American journal of physiology. Endocrinology and metabolism最新文献

{"title":"Concentrations of Adrenocorticotropic Hormone (ACTH_1-24) Too Low to Effect Cortisol Enhance Osteogenesis <i>In Vitro</i> and <i>In Vivo</i>.","authors":"Irina L Tourkova, Reed A Rankin, Quitterie C Larrouture, Steve F Dobrowolski, Carlos M Isales, Harry C Blair","doi":"10.1152/ajpendo.00084.2025","DOIUrl":"https://doi.org/10.1152/ajpendo.00084.2025","url":null,"abstract":"<p><p>After finding that minimal amounts of adrenocorticotropic hormone (ACTH_1-24) prevented osteonecrosis in rabbits, we studied bone formation at nanomolar ACTH_1-24, <i>in vivo</i> in rabbits, and <i>in vitro</i> in human osteoblasts. ACTH_1-24 in rabbits at 0.6 μg/kg/day had no measurable effect on cortisol. Groups of five rabbits given 0.6 μg/kg/day of ACTH_1-24 enhanced trabecular bone in the rabbit femoral head relative to saline-treated controls (controls), increased bone volume/total volume (BV/TV) by micro-computed tomography, p<0.03. Xylenol orange and calcein labeling <i>in vivo</i> showed increased trabecular bone formation with 0.6 μg/kg/day of ACTH_1-24, p = 0.0089 versus controls. In contrast, the cortex of the femoral shaft was unaffected, BV/TV p>0.95 ACTH_1-24 versus controls. Bone marrow mRNA by PCR showed no change in osteoclast markers, and confirmed increased osteoblast markers, p<0.05. <i>In vitro</i>, ACTH_1-24 elevated expression of Collagen 1, alkaline phosphatase (ALP), osteocalcin (BGLAP), and RunX2 in human osteoblasts differentiated on polyethylene terephthalate (PET) membranes. Optimal response was at 10^-9 to 10^-12 M. VEGF, VEGF receptors FLT-1 and FLK-1, and ACTH_1-24 receptors MC2R were upregulated at 10^-12 M ACTH_1-24. Pathway analysis included increased BMP2, Smad1, Wnt-1, β-Catenin and TGF-β pathways. Because bone-forming osteoblasts are metabolically highly active, we studied mRNA expression of mitochondrial complex 1 (NDUFA5, NDUFS2, NDUFB1, NDUFB6) members with key roles in energy production. This increased at 10^-12 M ACTH_1-24. An ELISA for mitochondrial complex 1 activity showed maximum activity at 10^-9 M and high activity at 10^-12 M ACTH_1-24. Thus, long-term very low dose ACTH_1-24 increases bone formation <i>in vivo</i> and <i>in vitro</i>.</p>","PeriodicalId":7594,"journal":{"name":"American journal of physiology. Endocrinology and metabolism","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145051542","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":"Supplementation with GPR120 (Ffar4) ligand omega-3 does not improve survival in murine sepsis models.","authors":"Susana Castelo Branco Ramos Nakandakari, Eric Isaac Elliott, Renan Fudoli Lins Vieira, Thaiane da Silva Rios, Andin Fosam, Isadora Carolina Betim Pavan, Maíra Maftoum Costa, Luiz Guilherme Salvino da Silva, Camila de Oliveira Ramos, Giovana Rios Gonçalves, Ngozi D Akingbesote, Davi Sidarta-Oliveira, Ana Paula Moreli, Renata Rosseto Braga, Ana Paula Pinto, Anna Eisenstein, Licio Augusto Velloso, Fernando Moreira Simabuco, José Rodrigo Pauli, Eduardo Rochete Ropelle, Adelino Sanchez Ramos da Silva, Andrew Wang, Rachel J Perry, Dennys Esper Cintra","doi":"10.1152/ajpendo.00147.2025","DOIUrl":"https://doi.org/10.1152/ajpendo.00147.2025","url":null,"abstract":"<p><p>Sepsis is a condition marked by physiologic dysregulation secondary to infection and is influenced by the nutritional state. Despite several preclinical studies and clinical trials examining nutrition and supplements in sepsis, there are no clear guidelines. Omega-3 fatty acids are poly-unsaturated fatty acids with anti-inflammatory properties, represented mainly by alpha-linolenic (ALA - C18:3), eicosapentaenoic (EPA - C20:5), and docosahexaenoic (DHA - C22:6). Since sepsis is characterized with high levels of inflammation and subsequent organ dysfunction, we hypothesised that omega-3 ingestion would improve sepsis survival by attenuating inflammation via activation of GPR120 in immune cells. Here, we aimed to experimentally explore the role of omega-3 and the receptor that mediates their anti-inflammatory functions, GPR120, during sepsis. To evaluate GPR120 functionality, acute