American journal of physiology. Endocrinology and metabolism最新文献

{"title":"The acute and chronic influence of exercise on mitochondrial dynamics in skeletal muscle.","authors":"Elya J Ritenis, Camila S Padilha, Matthew B Cooke, Christos G Stathis, Andrew Philp, Donny M Camera","doi":"10.1152/ajpendo.00311.2024","DOIUrl":"10.1152/ajpendo.00311.2024","url":null,"abstract":"<p><p>Exercise and nutritional modulation are potent stimuli for eliciting increases in mitochondrial mass and function. Collectively, these beneficial adaptations are increasingly recognized to coincide with improvements in skeletal muscle health. Mitochondrial dynamics of fission and fusion are increasingly implicated as having a central role in mediating aspects of key organelle adaptations that are seen with exercise. Exercise-induced mitochondrial adaptation dynamics that have been implicated are <i>1</i>) increases to mitochondrial turnover, resulting from elevated rates of mitochondrial synthesis (biogenesis) and degradative (mitophagy) processes and <i>2</i>) morphological changes to the three-dimensional (3-D) tubular network, known as the mitochondrial reticulum, that mitochondria form in skeletal muscle. Notably, mitochondrial fission has also been implicated in coordinating increases in mitophagy, following acute exercise. Furthermore, increased fusion following exercise training promotes increased connectivity of the mitochondrial reticulum and is associated with improved metabolism and mitochondrial function. However, the molecular basis and fashion in which exercise infers beneficial mitochondrial adaptations through mitochondrial dynamics remains to be fully elucidated. This review attempts to highlight recent developments investigating the effects of exercise on mitochondrial dynamics, while attempting to offer a perspective of the methodological refinements and potential variables, such as substrate/glycogen availability, which should be considered going forward.</p>","PeriodicalId":7594,"journal":{"name":"American journal of physiology. Endocrinology and metabolism","volume":" ","pages":"E198-E209"},"PeriodicalIF":4.2,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142492945","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":"Quantifying protein kinetics in vivo: influence of precursor dynamics on product labeling.","authors":"Huifang Yao, Seamus Kelley, Dan Zhou, Sophie VanSickle, Sheng-Ping Wang, Jennifer Piesvaux, Haihong Zhou, Hao Chen, David McKenney, David G McLaren, Jeanine E Ballard, Stephen F Previs","doi":"10.1152/ajpendo.00323.2024","DOIUrl":"10.1152/ajpendo.00323.2024","url":null,"abstract":"<p><p>Protein kinetics can be quantified by coupling stable isotope tracer methods with mass spectrometry readouts; however, interconnected decision points in the experimental design affect the complexity of the workflow and impact data interpretations. For example, choosing between a single bolus (pulse-chase) or a continuous exposure protocol influences subsequent decisions regarding when to measure and how to model the temporal labeling of a target protein. Herein, we examine the merits of in vivo tracer protocols, and we direct attention toward stable isotope tracer experiments that rely on administering a single bolus since these are generally more practical to use as compared with continuous administration protocols. We demonstrate how the interplay between precursor and product kinetics impacts downstream analytics and calculations by contrasting fast versus slow turnover precursors (e.g., ¹³C-leucine vs. ²H-water, respectively). Although the data collected here underscore certain advantages of using longer-lived precursors (e.g., ²H- or ¹⁸O-water), the results also highlight the influence of tracer recycling on measures of protein turnover. We discuss the impact of tracer recycling and consider how the sampling interval is critical for interpreting studies. Finally, we demonstrate that tracer recycling does not limit the ability to perform back-to-back studies of protein kinetics. It is possible to run experiments in which subjects are used as their own controls even though the precursor and product remain labeled following an initial tracer dosing.<b>NEW & NOTEWORTHY</b> We demonstrate a simple and robust protocol for measuring protein synthesis, the work considers problems encountered in experimental design. The logic can enable biologists with limited resources and/or can facilitate scenarios where higher throughput experiments are needed.