自引率: 3.5%
被引量: 39581
通过率: 暂无数据
审稿周期: 1.78
版面费用: 暂无数据
国人发稿量: 17
投稿须知/期刊简介:
Published by Elsevier Science. ISSN: 1550-4131.<br><br>Cell Metabolism publishes reports of novel results in any area of metabolic biology, from molecular and cellular biology to translational studies. The unifying theme is homeostatic mechanisms in health and disease, from simpler model systems all the way to the clinic. Published work should not only be of exceptional significance within its field, but also of interest to researchers outside the immediate area. Cell Metabolism also provides expert analysis and commentary on key findings in the field. The journal’s mission is to provide a forum for the exchange of ideas and concepts across the entire metabolic research community, cultivating new areas and fostering cross-disciplinary collaborations in basic research and clinical investigation.
期刊描述简介:
Published by Elsevier Science. ISSN: 1550-4131. Cell Metabolism publishes reports of novel results in any area of metabolic biology, from molecular and cellular biology to translational studies. The unifying theme is homeostatic mechanisms in health and disease, from simpler model systems all the way to the clinic. Published work should not only be of exceptional significance within its field, but also of interest to researchers outside the immediate area. Cell Metabolism also provides expert analysis and commentary on key findings in the field. The journal’s mission is to provide a forum for the exchange of ideas and concepts across the entire metabolic research community, cultivating new areas and fostering cross-disciplinary collaborations in basic research and clinical investigation.
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Cortical actions of thyroid hormone: An exploration and metabolism crossroad.
Classically, the central actions of thyroid hormones (THs) on metabolism occur within the hypothalamus. A recent article published in Cell by Sabatini and colleagues demonstrates that TH modulates cerebral cortical circuits of male mice, which might integrate exploratory behavior and whole-body metabolism.
被引量：- 发表：2024
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IL-22 resolves MASLD via enterocyte STAT3 restoration of diet-perturbed intestinal homeostasis.
被引量：- 发表：1970
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Myeloid beta-arrestin 2 depletion attenuates metabolic dysfunction-associated steatohepatitis via the metabolic reprogramming of macrophages.
被引量：- 发表：1970
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m(6)A mRNA methylation in brown fat regulates systemic insulin sensitivity via an inter-organ prostaglandin signaling axis independent of UCP1.
Brown adipose tissue (BAT) regulates systemic metabolism by releasing signaling lipids. N6-methyladenosine (m6A) is the most prevalent and abundant post-transcriptional mRNA modification and has been reported to regulate BAT adipogenesis and energy expenditure. Here, we demonstrate that the absence of m6A methyltransferase-like 14 (METTL14) modifies the BAT secretome to improve systemic insulin sensitivity independent of UCP1. Using lipidomics, we identify prostaglandin E2 (PGE2) and prostaglandin F2a (PGF2a) as BAT-secreted insulin sensitizers. PGE2 and PGF2a inversely correlate with insulin sensitivity in humans and protect mice from high-fat-diet-induced insulin resistance by suppressing specific AKT phosphatases. Mechanistically, METTL14-mediated m6A promotes the decay of PTGES2 and CBR1, the genes encoding PGE2 and PGF2a biosynthesis enzymes, in brown adipocytes via YTHDF2/3. Consistently, BAT-specific knockdown of Ptges2 or Cbr1 reverses the insulin-sensitizing effects in M14KO mice. Overall, these findings reveal a novel biological mechanism through which m6A-dependent regulation of the BAT secretome regulates systemic insulin sensitivity.
被引量：- 发表：1970
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SGLT2 inhibitor promotes ketogenesis to improve MASH by suppressing CD8(+) T cell activation.
被引量：- 发表：1970