inflammation was induced via lipopolysaccharide (LPS) treatment in Raw 264.7 cells, 3T3-L1 cells, bone marrow derived macrophages and primary adipocytes. To evaluate the impact of omega-3 in sepsis, C57BL/6J mice were supplemented with omega-3 before LPS administration or cecal ligation and puncture (CLP) surgery. GPR120 mRNA expression decreased during inflammation. Unexpectedly, omega-3 supplementation preceding CLP worsened sepsis survival in mice. In addition, omega-3 did not affect inflammatory markers such as TNFα, IL1}, IL10, and IL6. Overall, our findings that omega-3 do not influence inflammation or improve survival in sepsis are surprising given that omega-3 supplementation is recommended for the prevention of cardiovascular diseases due to its anti-inflammatory properties. The negative impact of omega-3 supplementation on survival in the CLP model raises caution for future clinical studies involving sepsis.</p>","PeriodicalId":7594,"journal":{"name":"American journal of physiology. Endocrinology and metabolism","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145051581","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":"Replicating human diabetes: insights from a novel animal model.","authors":"Silvia Teixidó-Trujillo, Esteban Porrini, Luis Manuel Menéndez-Quintanal, Armando Torres-Ramírez, Cecilia Fumero, Ana E Rodríguez-Rodríguez","doi":"10.1152/ajpendo.00226.2025","DOIUrl":"https://doi.org/10.1152/ajpendo.00226.2025","url":null,"abstract":"<p><p>Type 2 diabetes is considered the pandemic of the 21st century. The pathogenesis of diabetes is complex and multifactorial, and its understanding is crucial for its prevention and treatment. Nevertheless, the pathogenesis of beta cell dysfunction remains unclear. This gap in knowledge could be related to a lack of appropriate pre-clinical models of type 2 diabetes. Current animal models, mostly genotypic and monogenic, do not fully reflect the pathophysiology of type 2 diabetes or associated organ damage. Therefore, a new pre-clinical model is needed. In this study we present a non-genotypic animal model of diabetes that combines obesity and the treatment with the diabetogenic immunosuppressor Tacrolimus (TAC). Sprague Dawley male rats were fed with a high-fat diet to establish obesity and metabolic syndrome. Then, TAC was administered for 6-9 months to induce chronic hyperglycaemia. These animals showed a decrease in Langerhans islets area and number, and development of islet fibrosis. There were also changes in pancreatic insulin and glucagon content, imbalance in the alpha/beta cell ratio and decrease in the expression of essential transcription factors MafA, FOXO1A, PDX-1 and NeuroD1. Altogether, this could be a more appropriate animal model to study the pathophysiology of diabetes and, eventually, related organ damage.</p>","PeriodicalId":7594,"journal":{"name":"American journal of physiology. Endocrinology and metabolism","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145051549","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":"Protein intake counteracts alcohol intake in the regulation of postprandial FGF21 secretion in humans.","authors":"Stina Ramne, Teresa Duarte da Costa Seco, Katharina B Kuentzel, Trisha J Grevengoed, Jasmin P Hjerresen, Thomas Moritz, Torben Hansen, Anne Raben, Niels Grarup","doi":"10.1152/ajpendo.00265.2025","DOIUrl":"https://doi.org/10.1152/ajpendo.00265.2025","url":null,"abstract":"<p><p>FGF21 is a hormone secreted from the liver in response to various nutritional stressors, suggested to be acting to balance dietary intake through negative feedback regulation. This meal study aimed to investigate two different potential nutrient interactions on postprandial FGF21 secretion in healthy human participants: 1) between intake of alcohol and protein and 2) between intake of alcohol and vitamin A (retinol). In a 4-arm, randomized, double-blinded, cross-over meal study (NCT06105476), postprandial circulating concentrations of FGF21, glucose, insulin, ethanol, and acetate were compared after intake of four different test drinks containing alcohol, alcohol+protein, alcohol+retinol or retinol in 27 healthy humans. The postprandial FGF21 response to the alcohol+protein drink was severely attenuated compared to the alcohol drink. The FGF21 response to the alcohol+retinol drink was similar to the alcohol drink, while there was no FGF21 response to the drink with retinol only. In conclusion, intake of protein inhibited the secretory FGF21 response to alcohol intake, while retinol intake did not appear to influence FGF21 secretion.