Molecular Metabolism最新文献

{"title":"Control of Physiologic Glucose Homeostasis via Hypothalamic Modulation of Gluconeogenic Substrate Availability.","authors":"Jiaao Su, Abdullah Hashsham, Nandan Kodur, Carla Burton, Amanda Mancuso, Anjan Singer, Jennifer Wloszek, Abigail J Tomlinson, Warren T Yacawych, Jonathan N Flak, Kenneth T Lewis, Lily R Oles, Hiroyuki Mori, Nadejda Bozadjieva-Kramer, Adina F Turcu, Ormond A MacDougald, Martin G Myers, Alison H Affinati","doi":"10.1016/j.molmet.2025.102216","DOIUrl":"https://doi.org/10.1016/j.molmet.2025.102216","url":null,"abstract":"<p><strong>Objective: </strong>The brain mobilizes glucose in emergency situations such as hypoglycemia as well as during day-to-day physiology such as fasting. While most hypothalamic neuronal populations that contribute to glucose mobilization also contribute to other aspects of metabolism, neurons in the ventromedial nucleus of the hypothalamus that express the cholecystokinin b receptor (VMH^Cckbr neurons) support glucose production during hypoglycemia without controlling energy homeostasis. However, their role in day-to-day glucose physiology and the mechanisms they engage to support glucose mobilization is unclear.</p><p><strong>Methods: </strong>We used continuous glucose monitoring in mice with chronically silenced VMH^Cckbr neurons to establish whether these neurons are required during day-to-day glucose homeostasis. Tetanus-toxin based chronic silencing and acute optogenetic activation were followed by analysis of hepatic glucose metabolism and white adipose tissue lipolysis.</p><p><strong>Results: </strong>We found that VMH^Cckbr neurons support glucose homeostasis during short fasts and contribute to gluconeogenic substrate mobilization and lipolysis. VMH^Cckbr neurons mobilize glucose without depleting hepatic glycogen or increasing gluconeogenic gene expression, but instead mobilize glycerol in a β3-adrenergic receptor (β3-AR)-dependent manner. Restoring glycerol availability following VMH^Cckbr neuron silencing restores glucose. Finally, acute activation of VMH^Cckbr neurons mobilizes additional gluconeogenic substrates beyond glycerol.</p><p><strong>Conclusions: </strong>VMH^Cckbr neurons represent a distinct subset of glucose-mobilizing VMH neurons that support physiologic glucose homeostasis, likely through control of β3-AR-mediated gluconeogenic substrate mobilization and lipolysis. The presence of different glucose-mobilizing neuronal populations that engage distinct mechanisms in a context-dependent manner may provide the brain with flexibility to coordinate the appropriate glycemic response to different circumstances.</p>","PeriodicalId":18765,"journal":{"name":"Molecular Metabolism","volume":" ","pages":"102216"},"PeriodicalIF":7.0,"publicationDate":"2025-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144675299","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":"UCP2 MEDIATES MITOCHONDRIAL DYNAMICS TO INDUCE AgRP NEURONAL ACTIVITY.","authors":"Sungho Jin, Nal Ae Yoon, Zhong-Wu Liu, Ciro Menale, Jung Dae Kim, Nadia Diano, Sabrina Diano","doi":"10.1016/j.molmet.2025.102215","DOIUrl":"https://doi.org/10.1016/j.molmet.2025.102215","url":null,"abstract":"<p><strong>Objective: </strong>The hypothalamic agouti-related protein (AgRP)- expressing neurons regulate feeding and whole-body energy homeostasis. A growing body of evidence indicates that changes in mitochondrial dynamics, such as fission and fusion, play a crucial role in regulating AgRP neuronal activity. However, the mechanisms underlying this process remain to be elucidated. Here, we showed a role of mitochondrial UCP2-mediated mitochondrial dynamics in AgRP neurons in regulating AgRP neuronal activity and fasting-induced feeding behavior.</p><p><strong>Methods: </strong>We analyzed mitochondrial morphology, expression of activated dynamin-related protein 1 (DRP1), and mRNA expression levels of uncoupling protein 2 (Ucp2) in AgRP neurons of mice that were either in fed or fasted states. We then generated a mouse model in which Ucp2 was selectively deleted from adult AgRP neurons to assess the role of this mitochondrial protein in feeding behavior and whole-body energy metabolism.