Pub Date : 2022-10-19DOI: 10.1093/lifemeta/loac029
Guang Lu, Han-Ming Shen
CLN3 is a lysosomal transmembrane protein and loss of CLN3 mutation is known to cause a juvenile lethal neurodegenerative lysosomal storage disorder (LSD), called Batten disease. In a recent study published in Nature, Laqtom et al. reported a novel function of CLN3 in the clearance of glycerophospholipid from lysosomes via lysosomal efflux of glycerophosphodiesters (GPDs), not only establishing a deeper mechanistic understanding of Batten disease, also suggesting both the diagnostic and therapeutic potential of CLN3-GPDs in this type of neurodegenerative LSD.
{"title":"CLN3 clinches lysosomes in clearance of glycerophospholipids","authors":"Guang Lu, Han-Ming Shen","doi":"10.1093/lifemeta/loac029","DOIUrl":"https://doi.org/10.1093/lifemeta/loac029","url":null,"abstract":"\u0000 CLN3 is a lysosomal transmembrane protein and loss of CLN3 mutation is known to cause a juvenile lethal neurodegenerative lysosomal storage disorder (LSD), called Batten disease. In a recent study published in Nature, Laqtom et al. reported a novel function of CLN3 in the clearance of glycerophospholipid from lysosomes via lysosomal efflux of glycerophosphodiesters (GPDs), not only establishing a deeper mechanistic understanding of Batten disease, also suggesting both the diagnostic and therapeutic potential of CLN3-GPDs in this type of neurodegenerative LSD.","PeriodicalId":74074,"journal":{"name":"Life metabolism","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42835884","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}
Pub Date : 2022-10-10DOI: 10.1093/lifemeta/loac028
Yuqin Wang, Xinzhi Li, Cenxi Liu, Liying Zhou, Lei Shi, Zhiguo Zhang, Long Chen, Ming Gao, Lanyue Gao, Yuanyuan Xu, He Huang, Jin Li, Zheng Chen
Brown adipocyte maturation during postnatal development is essential for brown adipose tissue (BAT) to protect animals against cold. Impaired maturation of brown adipocytes leads to cold intolerance. However, the molecular mechanisms that determines maturation of brown adipocytes during postnatal development are not fully understood. Here we identify Wilms’ tumor 1-associating protein (WTAP) as an essential regulator in the postnatal development and maturation of BAT. BAT-specific knockout of Wtap (Wtap-BKO) severely impairs maturation of BAT in vivo by decreasing the expression of BAT-selective genes, leading to whitening of interscapular BAT (iBAT). Single nucleus RNA-sequencing analysis shows the dynamic changes of cell heterogeneity in iBAT of Wtap-BKO mice. Adult mice with WTAP deficiency in BAT display hypothermic and succumb to acute cold challenge. Mechanistically, WTAP deficiency decreases m 6A mRNA modification by reducing the protein stability of METTL3. BAT-specific overexpression of Mettl3 partially rescues the phenotypes observed in Wtap-BKO mice. These data demonstrate that WTAP/METTL3 plays an essential role in iBAT postnatal development and thermogenesis.