</p>","PeriodicalId":7594,"journal":{"name":"American journal of physiology. Endocrinology and metabolism","volume":" ","pages":"E173-E185"},"PeriodicalIF":4.2,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142612364","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":"L-type Calcium Channel Blockade Worsens Glucose Tolerance and β-Cell Function in C57BL6/J Mice Exposed to Intermittent Hypoxia.","authors":"Stanley M Chen-Cardenas, Tess A Baker, Larissa A Shimoda, Ernesto Bernal-Mizrachi, Naresh M Punjabi","doi":"10.1152/ajpendo.00001.2025","DOIUrl":"https://doi.org/10.1152/ajpendo.00001.2025","url":null,"abstract":"<p><p>Intermittent hypoxemia (IH), a pathophysiologic consequence of obstructive sleep apnea (OSA), adversely affects insulin sensitivity, insulin secretion, and glucose tolerance. Nifedipine, an L-type calcium channel blocker frequently used for treatment of hypertension, can also impair insulin sensitivity and secretion. However, the cumulative and interactive repercussions of IH and nifedipine on glucose homeostasis have not been previously investigated. Adult male C57BL6/J mice were exposed to either nifedipine or vehicle concurrently with IH or intermittent air (IA) over five days. IH exposure entailed cycling fractional inspired oxygen levels between 0.21 and 0.055 at a rate of 60 events per hour. Nifedipine (20 mg/kg/day) or vehicle was administered via subcutaneous osmotic pumps resulting in four groups of mice: IA-vehicle (control), IA-nifedipine, and IH-vehicle, IH-nifedipine. Compared to IA (control), IH increased fasting glucose (Mean Δ:33.0 mg/dl; p<0.001) and insulin (mean Δ: 0.53 ng/ml; p<0.001) with nifedipine having no independent effect. Furthermore, glucose tolerance was worse with nifedipine alone, and IH further exacerbated the impairment in glucose disposal (p=0.013 for interaction). Nifedipine also decreased glucose-stimulated insulin secretion and the insulinogenic index, with addition of IH attenuating those measures further. There were no discernible alterations in insulin biosynthesis/processing, insulin content, or islet morphology. These findings underscore the detrimental impact of IH on insulin sensitivity and glucose tolerance, while highlighting that nifedipine exacerbates these disturbances through impaired β- cell function. Consequently, cautious use of L-type calcium channel blockers is warranted in OSA patients, particularly in those at risk for type 2 diabetes.</p>","PeriodicalId":7594,"journal":{"name":"American journal of physiology. Endocrinology and metabolism","volume":" ","pages":""},"PeriodicalIF":4.2,"publicationDate":"2025-01-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142942596","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":"Hepatocyte HIF-2α aggravates NAFLD by inducing ferroptosis through increasing extracellular iron.","authors":"Shunkui Luo, Zhanjin Lu, Lingling Wang, Yun Li, Yingjuan Zeng, Hongyun Lu","doi":"10.1152/ajpendo.00287.2023","DOIUrl":"10.1152/ajpendo.00287.2023","url":null,"abstract":"<p><p>Recent research has illuminated the pivotal role of the hypoxia-inducible factor-2α (HIF-2α)/peroxisome proliferator-activated receptor alpha (PPARα) pathway in the progression of nonalcoholic fatty liver disease (NAFLD). Meanwhile, it has been reported that HIF-2α is involved in iron regulation, and that aberrant iron distribution leads to liver lipogenesis. Therefore, we hypothesize that HIF-2α exacerbates fatty liver by affecting iron distribution. To substantiate this hypothesis, we utilized liver-specific HIF-2α knockout mice and the LO2 cell line with overexpressed HIF-2α. HIF-2α overexpression (OE) was induced via lentiviral infection, followed by exposure to free fatty acids (FFAs) and deferoxamine (DFO). In animal experiments, hepatic HIF-2α knockout resulted in lower liver lipid levels, lower liver weight, and higher serum iron levels. Enrichment in autophagy, ferroptosis, and the PI3K-AKT pathway was demonstrated through Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis in the liver of mice. In vitro experiments showed that HIF-2α increased supernatant iron. In the HIF-2α OE group, the addition of FFA led to decreased levels of reduced glutathione (GSH) and glutathione peroxidase 4 (GPX4) protein, along with increased lipid peroxidation (LPO), cellular lipid droplets, and triglyceride content. Impressively, DFO intervention decreased supernatant iron, reversed these changes by increasing GSH and GPX4 levels, and simultaneously reduced LPO levels, cellular lipid droplets, and triglyceride content. In addition, the expression of proteins related to β-oxidation increased, and lipid deposition in hepatocytes improved, which may be associated with the PI3K/AKT pathway. In summary, our findings suggest that HIF-2α-mediated iron flux enhances NAFLD cell susceptibility to ferroptosis, thereby impacting lipid metabolism-related genes and contributing to lipid accumulation.