</p><p><strong>Results: </strong>We show fasting-induced AgRP neuronal activation is associated with UCP2-mediated mitochondrial fission and mitochondrial fatty acid utilization in AgRP neurons. In line with this, mice lacking UCP2 in AgRP neurons (Ucp2^AgRPKO) show attenuated fasting- or ghrelin-induced AgRP neuronal activation and feeding behaviors and exhibited a significant decrease in body weight and fat mass accompanied by a significant increase in energy expenditure.</p><p><strong>Conclusions: </strong>Altogether, our data revealed that UCP2-mediated mitochondrial dynamics and fatty acids oxidation in the hypothalamic AgRP neurons is necessary for AgRP neuronal function and fasting-induced food intake.</p>","PeriodicalId":18765,"journal":{"name":"Molecular Metabolism","volume":" ","pages":"102215"},"PeriodicalIF":7.0,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144668015","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":"Mitochondrial-targeted plastoquinone therapy prevents early onset muscle weakness that occurs before atrophy during ovarian cancer.","authors":"Luca J Delfinis, Shahrzad Khajehzadehshoushtar, Luke D Flewwelling, Nathaniel J Andrews, Madison C Garibotti, Shivam Gandhi, Aditya N Brahmbhatt, Brooke A Morris, Bianca Garlisi, Sylvia Lauks, Caroline Aitken, Leslie Ogilvie, Stavroula Tsitkanou, Jeremy A Simpson, Nicholas P Greene, Arthur J Cheng, Jim Petrik, Christopher G R Perry","doi":"10.1016/j.molmet.2025.102211","DOIUrl":"https://doi.org/10.1016/j.molmet.2025.102211","url":null,"abstract":"<p><p>Muscle loss with cancer causes weakness, worsens quality of life, and predicts reduced overall survival rates. Recently, muscle weakness was identified during early-stage cancer before atrophy develops. This discovery indicates that mechanisms independent of muscle loss must contribute to progressive weakness. While mitochondrial stress responses are associated with early-stage 'pre-cachexia' weakness, a causal relationship has not been established. Here, using a mouse model of metastatic ovarian cancer cachexia, we identified that the well-established mitochondrial-targeted plastoquinone SkQ1 partially prevents muscle weakness occurring before the development of atrophy in the diaphragm. Furthermore, SkQ1 improved force production during atrophy without preventing atrophy itself in the tibialis anterior and diaphragm. These findings indicate that atrophy-independent mechanisms of muscle weakness occur in different muscle types throughout ovarian cancer. Ovarian cancer reduced flexor digitorum brevis (FDB) whole muscle force production and myoplasmic free calcium ([Ca²⁺]_i) during contraction in intact single muscle fibers, both of which were prevented by SkQ1. Remarkably, changes in mitochondrial reactive oxygen species and pyruvate metabolism were heterogeneous across time and between muscle types which highlights a considerable complexity in the relationships between mitochondria and muscle remodeling throughout ovarian cancer. These discoveries identify that muscle weakness can occur independent of atrophy throughout ovarian cancer in a manner that is linked to improved calcium handling. The findings also demonstrate that mitochondrial-targeted therapies exert a robust effect in preserving muscle force early during ovarian cancer during the pre-atrophy period and in late stages once cachexia has become severe.</p>","PeriodicalId":18765,"journal":{"name":"Molecular Metabolism","volume":" ","pages":"102211"},"PeriodicalIF":7.0,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144668014","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":"Downstream interaction by glucagon-like peptide-1 and glucose-dependent insulinotropic polypeptide agonism is required for synergistic effects on body weight.","authors":"Claire H Feetham, Minrong Ai, Isabella Culotta, Alessia Costa, Jenna Hunter, Tamer Coskun, Paul J Emmerson, Giuseppe D'Agostino, Simon M Luckman","doi":"10.1016/j.molmet.2025.102214","DOIUrl":"https://doi.org/10.1016/j.molmet.2025.102214","url":null,"abstract":"<p><strong>Objective: </strong>Dual glucagon-like peptide-1 receptor and glucose-dependent insulinotropic polypeptide receptor agonists (GLP1RA and GIPRA, respectively) synergise to reduce body weight. Though this synergy depends on receptors within the brain, where and how this occurs is unclear.