{"title":"WTAP Regulates Postnatal Development of Brown Adipose Tissue by stabilizing METTL3 in mice","authors":"Yuqin Wang, Xinzhi Li, Cenxi Liu, Liying Zhou, Lei Shi, Zhiguo Zhang, Long Chen, Ming Gao, Lanyue Gao, Yuanyuan Xu, He Huang, Jin Li, Zheng Chen","doi":"10.1093/lifemeta/loac028","DOIUrl":"https://doi.org/10.1093/lifemeta/loac028","url":null,"abstract":"\u0000 Brown adipocyte maturation during postnatal development is essential for brown adipose tissue (BAT) to protect animals against cold. Impaired maturation of brown adipocytes leads to cold intolerance. However, the molecular mechanisms that determines maturation of brown adipocytes during postnatal development are not fully understood. Here we identify Wilms’ tumor 1-associating protein (WTAP) as an essential regulator in the postnatal development and maturation of BAT. BAT-specific knockout of Wtap (Wtap-BKO) severely impairs maturation of BAT in vivo by decreasing the expression of BAT-selective genes, leading to whitening of interscapular BAT (iBAT). Single nucleus RNA-sequencing analysis shows the dynamic changes of cell heterogeneity in iBAT of Wtap-BKO mice. Adult mice with WTAP deficiency in BAT display hypothermic and succumb to acute cold challenge. Mechanistically, WTAP deficiency decreases m 6A mRNA modification by reducing the protein stability of METTL3. BAT-specific overexpression of Mettl3 partially rescues the phenotypes observed in Wtap-BKO mice. These data demonstrate that WTAP/METTL3 plays an essential role in iBAT postnatal development and thermogenesis.","PeriodicalId":74074,"journal":{"name":"Life metabolism","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41274212","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}
Pub Date : 2022-10-10DOI: 10.1093/lifemeta/loac027
D. Carling
In a tour-de-force study by Zhang and colleagues recently published in Nature Metabolism, a newly identified aldolase inhibitor, Aldometanib, is shown to activate lysosomal AMPK. Remarkably, mice treated with Aldometanib have increased insulin sensitivity, lowered blood glucose, decreased hepatic steatosis and fibrosis and are long-lived, effects of which all appear to be mediated via activation of lysosomal AMPK.
{"title":"Inhibiting lysosomal aldolase: a magic bullet for AMPK activation in treating metabolic disease?","authors":"D. Carling","doi":"10.1093/lifemeta/loac027","DOIUrl":"https://doi.org/10.1093/lifemeta/loac027","url":null,"abstract":"\u0000 In a tour-de-force study by Zhang and colleagues recently published in Nature Metabolism, a newly identified aldolase inhibitor, Aldometanib, is shown to activate lysosomal AMPK. Remarkably, mice treated with Aldometanib have increased insulin sensitivity, lowered blood glucose, decreased hepatic steatosis and fibrosis and are long-lived, effects of which all appear to be mediated via activation of lysosomal AMPK.","PeriodicalId":74074,"journal":{"name":"Life metabolism","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44614874","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}
Pub Date : 2022-10-01DOI: 10.1093/lifemeta/loac025
Charles Brenner
It is central to biology that sequence conservation suggests functional conservation. Animal longevity is an emergent property of selected traits that integrates capacities to perform physical and mental functions after reproductive maturity. Though the yeast SIR2 gene was nominated as a longevity gene based on extended replicative longevity of old mother cells, this is not a selected trait: SIR2 is selected against in chronological aging and the direct targets of SIR2 in replicative lifespan are not conserved. Though it would be difficult to imagine how a gene that advantages 1 in 5 million yeast cells could have anticipated causes of aging in animals, overexpression of SIR2 homologs was tested in invertebrates for longevity. Because artifactual positive results were reported years before they were sorted out and because it was not known that SIR2 functions as a pro-aging gene in yeast chronological aging and in flies subject to amino acid deprivation, a global pursuit of longevity phenotypes was driven by a mixture of framing bias, confirmation bias and hype. Review articles that propagate these biases are so rampant that few investigators have considered how weak the case ever was for sirtuins as longevity genes. Acknowledging that a few positive associations between sirtuins and longevity have been identified after thousands of person-years and billions of dollars of effort, we review the data and suggest rejection of the notions that sirtuins 1) have any specific connection to lifespan in animals and 2) are primary mediators of the beneficial effects of NAD repletion.