<b>NEW & NOTEWORTHY</b> The experiment demonstrated that HIF-2α increased extracellular iron. In LO2 cells overexpressing HIF-2α, FFAs not only increased cellular lipid and triglyceride levels but also induced key features of ferroptosis, such as reduced GSH and GPX4 levels and increased LPO, despite the absence of cellular iron overload. These effects were reversed by lowering extracellular iron with DFO. Furthermore, DFO treatment increased β-oxidation protein expression and improved lipid deposition in hepatocytes, potentially through the PI3K/AKT pathway.</p>","PeriodicalId":7594,"journal":{"name":"American journal of physiology. Endocrinology and metabolism","volume":" ","pages":"E92-E104"},"PeriodicalIF":4.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142827115","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":"Enhanced quantification of α-cell suppression by hyperglycemia using a high-sensitivity glucagon assay.","authors":"Roy B Dyer, Marcello C Laurenti, Hannah E Christie, Sneha Mohan, Aoife M Egan, Chiara Dalla Man, Adrian Vella","doi":"10.1152/ajpendo.00301.2024","DOIUrl":"10.1152/ajpendo.00301.2024","url":null,"abstract":"<p><p>Accurate measurement of glucagon concentrations in a variety of conditions is necessary for subsequent estimation of glucagon secretion. Glucagon arises in the α-cell as a product of proglucagon processing. Modern two-site immunoassays have overcome prior problems with glucagon measurement caused by cross-reactivity with other proglucagon-derived fragments. However, in response to hyperglycemia, glucagon concentrations can fall below the limit of quantification of commercial immunoassays. This has implications for the characterization of α-cell function in health, in prediabetes, and in type 2 diabetes. An increase in the sensitivity of glucagon measurement was achieved by ethanol precipitation and concentration of the sample before measurement. Concentrating the sample sixfold enabled a decrease in the level of quantitation from 1.7 to 0.3 pmol/L with acceptable precision. To establish whether this enhanced high-sensitivity glucagon assay enhances the characterization of α-cell function in health and disease, we then estimated glucagon secretion rate (GSR) in four subjects. We subsequently used the relationship of GSR to glucose concentrations to characterize the α-cell response to glucose and demonstrate improved characterization of α-cell dysfunction in vivo.<b>NEW & NOTEWORTHY</b> We describe a method that lowers the limit of quantification of a glucagon immunoassay thereby enhancing the ability to differentiate between normal and abnormal α-cell responsiveness to glucagon.</p>","PeriodicalId":7594,"journal":{"name":"American journal of physiology. Endocrinology and metabolism","volume":" ","pages":"E62-E68"},"PeriodicalIF":4.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142798667","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":"Corrigendum for Bai et al., volume 296, 2009, p. E79-E88.","authors":"","doi":"10.1152/ajpendo.90539.2008_COR","DOIUrl":"10.1152/ajpendo.90539.2008_COR","url":null,"abstract":"","PeriodicalId":7594,"journal":{"name":"American journal of physiology. Endocrinology and metabolism","volume":"328 1","pages":"E137"},"PeriodicalIF":4.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142962011","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":"IGF-1 LR3 does not promote growth in late-gestation growth-restricted fetal sheep.","authors":"Alicia White, Jane Stremming, Stephanie R Wesolowski, Saif I Al-Juboori, Evgenia Dobrinskikh, Sean W Limesand, Laura D Brown, Paul J Rozance","doi":"10.1152/ajpendo.00259.2024","DOIUrl":"10.1152/ajpendo.00259.2024","url":null,"abstract":"<p><p>Insulin-like growth factor-1 (IGF-1) and insulin are important fetal anabolic hormones. Complications of pregnancy, such as placental insufficiency, can lead to fetal growth restriction (FGR) with low-circulating IGF-1 and insulin concentrations and attenuated glucose-stimulated insulin secretion (GSIS), which likely contribute to neonatal glucose dysregulation. We previously demonstrated that a 1-wk infusion of IGF-1 LR3, an IGF-1 analog with low affinity for IGF-binding proteins and high affinity for the IGF-1 receptor, at 6.6 µg·kg^-1·h^-1 into normal fetal sheep increased body weight but lowered insulin concentrations and GSIS. In this study, FGR fetal sheep received either IGF-1 LR3 treatment at 1.17 ± 0.12 μg·kg^-1·h^-1 (LR3; <i>n</i> = 7) or vehicle (VEH; <i>n</i> = 7) for 1 wk. Plasma insulin, glucose, oxygen, and amino acids were measured before starting treatment and at the end of the treatment period. GSIS was measured on the final treatment day. Fetal body weights, insulin, glucose, oxygen, and