so, than our understanding of the kidney and its central role in maintaining homeostasis.&lt;/p&gt;&lt;p&gt;The journal &lt;i&gt;Acta Physiologica&lt;/i&gt;, previously titled Acta Physiologica Scandinavica (1940–2005) and Skandinavisches Archiv für Physiologie (1889–1939) provide longstanding contributions to this field. For instance, in 1929, Norn found that the diurnal rhythm of urinary sodium, chloride, potassium, and water excretion could be reversed when studying a nurse on night shift.&lt;span&gt;&lt;sup&gt;5&lt;/sup&gt;&lt;/span&gt; In 1937, Krogh developed methods to study ion uptake and reported on the ability of the frog to absorb salt through the skin against large concentration gradients.&lt;span&gt;&lt;sup&gt;6&lt;/sup&gt;&lt;/span&gt; In 1951, Ussing and Zerahn published the development of an apparatus to simultaneously determine electric current and sodium transport through isolated frog skin,&lt;span&gt;&lt;sup&gt;7&lt;/sup&gt;&lt;/span&gt; now known as the Ussing chamber system. And in 1961 when Lassen et al, investigated the correlation between renal oxygen uptake and sodium reabsorption in the mammalian kidney.&lt;span&gt;&lt;sup&gt;8&lt;/sup&gt;&lt;/span&gt; These are just a few highlights and by no means an exhaustive overview of manuscripts published in Acta Physiologica on these topics. Furthermore, many manuscripts have been published within these","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"238 1","pages":""},"PeriodicalIF":6.3,"publicationDate":"2023-03-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apha.13958","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"5780558","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 parathyroid hormone on renal tubular calcium and phosphate handling","authors":"R. Todd Alexander,&nbsp;Henrik Dimke","doi":"10.1111/apha.13959","DOIUrl":"https://doi.org/10.1111/apha.13959","url":null,"abstract":"<p>Central to the maintenance of calcium homeostasis is the regulated reabsorption of calcium along the nephron. To this end, parathyroid hormone (PTH) is released from the parathyroid gland in response to lowered plasma calcium levels. This hormone acts through the PTH 1 receptor along the nephron to increase urinary phosphate excretion and decrease urinary calcium excretion. In the proximal tubule, PTH inhibits phosphate reabsorption by reducing the abundance of sodium phosphate cotransporters in the apical membrane. PTH likely decreases calcium reabsorption from the proximal tubule, by reducing the reabsorption of sodium, an event necessary for the paracellular movement of calcium across this segment. In the thick ascending limb (TAL), PTH increases calcium permeability and may increase the electrical driving force thereby increasing calcium reabsorption in the TAL. Finally, in the distal convolution, PTH acts to increase transcellular calcium reabsorption by increasing the activity and abundance of the apically expressed calcium channel TRPV5.</p>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"238 1","pages":""},"PeriodicalIF":6.3,"publicationDate":"2023-03-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apha.13959","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"5780541","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}