</p><p><strong>Methods: </strong>We employed a combination of neuroanatomical approaches in the mouse to investigate access of the dual GLP1RA/GIPRA, tirzepatide, and study the central targets engaged by single agonist, dual agonist and combined agonist treatments. Genetic manipulations were then used to further investigate the functional significance of specific brain regions and distinct neuronal subtypes.</p><p><strong>Results: </strong>We recorded penetration of fluorescently labelled tirzepatide limited mainly to circumventricular organs and confirmed the importance both GLP1R and GIPR in the dorsal vagal complex for the actions of systemically administered agonists. Receptor expression indicates GIPRA alone activates a distinct population of GABA neurons in the area postrema directly, but also neurotensin neurons in the central amygdala (Nts^CeA) indirectly. Disabling Nts^CeA neurons selectively reduces the synergistic effect of dual GLP1R/GIPR agonist administration on body weight.</p><p><strong>Conclusions: </strong>As with selective GLP1RA, the actions of dual GLP1RA/GIPA appear to be dependent on the dorsal vagal complex for their action, probably most importantly by gaining access through the area postrema. Downstream targets include the central amygdala where signals following dual receptor agonism interact. Specifically, Nts^CeA neurons are required for the full synergistic effect of dual receptor agonism on body weight.</p>","PeriodicalId":18765,"journal":{"name":"Molecular Metabolism","volume":" ","pages":"102214"},"PeriodicalIF":7.0,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144668013","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":"Subcutaneous Adipose Tissue-Secreted Proteins as Endocrine Regulators of Physical and Cognitive Function in Older Adults.","authors":"Cheehoon Ahn, Ian Tamburini, James A Sanford, Mingqi Zhou, Farah Gamie, Reichelle X Yeo, Carlos H Viesi, Maria Pino, Katie L Whytock, Lauren E Oberlin, Theresa Mau, Joshua N Adkins, Jamie N Justice, Ashlee N Wood, Zana M Ross, Paul D Piehowski, Chelsea M Hutchinson Bunch, Kirk I Erickson, Frederico G S Toledo, Nancy E Lane, Peggy M Cawthon, Anne B Newman, Stephen B Kritchevsky, Steven R Cummings, Bret H Goodpaster, Erin E Kershaw, Marcus M Seldin, Lauren M Sparks","doi":"10.1016/j.molmet.2025.102213","DOIUrl":"https://doi.org/10.1016/j.molmet.2025.102213","url":null,"abstract":"<p><p>Declines in skeletal muscle and cognitive function in older adults have been linked to abnormalities in abdominal subcutaneous adipose tissue (ASAT), yet the underlying molecular mediators remain poorly understood. Here, leveraging ASAT transcriptomics and explant-conditioned media proteomics from participants in the Study of Muscle, Mobility and Aging (SOMMA; age ≥70 years, n=229), we identified ASAT gene clusters and secreted proteins strongly associated with comprehensive assessments of physical and cognitive function in older adults. ASAT inflammation and secreted immunoglobulins were identified as key signatures of aging-associated physical and cognitive performance limitations. Systems genetics analysis confirmed secreted-SERPINF1 as a negative regulator of skeletal muscle contraction and highlighted its potential role in inducing inflammation in the heart in silico. Additionally, novel ASAT-secreted proteins such as NID2 and APOA4 were implicated in mediating ASAT crosstalk with skeletal muscle and brain in silico. Our framework provides insights into ASAT-driven tissue crosstalk underlying physical and cognitive performance in older adults and offers a valuable resource for understanding the role of ASAT in human aging.</p>","PeriodicalId":18765,"journal":{"name":"Molecular Metabolism","volume":" ","pages":"102213"},"PeriodicalIF":7.0,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144659678","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":"The Diabetes Gene Tcf7l2 Organizes Gene Expression in the Liver and Regulates Amino Acid Metabolism.","authors":"Joanna Krawczyk, William O'Connor, Pedro Vendramini, Mareike Schell, Kiran J Biddinger, Matt Kanke, George Pengo, Ivana Semova, Tiffany Fougeray, Marcia Haigis, Krishna G Aragam, Wouter H Lamers, Linus T Tsai, Praveen Sethupathy, Sudha B Biddinger","doi":"10.1016/j.molmet.2025.102208","DOIUrl":"https://doi.org/10.1016/j.molmet.2025.102208","url":null,"abstract":"<p><p>TCF7L2 harbors the strongest genetic association with diabetes identified thus far. However, its function in liver has remained unclear. Here, we find that