ArticleNature metabolism2022
Angiocrine polyamine production regulates adiposity.
Article in Nature metabolism, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 74 citations in OpenAlex.
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- Energy-Metabolism-Enhancing Probiotics Enhance the Therapeutic Response to a Glucagon-like Peptide-1 Receptor Agonist.Nutrients · 2026Article
- Adipose Tissue Engineering Biomaterials: Smart Scaffolds, Vascularization, and Clinical Frontiers.Biomolecules · 2026Review
- Arginase 1 promotes hepatic lipogenesis by regulating ERK2/PPARγ signaling in a non-canonical manner.Nature communications · 2026Article
- Optimizing adipogenic cocktail composition to enhance beige adipogenesis and evaluate thermogenic potential in primary mouse subcutaneous fat cell cultures.International journal of obesity (2005) · 2026Article
- Tryptophan and polyamine metabolism dysregulation serves as an early marker of high-fat diet-induced glucose intolerance.Journal of lipid research · 2026Article
- Metabolic syndrome promotes endometrial cancer by Oleic acid-mediated polyamine accumulation.Nature communications · 2025Article
- Tumor-Derived Polyamines Initiate Fat Wasting in Cancer Cachexia.bioRxiv : the preprint server for biology · 2025Article
- Defining the vascular niche of human adipose tissue across metabolic states.bioRxiv : the preprint server for biology · 2025Article
- Exercise-regulated lipolysis: Its role and mechanism in health and diseases.Journal of advanced research · 2025Review
- Fabricating Microfluidic Co-Cultures of Immortalized Cell Lines Uncovers Robust Design Principles for the Simultaneous Formation of Patterned, Vascularized, and Stem Cell-Derived Adipose Tissue.Small (Weinheim an der Bergstrasse, Germany) · 2025Article
- Unraveling the complexities of diet induced obesity and glucolipid dysfunction in metabolic syndrome.Diabetology & metabolic syndrome · 2025Review
- Somatic Uniparental Disomy of PTEN in Endothelial Cells Causes Vascular Malformations in Patients with PTEN Hamartoma Tumor Syndrome.Cancer discovery · 2025Article
- MEBOCOST maps metabolite-mediated intercellular communications using single-cell RNA-seq.Nucleic acids research · 2025Article
- Metabolic reaction fluxes as amplifiers and buffers of risk alleles for coronary artery disease.Molecular systems biology · 2025Article
- Microenvironmental determinants of endothelial cell heterogeneity.Nature reviews. Molecular cell biology · 2025Review
- Neurophysiological mechanisms of electroacupuncture in regulating pancreatic function and adipose tissue expansion.World journal of diabetes · 2025Article
- Secreted spermidine synthase reveals a paracrine role for PGC1α-induced growth suppression in prostate cancer.Cell death & disease · 2025Article
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30 authors at 13 institutions in 3 countries.
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Abstract
Reciprocal interactions between endothelial cells (ECs) and adipocytes are fundamental to maintain white adipose tissue (WAT) homeostasis, as illustrated by the activation of angiogenesis upon WAT expansion, a process that is impaired in obesity. However, the molecular mechanisms underlying the crosstalk between ECs and adipocytes remain poorly understood. Here, we show that local production of polyamines in ECs stimulates adipocyte lipolysis and regulates WAT homeostasis in mice. We promote enhanced cell-autonomous angiogenesis by deleting Pten in the murine endothelium. Endothelial Pten loss leads to a WAT-selective phenotype, characterized by reduced body weight and adiposity in pathophysiological conditions. This phenotype stems from enhanced fatty acid β-oxidation in ECs concomitant with a paracrine lipolytic action on adipocytes, accounting for reduced adiposity. Combined analysis of murine models, isolated ECs and human specimens reveals that WAT lipolysis is mediated by mTORC1-dependent production of polyamines by ECs. Our results indicate that angiocrine metabolic signals are important for WAT homeostasis and organismal metabolism.
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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.