{"title":"Sirtuins are Not Conserved Longevity Genes.","authors":"Charles Brenner","doi":"10.1093/lifemeta/loac025","DOIUrl":"https://doi.org/10.1093/lifemeta/loac025","url":null,"abstract":"<p><p>It is central to biology that sequence conservation suggests functional conservation. Animal longevity is an emergent property of selected traits that integrates capacities to perform physical and mental functions after reproductive maturity. Though the yeast <i>SIR2</i> gene was nominated as a longevity gene based on extended replicative longevity of old mother cells, this is not a selected trait: <i>SIR2</i> is selected against in chronological aging and the direct targets of <i>SIR2</i> in replicative lifespan are not conserved. Though it would be difficult to imagine how a gene that advantages 1 in 5 million yeast cells could have anticipated causes of aging in animals, overexpression of <i>SIR2</i> homologs was tested in invertebrates for longevity. Because artifactual positive results were reported years before they were sorted out and because it was not known that <i>SIR2</i> functions as a pro-aging gene in yeast chronological aging and in flies subject to amino acid deprivation, a global pursuit of longevity phenotypes was driven by a mixture of framing bias, confirmation bias and hype. Review articles that propagate these biases are so rampant that few investigators have considered how weak the case ever was for sirtuins as longevity genes. Acknowledging that a few positive associations between sirtuins and longevity have been identified after thousands of person-years and billions of dollars of effort, we review the data and suggest rejection of the notions that sirtuins 1) have any specific connection to lifespan in animals and 2) are primary mediators of the beneficial effects of NAD repletion.</p>","PeriodicalId":74074,"journal":{"name":"Life metabolism","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10081735/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9637428","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}
Pub Date : 2022-09-29DOI: 10.1093/lifemeta/loac026
Jinping Yang, Guli Xu, Yiming Xu, Pei Luo, Yexian Yuan, Lin Yao, Jingjing Zhou, Yunlong Zhu, Ishwari Gyawali, Chang Xu, Jinlong Feng, Zewei Ma, Yuxian Zeng, Songbo Wang, P. Gao, Canjun Zhu, Q. Jiang, G. Shu
In response to contraction during exercise, skeletal muscle growth and metabolism are dynamically regulated by nerve action, blood flow and metabolic feedback. α-ketoglutarate (AKG), a bioactive intermediate in the tricarboxylic acid cycle released during exercise, has been shown to promote skeletal muscle hypertrophy. However, the underlying mechanism of AKG in regulating skeletal muscle development and metabolism is still less known. 2-Oxoglutarate receptor 1 (OXGR1), the endogenous AKG receptor, is found to be distributed in the vascular smooth muscle (VSM) of skeletal muscles. OXGR1 knockout results in skeletal muscle atrophy, accompanied by decreased expression of myosin heavy chain I (MyHC I), capillary density, and endurance exercise capacity. Furthermore, the study found that dietary AKG supplementation increased mice endurance exercise distance, MyHC I/MyHC IIb ratio, arteriole and capillary densities in skeletal muscle. Meanwhile, acute AKG administration gradually increased the blood flow in the lower limbs. Further, by using OXGR1 global knock-out and OXGR1 VSM specific (MYH11-Cre × OXGR1-FloxP) knockdown models, we found that OXGR1 in VSM is essential for AKG-induced improvement of skeletal muscle performances. According to the in vitro study, AKG expanded the cell area in VSM with a decreased intracellular pH (pHi) by OXGR1. Our results demonstrated a novel role of AKG/OXGR1 in VSM of skeletal muscle to regulate blood flow and then enhance slow muscle fiber conversion and capillarization. These findings provide a theoretical basis for the AKG/OXGR1 signaling pathway to maintain human muscle function and improve meat production and livestock and poultry meat quality.