liver-specific deletion Tcf7l2 has little effect on plasma glucose, but disrupts hepatic zonation. That is, in the normal liver, many genes show gradients of expression across the liver lobule; in the absence of Tcf7l2, these gradients collapse. One major consequence is the disorganization of glutamine metabolism, with a loss of the glutamine production program, ectopic expression of the glutamine consumption program, and a decrease in glutamine levels. In parallel, metabolomic profiling shows glutamine to be the most significantly decreased metabolite in the plasma of individuals harboring the rs7903146 variant in TCF7L2. Taken together, these data indicate that hepatic TCF7L2 has a secondary role in glycemic control, but a primary role in maintaining transcriptional architecture and glutamine homeostasis.</p>","PeriodicalId":18765,"journal":{"name":"Molecular Metabolism","volume":" ","pages":"102208"},"PeriodicalIF":7.0,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144659679","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":"p21-activated kinases (PAKs) regulate FGF1/PDE4D antilipolytic pathway and insulin resistance in adipocytes.","authors":"Judith Seigner, Johannes Krier, David Spähn, Leontine Sandforth, Judith L Nono, Robert Lukowski, Andreas L Birkenfeld, Gencer Sancar","doi":"10.1016/j.molmet.2025.102210","DOIUrl":"10.1016/j.molmet.2025.102210","url":null,"abstract":"<p><p>Increasing evidence suggests that adipose tissue plays a key role in the development, progression, and treatment of the globally epidemic disease type 2 diabetes (T2D). For example, adipose tissue dysfunction, lipotoxicity, and insulin resistance (IR) are major contributors and targets for the treatment of T2D. We previously identified the Fibroblast growth factor 1 (FGF1)/Phosphodiesterase 4D (PDE4D) pathway, which lowers plasma glucose concentration by suppressing lipolysis in adipose tissue and ultimately regulating hepatic glucose production in obese insulin-resistant mice. While phosphorylation of PDE4D is critical for its activity, the upstream signaling mechanisms remain unclear. In this study, we identified p21-activated kinases (PAKs) as regulator of PDE4D phosphorylation and suppression of lipolysis by FGF1. Inhibition of PAK-induced cAMP accumulation prevented antilipolytic function of FGF1, and reversed suppression of lipolysis caused by PDE4D overexpression, linking PAKs to the regulation of cAMP by PDE4D in murine adipocytes in vitro. Chronic inhibition of PAKs decreased lipid accumulation in both mouse and human adipocyte cultures, lowered expression of adipogenic markers, and induced IR, suggesting a previously unidentified role of PAKs in adipocyte function and differentiation. We conclude that PAKs play a crucial role in regulating the FGF1/PDE4D antilipolytic pathway, adipogenesis and IR, thereby highlighting their potential as therapeutic targets for T2D.</p>","PeriodicalId":18765,"journal":{"name":"Molecular Metabolism","volume":" ","pages":"102210"},"PeriodicalIF":7.0,"publicationDate":"2025-07-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144637670","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":"Fructose-induced synaptic and neuronal adaptations at neuropeptide Y/agouti-related peptide neurons.","authors":"Mikayla A Payant, Aditi S Sankhe, Persephone A Miller, Sarah S Vieira, Yasmina Dumiaty, Jenny Phy-Lim, Zachary L Levy, Melissa J Chee","doi":"10.1016/j.molmet.2025.102209","DOIUrl":"10.1016/j.molmet.2025.102209","url":null,"abstract":"<p><p>Fructose is a naturally-occurring sugar, consumed in excess as sweeteners, and is linked to the development of obesity. Fructose is consumed with glucose (dextrose) in added sugars, but while dextrose produces satiety, excessive fructose intake promotes hyperphagia through the brain. However, the neurological effects of dietary fructose are not clearly defined. We fed male and female mice standard chow, a 60% high fructose, or 60% high dextrose diet and found that fructose- and dextrose-fed mice ate more calories and gained more body fat despite increasing fat oxidation and energy expenditure. Their metabolic syndromes were more prominent in male mice, who also developed glucose intolerance. To define the neurological effects underlying the obesogenic actions of fructose, we performed ex vivo patch-clamp recordings from orexigenic