</p>","PeriodicalId":7594,"journal":{"name":"American journal of physiology. Endocrinology and metabolism","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145032697","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":"Respiratory Resilience as Form Fades: Skeletal Muscle Mitochondrial Adaptation in Aging.","authors":"John Noone","doi":"10.1152/ajpendo.00369.2025","DOIUrl":"10.1152/ajpendo.00369.2025","url":null,"abstract":"","PeriodicalId":7594,"journal":{"name":"American journal of physiology. Endocrinology and metabolism","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144939081","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":"Defective medium-chain fatty acid β-oxidation in the liver alters the fat preference and induces hepatic steatosis and glucose intolerance.","authors":"Tsugunori Maruyama, Sho Matsui, Satoshi Tsuzuki, Takahiro Horie, Koh Ono, Tsutomu Sasaki","doi":"10.1152/ajpendo.00276.2025","DOIUrl":"https://doi.org/10.1152/ajpendo.00276.2025","url":null,"abstract":"<p><p>Long-chain triglycerides (LCTs) exert obesogenic effects, whereas medium-chain triglycerides (MCTs) exert antiobesity effects. To date, most studies examining the distinct effects of MCTs and LCTs have been conducted under extreme conditions using high-fat diets (45-60 kcal% fat). In this study, we aimed to investigate the health effects of varying MCT/LCT intake ratios in 30 kcal% high-fat diets, using liver-specific medium-chain acyl-CoA dehydrogenase (MCAD)-deficient (MCAD^L-/-) mice. Since this fat level more closely resembles the human diet without causing overeating, it allows for a purer assessment of the metabolic effects of the MCT/LCT intake ratios compared with the results of studies using extreme high-fat conditions. We fed MCAD^L-/- mice 30 kcal% fat MCT and LCT diets for 12 wk. Notably, MCAD^L-/- mice consumed the LCT diet more than the MCT diet, without any difference in the total caloric intake. Despite no difference in body weight, MCAD^L-/- mice exhibited impaired glucose tolerance and elevated hepatic triacylglycerol and cholesterol levels. Moreover, lipid droplet size and gene expression levels of some inflammatory markers increased in the adipose tissues of MCAD^L-/- mice. Overall, these results suggest that the intact metabolism of medium-chain fatty acids in the liver is crucial for dietary fat preference regulation. Furthermore, antiobesity effects of MCTs are observed even when the percentage of MCT intake is increased without altering the total fat intake.<b>NEW & NOTEWORTHY</b> Medium-chain triglycerides (MCTs) exert antiobesity effects; however, whether these antiobesity effects are observed when the MCT/long-chain triglyceride intake is altered using a high-fat diet (30 kcal% fat) remains unclear. This study found that impaired medium-chain fatty acid metabolism in the liver reduced MCT preference, without altering the total fat intake, resulting in metabolic dysfunction. Therefore, increasing the MCT ratio in dietary fats possibly reduces the risk of obesity.</p>","PeriodicalId":7594,"journal":{"name":"American journal of physiology. Endocrinology and metabolism","volume":"329 3","pages":"E433-E440"},"PeriodicalIF":3.1,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144939052","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":"New insights into lactate in exercise adaptations: does protein lactylation play a role?","authors":"Zhen Wang, Lin Zhu","doi":"10.1152/ajpendo.00225.2025","DOIUrl":"10.1152/ajpendo.00225.2025","url":null,"abstract":"<p><p>Physical activity and exercise are widely recognized as effective ways to promote physical fitness and prevent disease; however, their underlying molecular mechanisms remain to be fully elucidated. Within