Cell metabolismPub Date : 2024-10-01Epub Date: 2024-08-26DOI: 10.1016/j.cmet.2024.07.021
Esther W Lim, Regis J Fallon, Caleb Bates, Yoichiro Ideguchi, Takayuki Nagasaki, Michal K Handzlik, Emeline Joulia, Roberto Bonelli, Courtney R Green, Brendan R E Ansell, Maki Kitano, Ilham Polis, Amanda J Roberts, Shigeki Furuya, Rando Allikmets, Martina Wallace, Martin Friedlander, Christian M Metallo, Marin L Gantner
{"title":"Serine and glycine physiology reversibly modulate retinal and peripheral nerve function.","authors":"Esther W Lim, Regis J Fallon, Caleb Bates, Yoichiro Ideguchi, Takayuki Nagasaki, Michal K Handzlik, Emeline Joulia, Roberto Bonelli, Courtney R Green, Brendan R E Ansell, Maki Kitano, Ilham Polis, Amanda J Roberts, Shigeki Furuya, Rando Allikmets, Martina Wallace, Martin Friedlander, Christian M Metallo, Marin L Gantner","doi":"10.1016/j.cmet.2024.07.021","DOIUrl":"10.1016/j.cmet.2024.07.021","url":null,"abstract":"<p><p>Metabolic homeostasis is maintained by redundant pathways to ensure adequate nutrient supply during fasting and other stresses. These pathways are regulated locally in tissues and systemically via the liver, kidney, and circulation. Here, we characterize how serine, glycine, and one-carbon (SGOC) metabolism fluxes across the eye, liver, and kidney sustain retinal amino acid levels and function. Individuals with macular telangiectasia (MacTel), an age-related retinal disease with reduced circulating serine and glycine, carrying deleterious alleles in SGOC metabolic enzymes exhibit an exaggerated reduction in circulating serine. A Phgdh<sup>+/</sup><sup>-</sup> mouse model of this haploinsufficiency experiences accelerated retinal defects upon dietary serine/glycine restriction, highlighting how otherwise silent haploinsufficiencies can impact retinal health. We demonstrate that serine-associated retinopathy and peripheral neuropathy are reversible, as both are restored in mice upon serine supplementation. These data provide molecular insights into the genetic and metabolic drivers of neuro-retinal dysfunction while highlighting therapeutic opportunities to ameliorate this pathogenesis.</p>","PeriodicalId":93927,"journal":{"name":"Cell metabolism","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142082835","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell metabolismPub Date : 2024-10-01Epub Date: 2024-08-20DOI: 10.1016/j.cmet.2024.07.017
Brendan Cordeiro, Jeeyoon Jennifer Ahn, Saurabh Gawde, Carmen Ucciferri, Nuria Alvarez-Sanchez, Xavier S Revelo, Natalie Stickle, Kaylea Massey, David G Brooks, Joel M Guthridge, Gabriel Pardo, Daniel A Winer, Robert C Axtell, Shannon E Dunn
{"title":"Obesity intensifies sex-specific interferon signaling to selectively worsen central nervous system autoimmunity in females.","authors":"Brendan Cordeiro, Jeeyoon Jennifer Ahn, Saurabh Gawde, Carmen Ucciferri, Nuria Alvarez-Sanchez, Xavier S Revelo, Natalie Stickle, Kaylea Massey, David G Brooks, Joel M Guthridge, Gabriel Pardo, Daniel A Winer, Robert C Axtell, Shannon E Dunn","doi":"10.1016/j.cmet.2024.07.017","DOIUrl":"10.1016/j.cmet.2024.07.017","url":null,"abstract":"<p><p>Obesity has been implicated in the rise of autoimmunity in women. We report that obesity induces a serum protein signature that is associated with T helper 1 (Th1), interleukin (IL)-17, and multiple sclerosis (MS) signaling pathways selectively in human females. Females, but not male mice, subjected to diet-induced overweightness/obesity (DIO) exhibited upregulated Th1/IL-17 inflammation in the central nervous system during experimental autoimmune encephalomyelitis, a model of MS. This was associated with worsened disability and a heightened expansion of myelin-specific Th1 cells in the peripheral lymphoid organs. Moreover, at steady state, DIO increased serum levels of interferon (IFN)-α and potentiated STAT1 expression and IFN-γ production by naive CD4<sup>+</sup> T cells uniquely in female mice. This T cell phenotype was driven by increased adiposity and was prevented by the removal of ovaries or knockdown of the type I IFN receptor in T cells. Our findings offer a mechanistic explanation of how obesity enhances autoimmunity.