Neuropeptide Y/agouti-related peptide (NPY/AgRP) neurons in the arcuate nucleus. Fructose feeding uniquely increased synaptic excitation at NPY/AgRP neurons, which remained elevated with sustained fructose exposure; this excitation may arise from glutamatergic neurons in the dorsomedial hypothalamic nucleus. Terminating fructose feeding reversed this synaptic excitation at male but not female NPY/AgRP neurons. Furthermore, chronic but not acute fructose feeding in male mice also irreversibly activated NPY/AgRP neurons even following fructose withdrawal. Interestingly, despite sex-dependent fructose-mediated plasticity at NPY/AgRP neurons, a prolonged fructose withdrawal increased innate fructose preference in both male and female mice. Taken together, these findings showed that fructose elicited synaptic and neuronal excitation at NPY/AgRP neurons that can be long-lasting. These actions are consistent with that seen during hunger and may thus promote hyperphagia in the expression of fructose-mediated obesity.</p>","PeriodicalId":18765,"journal":{"name":"Molecular Metabolism","volume":" ","pages":"102209"},"PeriodicalIF":7.0,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144626646","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":"Muscle very long-chain ceramides associate with insulin resistance independently of obesity.","authors":"Søren Madsen, Harry B Cutler, Kristen C Cooke, Meg Potter, Jasmine Khor, Christoph D Rau, Stewart Wc Masson, Anna Howell, Zora Modrusan, Anthony S Don, Jacqueline Stöckli, Alexis Diaz Vegas, David E James","doi":"10.1016/j.molmet.2025.102212","DOIUrl":"https://doi.org/10.1016/j.molmet.2025.102212","url":null,"abstract":"<p><p>Lipids, in particular ceramides and diacylglycerols (DAGs), are implicated in insulin resistance (IR), however their precise roles remain unclear. Here, we leverage natural genetic variation to examine muscle lipids and systemic IR in 399 Diversity Outbred Australia mice fed either chow or a high-fat diet. Adipose tissue mass was significantly associated with 55% of muscle lipid features and whole-body insulin sensitivity, with DAGs as the only lipid class enriched in this association. To disentangle the contribution of adiposity and muscle lipids to whole-body insulin sensitivity, we employed two independent approaches: (1) a linear model correcting muscle lipid features for adipose tissue mass to assess their relationship with insulin sensitivity, and (2) stratifying mice into insulin sensitivity quartiles within adiposity bins. Both revealed that very long-chain ceramides, but not DAGs, were linked to IR. RNA sequencing and proteomics from the same muscles further associated these very long-chain ceramides with cellular stress, mitochondrial dysfunction, and protein synthesis. Meanwhile, DAGs correlated with leptin gene expression in skeletal muscle, suggesting they originate from contaminating adipocytes rather than myocytes per se. We propose that many muscle lipids, including DAGs, associate with muscle and systemic IR due to accumulation of adipose tissue rather than directly influencing muscle insulin sensitivity. By addressing the relationship between adiposity and metabolic state, we identified very long-chain muscle ceramides as being highly associated with IR independently of adiposity.</p>","PeriodicalId":18765,"journal":{"name":"Molecular Metabolism","volume":" ","pages":"102212"},"PeriodicalIF":7.0,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144626723","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 to “IL-6 decodes sex and diet-dependent circadian and metabolic rhythms” [Mol Metabol 97 (2025) 102171]","authors":"Antía González-Vila ,&nbsp;Ali Mohammad Ibrahim-Alasoufi ,&nbsp;María Luengo-Mateos ,&nbsp;Víctor Pardo-García ,&nbsp;Alejandro Diaz-López ,&nbsp;Belén Fernández-Rodríguez ,&nbsp;Matti Poutanen ,&nbsp;Claes Ohlsson ,&nbsp;Manuel Tena-Sempere ,&nbsp;Carlos Diéguez-González ,&nbsp;María Del Carmen García-García ,&nbsp;Olga Barca-Mayo","doi":"10.1016/j.molmet.2025.102198","DOIUrl":"10.1016/j.molmet.2025.102198","url":null,"abstract":"","PeriodicalId":18765,"journal":{"name":"Molecular Metabolism","volume":"99 ","pages":"Article 102198"},"PeriodicalIF":7.0,"publicationDate":"2025-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144567574","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}