the last few years, the discovery of lactylation has propelled the well-known exercise metabolite lactate into the scientific spotlight. As the end product of glycolysis, lactate was initially considered to be a \"metabolic waste\" leading to muscle fatigue; however, subsequent studies have demonstrated the importance of lactate as an energy substrate and a signal transduction molecule to coordinate various physiological processes. Importantly, the novel posttranslational modification, lactylation, establishes a bridge between lactate and epigenetics, and provides new perspectives for understanding the role of lactate in exercise-mediated health promotion. Although some recent evidence in rodents suggests that exercise increases protein lactylation, there are mixed findings in this area, with limited human studies showing no effects. This review summarizes current knowledge of exercise-mediated lactylation, why mixed findings in the literature may exist, and suggests future research that can add further clarity to this area of molecular biology.</p>","PeriodicalId":7594,"journal":{"name":"American journal of physiology. Endocrinology and metabolism","volume":" ","pages":"E405-E419"},"PeriodicalIF":3.1,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144820363","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":"Early complete weaning in mice induces hepatic steatosis, which is associated with changes in phospholipids, metabolites, gene expression, and epigenome.","authors":"Haruka Adachi, Shiori Ishiyama, Kentaro Yoshimura, Hirotake Kasai, Kazuki Mochizuki","doi":"10.1152/ajpendo.00184.2025","DOIUrl":"10.1152/ajpendo.00184.2025","url":null,"abstract":"<p><p>Early complete weaning may increase the risk of developing metabolic diseases. This study investigated whether early complete weaning in mice leads to the development of steatosis. Institute of Cancer Research (ICR) mouse male pups were weaned at 17 days [early complete weaning (EW)] or 21 days [normal complete weaning (NW)] and subsequently fed the AIN93G diet until 32 weeks of age. We measured the diameter of lipid droplets, primary metabolites, protein expression related to phospholipid synthesis, and histone modifications of the <i>Pemt</i> in the liver. The lipid droplet diameter was larger in EW mice than in NW mice. A set of phosphatidylcholine (PC) species, particularly PC(38:6), demonstrated lower mRNA and protein expression of <i>Pemt</i> and methylenetetrahydrofolate reductase, as well as decreased primary metabolites related to <i>S</i>-adenosylmethionine/choline, and a reduction in an antioxidative marker in EW mice. Moreover, histone methylation (H3K4 tri-methyl and H3K36 di-/tri-methyl) and acetylation around <i>Pemt</i> were also lower in these mice. The steatosis development due to early complete weaning in mice is closely and positively associated with a reduced amount of PC.<b>NEW & NOTEWORTHY</b> The development of steatosis due to early complete weaning in mice is closely positively associated with a reduced amount of PC and related metabolites, transcriptome changes including <i>Pemt</i>, and alterations in histone modifications around <i>Pemt.</i></p>","PeriodicalId":7594,"journal":{"name":"American journal of physiology. Endocrinology and metabolism","volume":" ","pages":"E455-E462"},"PeriodicalIF":3.1,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144726520","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":"Lipidome profile of Cystic Fibrosis Related Diabetes, Type 1 and Type 2 Diabetes Mellitus: potential links to inflammation and glucose and lipid metabolism.","authors":"Alessandra Mingione, Cristian Loretelli, Michele Dei Cas, Francesca Pivari, Matteo Barcella, Ivan Merelli, Aida Zulueta, Rita Paroni, Letizia Corinna Morlacchi, Valentina Vaira, Francesca Gillani, Marco Piccoli, Luigi Anastasia, Elisabetta Albi, Ilaria Righi, Mario Nosotti, Paolo Fiorina, Anna Caretti, Lorenzo Rosso, Franco Folli, Paola Signorelli","doi":"10.1152/ajpendo.00293.2024","DOIUrl":"https://doi.org/10.1152/ajpendo.00293.2024","url":null,"abstract":"<p><p>Cystic Fibrosis (CF) is a genetic disease that primarily affects the