</p>","PeriodicalId":93927,"journal":{"name":"Cell metabolism","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11463735/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142019843","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell metabolismPub Date : 2024-10-01Epub Date: 2024-08-16DOI: 10.1016/j.cmet.2024.07.016
Traci E LaMoia, Brandon T Hubbard, Mateus T Guerra, Ali Nasiri, Ikki Sakuma, Mario Kahn, Dongyan Zhang, Russell P Goodman, Michael H Nathanson, Yasemin Sancak, Mark Perelis, Vamsi K Mootha, Gerald I Shulman
{"title":"Cytosolic calcium regulates hepatic mitochondrial oxidation, intrahepatic lipolysis, and gluconeogenesis via CAMKII activation.","authors":"Traci E LaMoia, Brandon T Hubbard, Mateus T Guerra, Ali Nasiri, Ikki Sakuma, Mario Kahn, Dongyan Zhang, Russell P Goodman, Michael H Nathanson, Yasemin Sancak, Mark Perelis, Vamsi K Mootha, Gerald I Shulman","doi":"10.1016/j.cmet.2024.07.016","DOIUrl":"10.1016/j.cmet.2024.07.016","url":null,"abstract":"<p><p>To examine the roles of mitochondrial calcium Ca<sup>2+</sup> ([Ca<sup>2+</sup>]<sub>mt</sub>) and cytosolic Ca<sup>2+</sup> ([Ca<sup>2+</sup>]<sub>cyt</sub>) in the regulation of hepatic mitochondrial fat oxidation, we studied a liver-specific mitochondrial calcium uniporter knockout (MCU KO) mouse model with reduced [Ca<sup>2+</sup>]<sub>mt</sub> and increased [Ca<sup>2+</sup>]<sub>cyt</sub> content. Despite decreased [Ca<sup>2+</sup>]<sub>mt</sub>, deletion of hepatic MCU increased rates of isocitrate dehydrogenase flux, α-ketoglutarate dehydrogenase flux, and succinate dehydrogenase flux in vivo. Rates of [<sup>14</sup>C<sub>16</sub>]palmitate oxidation and intrahepatic lipolysis were increased in MCU KO liver slices, which led to decreased hepatic triacylglycerol content. These effects were recapitulated with activation of CAMKII and abrogated with CAMKII knockdown, demonstrating that [Ca<sup>2+</sup>]<sub>cyt</sub> activation of CAMKII may be the primary mechanism by which MCU deletion promotes increased hepatic mitochondrial oxidation. Together, these data demonstrate that hepatic mitochondrial oxidation can be dissociated from [Ca<sup>2+</sup>]<sub>mt</sub> and reveal a key role for [Ca<sup>2+</sup>]<sub>cyt</sub> in the regulation of hepatic fat mitochondrial oxidation, intrahepatic lipolysis, gluconeogenesis, and lipid accumulation.</p>","PeriodicalId":93927,"journal":{"name":"Cell metabolism","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11446666/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141997077","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell metabolismPub Date : 2024-09-03Epub Date: 2024-08-19DOI: 10.1016/j.cmet.2024.07.019
Qinqin He, Liwei Ji, Yanyan Wang, Yarong Zhang, Haiyan Wang, Junyan Wang, Qing Zhu, Maodi Xie, Wei Ou, Jun Liu, Kuo Tang, Kening Lu, Qingmei Liu, Jian Zhou, Rui Zhao, Xintian Cai, Nanfang Li, Yang Cao, Tao Li
{"title":"Acetate enables metabolic fitness and cognitive performance during sleep disruption.","authors":"Qinqin He, Liwei Ji, Yanyan Wang, Yarong Zhang, Haiyan Wang, Junyan Wang, Qing Zhu, Maodi Xie, Wei Ou, Jun Liu, Kuo Tang, Kening Lu, Qingmei Liu, Jian Zhou, Rui Zhao, Xintian Cai, Nanfang Li, Yang Cao, Tao Li","doi":"10.1016/j.cmet.2024.07.019","DOIUrl":"10.1016/j.cmet.2024.07.019","url":null,"abstract":"<p><p>Sleep is essential for overall health, and its disruption is linked to increased risks of metabolic, cognitive, and cardiovascular dysfunctions; however, the molecular mechanisms remain poorly understood. This study investigated how sleep disturbances contribute