{"title":"AKG/OXGR1 promotes skeletal muscle blood flow and metabolism by relaxing vascular smooth muscle","authors":"Jinping Yang, Guli Xu, Yiming Xu, Pei Luo, Yexian Yuan, Lin Yao, Jingjing Zhou, Yunlong Zhu, Ishwari Gyawali, Chang Xu, Jinlong Feng, Zewei Ma, Yuxian Zeng, Songbo Wang, P. Gao, Canjun Zhu, Q. Jiang, G. Shu","doi":"10.1093/lifemeta/loac026","DOIUrl":"https://doi.org/10.1093/lifemeta/loac026","url":null,"abstract":"\u0000 In response to contraction during exercise, skeletal muscle growth and metabolism are dynamically regulated by nerve action, blood flow and metabolic feedback. α-ketoglutarate (AKG), a bioactive intermediate in the tricarboxylic acid cycle released during exercise, has been shown to promote skeletal muscle hypertrophy. However, the underlying mechanism of AKG in regulating skeletal muscle development and metabolism is still less known. 2-Oxoglutarate receptor 1 (OXGR1), the endogenous AKG receptor, is found to be distributed in the vascular smooth muscle (VSM) of skeletal muscles. OXGR1 knockout results in skeletal muscle atrophy, accompanied by decreased expression of myosin heavy chain I (MyHC I), capillary density, and endurance exercise capacity. Furthermore, the study found that dietary AKG supplementation increased mice endurance exercise distance, MyHC I/MyHC IIb ratio, arteriole and capillary densities in skeletal muscle. Meanwhile, acute AKG administration gradually increased the blood flow in the lower limbs. Further, by using OXGR1 global knock-out and OXGR1 VSM specific (MYH11-Cre × OXGR1-FloxP) knockdown models, we found that OXGR1 in VSM is essential for AKG-induced improvement of skeletal muscle performances. According to the in vitro study, AKG expanded the cell area in VSM with a decreased intracellular pH (pHi) by OXGR1. Our results demonstrated a novel role of AKG/OXGR1 in VSM of skeletal muscle to regulate blood flow and then enhance slow muscle fiber conversion and capillarization. These findings provide a theoretical basis for the AKG/OXGR1 signaling pathway to maintain human muscle function and improve meat production and livestock and poultry meat quality.","PeriodicalId":74074,"journal":{"name":"Life metabolism","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49349853","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}
Pub Date : 2022-09-22DOI: 10.1093/lifemeta/loac024
Tian Ma, Zixin Deng
In a recent study published in Nature, Zhang et al. employed an innovative approach by reprogramming and engineering yeast strain for combined biosynthesis of vindoline and catharanthine, followed by an additional in vitro chemical step for the successful synthesis of the anticancer vinblastine.
{"title":"Reprograming yeast for anticancer vinblastine synthesis","authors":"Tian Ma, Zixin Deng","doi":"10.1093/lifemeta/loac024","DOIUrl":"https://doi.org/10.1093/lifemeta/loac024","url":null,"abstract":"\u0000 In a recent study published in Nature, Zhang et al. employed an innovative approach by reprogramming and engineering yeast strain for combined biosynthesis of vindoline and catharanthine, followed by an additional in vitro chemical step for the successful synthesis of the anticancer vinblastine.","PeriodicalId":74074,"journal":{"name":"Life metabolism","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47399855","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}
Pub Date : 2022-09-17DOI: 10.1093/lifemeta/loac023
Bin Liang, J. Watts
In a recent paper published in Life Metabolism, Zhu et al. revealed that mutations that reduce phosphatidylcholine (PC) synthesis rescue embryonic lethality but exacerbate lipid droplet (LD) abnormalities in C. elegans seipin mutants, demonstrating distinct roles for Seipin in embryogenesis and LD formation.