pancreas and lungs. CF dyslipidaemia is characterized by decreased circulating lipids and increased ectopic lipid deposition in liver, pancreas, and lungs. Pancreatic exocrine insufficiency precedes the onset of CF related diabetes (CFRD). We hypothesized that different mechanisms contribute to CFRD development and progression, including features of Type 1 and Type 2 diabetes mellitus (T1DM and T2DM). Thus, we compared their plasma inflammatory, metabolic/hormonal, and lipidomic profiles, using Luminex assays and untargeted mass spectrometry analyses. Then, we compared the lipidomic profiles of lung biopsies and plasma extracellular vesicles (EVs) of CFRD and patients with other lung diseases (LD). Inflammatory cytokines (IL6 and IL1β) and chemokines (IL8 and MCP-1) were increased in the plasma of CFRD as compared with T1DM, whereas only cytokines increased when comparing with T2DM. Low insulin and C-peptide characterized CFRD and T1DM. Phosphatidylcholine, phosphatidylethanolamine and storage lipids were reduced and free fatty acids (FA) were increased in CFRD plasma compared with T1DM and T2DM. When comparing CFRD with LD, systemic inflammation was increased to a similar extent. Increased levels of sphingolipids, glycerolipids, acylcarnitines were found in lung biopsies of CFRD as compared to LD. Increased triacylglycerols in lung biopsies positively correlated with lung inflammatory infiltrates (CD68 positive cells) of CFRD patients. In conclusion, CFRD is characterized by altered lipid metabolism, insulin deficiency and insulin resistance, partially overlapping with both T1DM and T2DM. CFRD also involves ectopic lung lipids accumulation correlating with increased <i>in situ</i> inflammation.</p>","PeriodicalId":7594,"journal":{"name":"American journal of physiology. Endocrinology and metabolism","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144939043","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":"Estrogen signaling is necessary for the sex difference in simulated jet lag in mice.","authors":"Maria A Venegas, Nicholas Westray, Samuel Nwadialo, Yuriko Katsumata, Julie S Pendergast","doi":"10.1152/ajpendo.00268.2025","DOIUrl":"https://doi.org/10.1152/ajpendo.00268.2025","url":null,"abstract":"<p><p>The circadian system coordinates 24-hour cycles of internal biological processes with the environmental light-dark cycle. Abrupt shifts in the timing of the light-dark cycle misalign internal circadian clocks with the environment and cause jet lag until resynchronization occurs. The objective of this study was to investigate the sex difference in simulated jet lag in mice. Female mice resynchronized faster than male mice to 6-hour advances of the light-dark cycle that mimicked eastward travel. Circulating estradiol was necessary and sufficient for rapid resynchronization in female mice since ovariectomized females resynchronized slower than mice treated with estradiol. Disabling estrogen receptor alpha (ERα), but not ERβ or G-protein coupled estrogen receptor 1 (GPER1), abolished the sex difference in resynchronization. To investigate ERα-dependent mechanisms that regulate the rate of resynchronization, we measured the endogenous circadian period and the magnitudes of phase shifts to light pulses in male and female wild-type and ERα knockout mice. Wild-type females had shorter periods and greater phase delays in response to light pulses given in the early subjective night than male mice. Disabling ERα abolished the these sex differences by lengthening circadian period and reducing the magnitudes of phase delays. Together these data suggest that ERα alters the rate of resynchronization to shifted light-dark cycles by regulating period length and phase shift magnitude in female mice. Understanding the mechanisms underlying the sex difference in resynchronization to shifted light-dark cycles can be used to develop strategies to alleviate jet lag and circadian misalignment.</p>","PeriodicalId":7594,"journal":{"name":"American journal of physiology. Endocrinology and metabolism","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144939019","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}