to metabolic imbalance and cognition impairment using a chronic sleep fragmentation (SF) mouse model. SF mice exhibited impaired cognition, glucose metabolism, and insulin sensitivity compared with controls. We identified increased acetate levels in hypothalamic astrocytes as a defensive response in SF mice. Through acetate infusion or astrocyte-specific Acss1 deletion to elevate acetate levels, we observed mitigated metabolic and cognitive impairments in SF mice. Mechanistically, acetate binds and activates pyruvate carboxylase, thereby restoring glycolysis and the tricarboxylic acid cycle. Among individuals most commonly affected by SF, patients with obstructive sleep apnea exhibited elevated acetate levels when coupled with type 2 diabetes. Our study uncovers the protective effect of acetate against sleep-induced metabolic and cognitive impairments.</p>","PeriodicalId":93927,"journal":{"name":"Cell metabolism","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142010118","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"TNF compromises intestinal bile-acid tolerance dictating colitis progression and limited infliximab response.","authors":"Mengqi Zheng, Yunjiao Zhai, Yanbo Yu, Jing Shen, Shuzheng Chu, Enrico Focaccia, Wenyu Tian, Sui Wang, Xuesong Liu, Xi Yuan, Yue Wang, Lixiang Li, Bingcheng Feng, Zhen Li, Xiaohuan Guo, Ju Qiu, Cuijuan Zhang, Jiajie Hou, Yiyuan Sun, Xiaoyun Yang, Xiuli Zuo, Mathias Heikenwalder, Yanqing Li, Detian Yuan, Shiyang Li","doi":"10.1016/j.cmet.2024.06.008","DOIUrl":"10.1016/j.cmet.2024.06.008","url":null,"abstract":"<p><p>The intestine constantly encounters and adapts to the external environment shaped by diverse dietary nutrients. However, whether and how gut adaptability to dietary challenges is compromised in ulcerative colitis is incompletely understood. Here, we show that a transient high-fat diet exacerbates colitis owing to inflammation-compromised bile acid tolerance. Mechanistically, excessive tumor necrosis factor (TNF) produced at the onset of colitis interferes with bile-acid detoxification through the receptor-interacting serine/threonine-protein kinase 1/extracellular signal-regulated kinase pathway in intestinal epithelial cells, leading to bile acid overload in the endoplasmic reticulum and consequent apoptosis. In line with the synergy of bile acids and TNF in promoting gut epithelial damage, high intestinal bile acids correlate with poor infliximab response, and bile acid clearance improves infliximab efficacy in experimental colitis. This study identifies bile acids as an \"opportunistic pathogenic factor\" in the gut that would represent a promising target and stratification criterion for ulcerative colitis prevention/therapy.</p>","PeriodicalId":93927,"journal":{"name":"Cell metabolism","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141545705","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell metabolismPub Date : 2024-09-03Epub Date: 2024-08-19DOI: 10.1016/j.cmet.2024.07.018
Lan Yan, Yajie Wang, Haidong Hu, Diran Yang, Wenjing Wang, Zhihua Luo, Yangze Wang, Fengzhen Yang, Kwok-Fai So, Li Zhang
{"title":"Physical exercise mediates cortical synaptic protein lactylation to improve stress resilience.","authors":"Lan Yan, Yajie Wang, Haidong Hu, Diran Yang, Wenjing Wang, Zhihua Luo, Yangze Wang, Fengzhen Yang, Kwok-Fai So, Li Zhang","doi":"10.1016/j.cmet.2024.07.018","DOIUrl":"10.1016/j.cmet.2024.07.018","url":null,"abstract":"<p><p>Lactate is a critical metabolite during the body's adaption to exercise training, which effectively relieves anxiety-like disorders. The biological mechanism of lactate in the exercise-mediated anxiolytic effect has, however, not been comprehensively investigated. Here, we report that exercise-induced lactate markedly potentiates the lactylation of multiple synaptic proteins, among which synaptosome-associated protein 91 (SNAP91) is the critical molecule for synaptic functions. Both anatomical evidence and in vivo recording data showed that the lactylation of SNAP91 confers resilience against chronic restraint stress (CRS) via potentiating synaptic structural formation and neuronal activity in the medial prefrontal cortex (mPFC). More interestingly, exercise-potentiated lactylation of SNAP91 is necessary for the prevention of anxiety-like behaviors in CRS mice. These results collectively suggest a previously unrecognized non-histone lactylation in the brain for modulating mental functions and provide evidence for the brain's metabolic adaption during exercise paradigms.</p>","PeriodicalId":93927,"journal":{"name":"Cell metabolism","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142010119","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell metabolismPub Date : 2024-07-02Epub Date: 2024-06-14DOI: 10.1016/j.cmet.2024.05.010
Ajit Regmi, Eitaro Aihara, Michael E Christe, Gabor Varga, Thomas P Beyer, Xiaoping Ruan, Emily Beebe, Libbey S O'Farrell, Melissa A Bellinger, Aaron K Austin, Yanzhu Lin, Haitao Hu, Debra L Konkol, Samantha Wojnicki, Adrienne K Holland, Jessica L Friedrich, Robert A Brown, Amanda S Estelle, Hannah S Badger, Gabriel S Gaidosh, Sander Kooijman, Patrick C N Rensen, Tamer Coskun, Melissa K Thomas, William Roell
{"title":"Tirzepatide modulates the regulation of adipocyte nutrient metabolism through long-acting activation of the GIP receptor.","authors":"Ajit Regmi, Eitaro Aihara, Michael E Christe, Gabor Varga, Thomas P Beyer, Xiaoping Ruan, Emily Beebe, Libbey S O'Farrell, Melissa A Bellinger, Aaron K Austin, Yanzhu Lin, Haitao Hu, Debra L Konkol, Samantha Wojnicki, Adrienne K Holland, Jessica L Friedrich, Robert A Brown, Amanda S Estelle, Hannah S Badger, Gabriel S Gaidosh, Sander Kooijman, Patrick C N Rensen, Tamer Coskun, Melissa K Thomas, William Roell","doi":"10.1016/j.cmet.2024.05.010","DOIUrl":"10.1016/j.cmet.2024.05.010","url":null,"abstract":"<p><p>Tirzepatide, a glucose-dependent insulinotropic polypeptide/glucagon-like peptide 1 receptor (GIPR/GLP-1R) agonist, has, in clinical trials, demonstrated greater reductions in glucose, body weight, and triglyceride levels compared with selective GLP-1R agonists in people with type 2 diabetes (T2D). However, cellular mechanisms by which GIPR agonism may contribute to these improved efficacy outcomes have not been fully defined. Using human adipocyte and mouse models, we investigated how long-acting GIPR agonists regulate fasted and fed adipocyte functions. In functional assays, GIPR agonism enhanced insulin signaling, augmented glucose uptake, and increased the conversion of glucose to glycerol in a cooperative manner with insulin; however, in the absence of insulin, GIPR agonists increased lipolysis. In diet-induced obese mice treated with a long-acting GIPR agonist, circulating triglyceride levels were reduced during oral lipid challenge, and lipoprotein-derived fatty acid uptake into adipose tissue was increased. Our findings support a model for long-acting GIPR agonists to modulate both fasted and fed adipose tissue function differentially by cooperating with insulin to augment glucose and lipid clearance in the fed state while enhancing lipid release when insulin levels are reduced in the fasted state.</p>","PeriodicalId":93927,"journal":{"name":"Cell metabolism","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141328142","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell metabolismPub Date : 2024-07-02Epub Date: 2024-06-13DOI: 10.1016/j.cmet.2024.05.014
Zheng Wu, Divya Bezwada, Feng Cai, Robert C Harris, Bookyung Ko, Varun Sondhi, Chunxiao Pan, Hieu S Vu, Phong T Nguyen, Brandon Faubert, Ling Cai, Hongli Chen, Misty Martin-Sandoval, Duyen Do, Wen Gu, Yuanyuan Zhang, Yuannyu Zhang, Bailey Brooks, Sherwin Kelekar, Lauren G Zacharias, K Celeste Oaxaca, Joao S Patricio, Thomas P Mathews, Javier Garcia-Bermudez, Min Ni, Ralph J DeBerardinis