{"title":"Less is more: seipin, phospholipids, and embryogenesis","authors":"Bin Liang, J. Watts","doi":"10.1093/lifemeta/loac023","DOIUrl":"https://doi.org/10.1093/lifemeta/loac023","url":null,"abstract":"\u0000 In a recent paper published in Life Metabolism, Zhu et al. revealed that mutations that reduce phosphatidylcholine (PC) synthesis rescue embryonic lethality but exacerbate lipid droplet (LD) abnormalities in C. elegans seipin mutants, demonstrating distinct roles for Seipin in embryogenesis and LD formation.","PeriodicalId":74074,"journal":{"name":"Life metabolism","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42477544","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}
Pub Date : 2022-09-15DOI: 10.1093/lifemeta/loac022
Shudi Luo, Xiaoming Jiang, Zhimin Lu
The Warburg effect is critical for tumor growth. A new study showed that cold acclimatization activates brown adipose tissue, reduces blood glucose levels, and subsequently blunts aerobic glycolysis in cancer and tumor growth
{"title":"Coldness impedes tumor growth","authors":"Shudi Luo, Xiaoming Jiang, Zhimin Lu","doi":"10.1093/lifemeta/loac022","DOIUrl":"https://doi.org/10.1093/lifemeta/loac022","url":null,"abstract":"\u0000 The Warburg effect is critical for tumor growth. A new study showed that cold acclimatization activates brown adipose tissue, reduces blood glucose levels, and subsequently blunts aerobic glycolysis in cancer and tumor growth","PeriodicalId":74074,"journal":{"name":"Life metabolism","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42337618","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}
Pub Date : 2022-09-08DOI: 10.1093/lifemeta/loac021
Jinglin Zhu, S. Lam, Lei-lei Yang, Jingjing Liang, Mei Ding, G. Shui, Xun Huang
Seipin plays a vital role in lipid droplet homeostasis and its deficiency causes congenital generalized lipodystrophy type II in humans. It is not known whether the physiological defects are all caused by cellular lipid droplet defects. Loss-of-function mutation of seip-1, the C. elegans seipin ortholog, causes embryonic lethality and lipid droplet abnormality. We uncover nhr-114 and spin-4 as two suppressors of seip-1 embryonic lethality. Mechanistically, nhr-114 and spin-4 act in the “B12-one-carbon cycle-phosphatidylcholine (PC)” axis and reducing PC synthesis suppresses the embryonic lethality of seip-1 mutants. Conversely, PC deficiency enhances the lipid droplet abnormality of seip-1 mutants. The suppression of seip-1 embryonic lethality by PC reduction requires polyunsaturated fatty acid (PUFA). In addition, the suppression is enhanced by knockdown of phospholipid scramblase epg-3. Therefore, seipin and phosphatidylcholine exhibit opposite actions in embryogenesis, while they function similarly in lipid droplet homeostasis. Our results demonstrate that seipin-mediated embryogenesis is independent of lipid droplet homeostasis.
{"title":"Reduced phosphatidylcholine synthesis suppresses the embryonic lethality of seipin deficiency","authors":"Jinglin Zhu, S. Lam, Lei-lei Yang, Jingjing Liang, Mei Ding, G. Shui, Xun Huang","doi":"10.1093/lifemeta/loac021","DOIUrl":"https://doi.org/10.1093/lifemeta/loac021","url":null,"abstract":"\u0000 Seipin plays a vital role in lipid droplet homeostasis and its deficiency causes congenital generalized lipodystrophy type II in humans. It is not known whether the physiological defects are all caused by cellular lipid droplet defects. Loss-of-function mutation of seip-1, the C. elegans seipin ortholog, causes embryonic lethality and lipid droplet abnormality. We uncover nhr-114 and spin-4 as two suppressors of seip-1 embryonic lethality. Mechanistically, nhr-114 and spin-4 act in the “B12-one-carbon cycle-phosphatidylcholine (PC)” axis and reducing PC synthesis suppresses the embryonic lethality of seip-1 mutants. Conversely, PC deficiency enhances the lipid droplet abnormality of seip-1 mutants. The suppression of seip-1 embryonic lethality by PC reduction requires polyunsaturated fatty acid (PUFA). In addition, the suppression is enhanced by knockdown of phospholipid scramblase epg-3. Therefore, seipin and phosphatidylcholine exhibit opposite actions in embryogenesis, while they function similarly in lipid droplet homeostasis. Our results demonstrate that seipin-mediated embryogenesis is independent of lipid droplet homeostasis.","PeriodicalId":74074,"journal":{"name":"Life metabolism","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45950703","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}
Pub Date : 2022-09-01DOI: 10.1093/lifemeta/loac020
Xiu-Fang Xin, Jian-Min Zhou
{"title":"Impaired condensate formation is to blame for failed disease resistance in plants","authors":"Xiu-Fang Xin, Jian-Min Zhou","doi":"10.1093/lifemeta/loac020","DOIUrl":"https://doi.org/10.1093/lifemeta/loac020","url":null,"abstract":"","PeriodicalId":74074,"journal":{"name":"Life metabolism","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42553266","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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