GSIS were not different between groups. Amino acid concentrations decreased in LR3 (baseline vs. final individual means comparison <i>P</i> = 0.0232) but not in VEH (<i>P</i> = 0.3866). In summary, a 1-wk IGF-1 LR3 treatment did not improve growth in FGR fetuses. Insulin concentrations and GSIS were not attenuated by IGF-1 LR3, yet circulating amino acids decreased, which could reflect increased amino acid utilization. We speculate that maintaining amino acid concentrations or raising insulin, glucose, and/or oxygen concentrations to values consistent with normally growing fetuses during IGF-1 LR3 treatment may be necessary to increase fetal growth in the setting of placental insufficiency and FGR.<b>NEW & NOTEWORTHY</b> IGF-1 LR3 treatment administered directly into growth-restricted fetal sheep circulation did not improve fetal growth or attenuate circulating insulin or fetal GSIS. Importantly, IGF-1 LR3 treatment reduced circulating amino acids, notably branched-chain amino acids, which have been shown to potentiate GSIS and protein accretion supporting fetal growth.</p>","PeriodicalId":7594,"journal":{"name":"American journal of physiology. Endocrinology and metabolism","volume":" ","pages":"E116-E125"},"PeriodicalIF":4.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11901354/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142826600","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":"The mitochondrial lactate oxidation complex: endpoint for carbohydrate carbon disposal.","authors":"Robert G Leija, Jose A Arevalo, Dianna Xing, José Pablo Vázquez-Medina, George A Brooks","doi":"10.1152/ajpendo.00306.2024","DOIUrl":"10.1152/ajpendo.00306.2024","url":null,"abstract":"<p><p>The lactate shuttle concept has revolutionized our understanding and study of metabolism in physiology, biochemistry, intermediary metabolism, nutrition, and medicine. Seminal findings of the mitochondrial lactate oxidation complex (mLOC) elucidated the architectural structure of its components. Here, we report that the mitochondrial pyruvate carrier (mPC) is an additional member of the mLOC in mouse muscle and C2C12 myoblasts and myotubes. Immunoblots, mass spectrometry, and co-immunoprecipitation experiments of mitochondrial preparations revealed abundant amounts of mitochondrial lactate dehydrogenase (mLDH), monocarboxylate transporter (mMCT), basigin (CD147), cytochrome oxidase (COx), and pyruvate carriers 1 and 2 (mPC1 and 2). In addition, using confocal laser scanning microscopy (CLSM) and in situ proximity ligation, we also demonstrated planar and three-dimensional (3-D) colocalization of pyruvate and lactate transporters with COx in fixed mouse skeletal muscle sections and C2C12 myoblasts and myotubes skeletal muscle sections, mouse muscle and C2C12 myoblasts and myotubes myotubes, and C2C12 myoblasts. This work serves as a landmark for configuring the final pathway of carbohydrate oxidation.<b>NEW & NOTEWORTHY</b> We expand on knowledge of the architectural design of the mitochondrial lactate oxidation complex (mLOC); key members are: mitochondrial lactate dehydrogenase (mLDH), monocarboxylate transporter 1 (mMCT1), cytochrome oxidase (COx), basigin scaffolding protein (CD147), and the mitochondrial pyruvate carrier (mPC). The mLOC is key in creating the lower end of the concentration gradient for disposal of lactate and pyruvate.</p>","PeriodicalId":7594,"journal":{"name":"American journal of physiology. Endocrinology and metabolism","volume":" ","pages":"E126-E136"},"PeriodicalIF":4.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142881083","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":"Chronic inorganic nitrate supplementation does not improve metabolic health and worsens disease progression in mice with diet-induced obesity.","authors":"Alice P Sowton, Lorenz M W Holzner, Fynn N Krause, Ruby Baxter, Gabriele Mocciaro, Dominika K Krzyzanska, Magdalena Minnion, Katie A O'Brien, Matthew C Harrop, Paula M Darwin, Benjamin D Thackray, Michele Vacca, Martin Feelisch, Julian L Griffin, Andrew J Murray","doi":"10.1152/ajpendo.00256.2024","DOIUrl":"10.1152/ajpendo.00256.2024","url":null,"abstract":"<p><p>Inorganic nitrate (NO₃^-) has been proposed to be of therapeutic use as a dietary supplement in obesity and related conditions including the metabolic syndrome (MetS), type II diabetes, and metabolic dysfunction-associated steatotic liver disease (MASLD). Administration of NO₃^- to endothelial nitric oxide synthase-deficient mice reversed aspects of MetS; however, the impact of NO₃^- supplementation in diet-induced obesity is not well understood. Here we investigated the whole body metabolic phenotype and cardiac and hepatic metabolism in