Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 50% of its field
1 · What the graph read from it
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
2 · The registry
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
3 · Its place in the literature
Who cites it
1 citing paper in PubMed, 5 citations in OpenAlex.
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what money
Authors and funding
14 authors at 6 institutions in 1 country.
Ruoxuan BaoThe Molecular and Cell Biology Research Lab of the Institutes of Biomedical Sciences and the School of Basic Medical Sciences, Fudan University, Shanghai, 200032, China.
Yongmei MengCollege of Traditional Mongolian Medicine, Inner Mongolia Medical University, Mongolia, 010110, China.
Haibo ZhangKey Laboratory of Tropical Marine Bioresources and Ecology, Guangdong Key Laboratory of Marine Materia Medica, Institution of South China Sea Ecology and Environmental Engineering, South China Sea Institute of Oceanology, Chinese Academy of Sciences, Guangzhou, 510301, China.ORCID 0000-0003-3796-5095
Chen YangKey Laboratory of Metabolism and Molecular Medicine, the Ministry of Education, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fudan University, Shanghai, 200032, China.
Wei LiDepartment of Medicinal Chemistry, China Pharmaceutical University, Nanjing, Jiangsu, 210009, China.ORCID 0000-0003-0388-1467
Cheng ZhangThe Molecular and Cell Biology Research Lab of the Institutes of Biomedical Sciences and the School of Basic Medical Sciences, Fudan University, Shanghai, 200032, China.ORCID 0000-0002-9218-5019
Jinye ZhangThe Molecular and Cell Biology Research Lab of the Institutes of Biomedical Sciences and the School of Basic Medical Sciences, Fudan University, Shanghai, 200032, China.ORCID 0000-0002-8947-2607
Renqiang SunThe Molecular and Cell Biology Research Lab of the Institutes of Biomedical Sciences and the School of Basic Medical Sciences, Fudan University, Shanghai, 200032, China.
Zengxia LiKey Laboratory of Metabolism and Molecular Medicine, the Ministry of Education, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fudan University, Shanghai, 200032, China.
Wei JiangKey Laboratory of Metabolism and Molecular Medicine, the Ministry of Education, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fudan University, Shanghai, 200032, China.ORCID 0000-0001-7615-0900
Chensong ZhangState Key Laboratory for Cellular Stress Biology, School of Life Sciences, Xiamen University, Xiamen, Fujian, 361102, China.
Changsheng ZhangKey Laboratory of Tropical Marine Bioresources and Ecology, Guangdong Key Laboratory of Marine Materia Medica, Institution of South China Sea Ecology and Environmental Engineering, South China Sea Institute of Oceanology, Chinese Academy of Sciences, Guangzhou, 510301, China. czhang@scsio.ac.cn.ORCID 0000-0003-2349-3138
Hai-Xin YuanThe Molecular and Cell Biology Research Lab of the Institutes of Biomedical Sciences and the School of Basic Medical Sciences, Fudan University, Shanghai, 200032, China. yuanhaixin@fudan.edu.cn.ORCID 0000-0002-1624-3934
Yongjun DangKey Laboratory of Metabolism and Molecular Medicine, the Ministry of Education, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fudan University, Shanghai, 200032, China. yongjundang@fudan.edu.cn.ORCID 0000-0001-7237-1132
Fudan University · CNXiamen University · CNShanghai Medical College of Fudan University · CNChina Pharmaceutical University · CNChinese Academy of Sciences · CNInner Mongolia Medical University · CN
Funding
National Natural Science Foundation of China (National Science Foundation of China) 21977115National Natural Science Foundation of China (National Science Foundation of China) 31970684National Natural Science Foundation of China (National Science Foundation of China) 81820108030
6 · The paper itself
Abstract
Obesity is an epidemic affecting 13% of the global population and increasing the risk of many chronic diseases. However, only several drugs are licensed for pharmacological intervention for the treatment of obesity. As a master regulator of metabolism, the therapeutic potential of AMPK is widely recognized and aggressively pursued for the treatment of metabolic diseases. We found that elaiophylin (Ela) rapidly activates AMPK in a panel of cancer-cell lines, as well as primary hepatocytes and adipocytes. Meanwhile, Ela inhibits the mTORC1 complex, turning on catabolism and turning off anabolism together with AMPK. In vitro and in vivo studies showed that Ela does not activate AMPK directly, instead, it increases cellular AMP/ATP and ADP/ATP ratios, leading to AMPK phosphorylation in a LKB1-dependent manner. AMPK activation induced by Ela caused changes in diverse metabolic genes, thereby promoting glucose consumption and fatty acid oxidation. Importantly, Ela activates AMPK in mouse liver and adipose tissue. As a consequence, it reduces body weight and blood glucose levels and improves glucose and insulin tolerance in both ob/ob and high-fat diet-induced obese mouse models. Our study has identified a novel AMPK activator as a candidate drug for the treatment of obesity and its associated chronic diseases.
Indexed as
AMP-Activated Protein KinasesAnimalsBiological ProductsBody WeightDrug DiscoveryGlucoseHumansMacrolidesMaleMiceMice, ObeseAMP-Activated Protein KinasesBiological ProductselaiophylinGlucoseMacrolides
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.
Elaiophylin reduces body weight and lowers glucose levels in obese mice by activating AMPK. · full record | OpenQuestion