{"title":"Electron transport chain inhibition increases cellular dependence on purine transport and salvage.","authors":"Zheng Wu, Divya Bezwada, Feng Cai, Robert C Harris, Bookyung Ko, Varun Sondhi, Chunxiao Pan, Hieu S Vu, Phong T Nguyen, Brandon Faubert, Ling Cai, Hongli Chen, Misty Martin-Sandoval, Duyen Do, Wen Gu, Yuanyuan Zhang, Yuannyu Zhang, Bailey Brooks, Sherwin Kelekar, Lauren G Zacharias, K Celeste Oaxaca, Joao S Patricio, Thomas P Mathews, Javier Garcia-Bermudez, Min Ni, Ralph J DeBerardinis","doi":"10.1016/j.cmet.2024.05.014","DOIUrl":"10.1016/j.cmet.2024.05.014","url":null,"abstract":"<p><p>Mitochondria house many metabolic pathways required for homeostasis and growth. To explore how human cells respond to mitochondrial dysfunction, we performed metabolomics in fibroblasts from patients with various mitochondrial disorders and cancer cells with electron transport chain (ETC) blockade. These analyses revealed extensive perturbations in purine metabolism, and stable isotope tracing demonstrated that ETC defects suppress de novo purine synthesis while enhancing purine salvage. In human lung cancer, tumors with markers of low oxidative mitochondrial metabolism exhibit enhanced expression of the salvage enzyme hypoxanthine phosphoribosyl transferase 1 (HPRT1) and high levels of the HPRT1 product inosine monophosphate. Mechanistically, ETC blockade activates the pentose phosphate pathway, providing phosphoribosyl diphosphate to drive purine salvage supplied by uptake of extracellular bases. Blocking HPRT1 sensitizes cancer cells to ETC inhibition. These findings demonstrate how cells remodel purine metabolism upon ETC blockade and uncover a new metabolic vulnerability in tumors with low respiration.</p>","PeriodicalId":93927,"journal":{"name":"Cell metabolism","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11240302/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141322228","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell metabolismPub Date : 2024-06-04Epub Date: 2024-03-14DOI: 10.1016/j.cmet.2024.02.014
Ever Espino-Gonzalez, Emilie Dalbram, Rémi Mounier, Julien Gondin, Jean Farup, Niels Jessen, Jonas T Treebak
{"title":"Impaired skeletal muscle regeneration in diabetes: From cellular and molecular mechanisms to novel treatments.","authors":"Ever Espino-Gonzalez, Emilie Dalbram, Rémi Mounier, Julien Gondin, Jean Farup, Niels Jessen, Jonas T Treebak","doi":"10.1016/j.cmet.2024.02.014","DOIUrl":"10.1016/j.cmet.2024.02.014","url":null,"abstract":"<p><p>Diabetes represents a major public health concern with a considerable impact on human life and healthcare expenditures. It is now well established that diabetes is characterized by a severe skeletal muscle pathology that limits functional capacity and quality of life. Increasing evidence indicates that diabetes is also one of the most prevalent disorders characterized by impaired skeletal muscle regeneration, yet underlying mechanisms and therapeutic treatments remain poorly established. In this review, we describe the cellular and molecular alterations currently known to occur during skeletal muscle regeneration in people with diabetes and animal models of diabetes, including its associated comorbidities, e.g., obesity, hyperinsulinemia, and insulin resistance. We describe the role of myogenic and non-myogenic cell types on muscle regeneration in conditions with or without diabetes. Therapies for skeletal muscle regeneration and gaps in our knowledge are also discussed, while proposing future directions for the field.</p>","PeriodicalId":93927,"journal":{"name":"Cell metabolism","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140137620","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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