mice fed a high-fat, high-sucrose (HFHS) diet for up to 12 mo of age, supplemented with 1 mM NaNO₃ (or NaCl) in their drinking water. HFHS feeding was associated with a progressive obesogenic and diabetogenic phenotype, which was not ameliorated by NO₃^-. Furthermore, HFHS-fed mice supplemented with NO₃^- showed elevated levels of cardiac fibrosis and accelerated progression of MASLD including development of hepatocellular carcinoma in comparison with NaCl-supplemented mice. NO₃^- did not enhance mitochondrial β-oxidation capacity in any tissue assayed and did not suppress hepatic lipid accumulation, suggesting it does not prevent lipotoxicity. We conclude that NO₃^- is ineffective in preventing the metabolic consequences of an obesogenic diet and may instead be detrimental to metabolic health against the background of HFHS feeding. This is the first report of an unfavorable effect of long-term nitrate supplementation in the context of the metabolic challenges of overfeeding, warranting urgent further investigation into the mechanism of this interaction.<b>NEW & NOTEWORTHY</b> Inorganic nitrate has been suggested to be of therapeutic benefit in obesity-related conditions, as it increases nitric oxide bioavailability, enhances mitochondrial β-oxidation, and reverses metabolic syndrome in <i>eNOS^-/-</i> mice. However, we here show that over 12 months nitrate was ineffective in preventing metabolic consequences in high fat, high sucrose-fed mice and worsened aspects of metabolic health, impairing cholesterol handling, increasing cardiac fibrosis, and exacerbating steatotic liver disease progression, with acceleration to hepatocellular carcinoma.</p>","PeriodicalId":7594,"journal":{"name":"American journal of physiology. Endocrinology and metabolism","volume":" ","pages":"E69-E91"},"PeriodicalIF":4.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142798705","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":"Studies on cortisol, corticosterone, and 17β-estradiol indicate these steroids have no role in stress or reproduction in the common octopus (<i>Octopus vulgaris</i>).","authors":"Benjamin H Maskrey, Carolina Costas, Luís Méndez-Martínez, Laura Guerrero-Peña, Ricardo Tur, Pablo García, Pablo Touriñan, David Chavarrias, Adelino V Canario, Alex P Scott, Josep Rotllant","doi":"10.1152/ajpendo.00251.2024","DOIUrl":"10.1152/ajpendo.00251.2024","url":null,"abstract":"<p><p>The common octopus (<i>Octopus vulgaris</i>) is a promising candidate for aquaculture diversification, particularly in Europe. As interest in octopus farming grows, animal welfare concerns arise. In bony vertebrates (teleosts and tetrapods), measurements of the levels of corticosterone or cortisol have been successfully used as indicators of stress and welfare. Here, it is explored whether octopuses also produce cortisol or corticosterone and, if so, whether they are released into the water in response to stress (as can be done in teleosts and amphibians). The ability of the octopus to absorb cortisol from the water is also investigated-with another steroid, the principle vertebrate estrogen, 17β-estradiol (E₂), being used as a positive uptake control. In this study, using liquid chromatography tandem mass spectrometry techniques, it was found that octopus hemolymph did not contain either cortisol, corticosterone, cortisone (a common metabolite of cortisol), or E₂. Nor were any of the corticosteroids consistently found in the water in which stressed octopuses were held. The results support the evolutionary argument that octopuses are unlikely to exhibit a stress response mediated by vertebrate-like corticosteroids. Octopus demonstrated a low ability to absorb cortisol from the water (<2% over 24 h) but showed a high ability to absorb E₂ from water (92% over 24 h). In this latter respect, the octopus is similar to other mollusks. The finding calls into doubt the origin of the E₂ measured in this species.<b>NEW & NOTEWORTHY</b> This study demonstrates that common octopuses (<i>Octopus vulgaris</i> Cuvier 1797) do not produce cortisol, cortisone, or corticosterone in response to stress. Using liquid chromatography tandem mass spectrometry, it was also shown that octopuses have a low absorption rate of cortisol from water but a high absorption rate of 17β-estradiol (E2). The findings support the evolutionary argument that octopuses are unlikely to exhibit a stress response mediated by vertebrate-like corticosteroids.</p>","PeriodicalId":7594,"journal":{"name":"American journal of physiology. Endocrinology and metabolism","volume":" ","pages":"E105-E115"},"PeriodicalIF":4.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142805599","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}