ArticleeLife2014
Adipocyte ALK7 links nutrient overload to catecholamine resistance in obesity.
Article in eLife, 2014. 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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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.
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Who cites it
44 citing papers in PubMed, 83 citations in OpenAlex.
- SLIT3 fragments orchestrate neurovascular expansion and thermogenesis in brown adipose tissue.Nature communications · 2026Article
- A consensus guide to preclinical indirect calorimetry experiments.Nature metabolism · 2025Review
- Nerve-associated macrophages control adipose homeostasis across lifespan and restrain age-related inflammation.Nature aging · 2025Article
- Activin Actions in Adipocytes.The Journal of clinical endocrinology and metabolism · 2025Review
- Acute regulation of murine adipose tissue lipolysis and insulin resistance by the TGFβ superfamily protein GDF3.Nature communications · 2025Article
- High-throughput transcriptome analysis reveals a developmental increase in Acvr1c which mediates epigenetic repression of the gene encoding the pubertal brake, Makorin ring finger protein 3.NAR molecular medicine · 2025Article
- Activin E is a new guardian protecting against hepatic steatosis via inhibiting lipolysis in white adipose tissue.Experimental & molecular medicine · 2025Article
- Immunoneuroendocrine, Stress, Metabolic, and Behavioural Responses in High-Fat Diet-Induced Obesity.Nutrients · 2024Article
- Activin E is a transforming growth factor β ligand that signals specifically through activin receptor-like kinase 7.The Biochemical journal · 2024Article
- Human ACVR1C missense variants that correlate with altered body fat distribution produce metabolic alterations of graded severity in knock-in mutant mice.Molecular metabolism · 2024Article
- Hepatic Activin E mediates liver-adipose inter-organ communication, suppressing adipose lipolysis in response to elevated serum fatty acids.Molecular metabolism · 2023Article
- Adipose tissue lipid metabolism: lipolysis.Current opinion in genetics & development · 2023Review
- Adipose METTL14-Elicited NAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Activin E-ACVR1C cross talk controls energy storage via suppression of adipose lipolysis in mice.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- The adipocyte supersystem of insulin and cAMP signaling.Trends in cell biology · 2023Review
- Brown Adipose Tissue-A Translational Perspective.Endocrine reviews · 2023Review
- Targeting activin receptor-like kinase 7 ameliorates adiposity and associated metabolic disorders.JCI insight · 2023Article
- Loss of adipose TET proteins enhances β-adrenergic responses and protects against obesity by epigenetic regulation of β3-AR expression.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Article
- Identification of Rare Loss-of-Function Genetic Variation Regulating Body Fat Distribution.The Journal of clinical endocrinology and metabolism · 2022Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Obesity is associated with blunted β-adrenoreceptor (β-AR)-mediated lipolysis and lipid oxidation in adipose tissue, but the mechanisms linking nutrient overload to catecholamine resistance are poorly understood. We report that targeted disruption of TGF-β superfamily receptor ALK7 alleviates diet-induced catecholamine resistance in adipose tissue, thereby reducing obesity in mice. Global and fat-specific Alk7 knock-out enhanced adipose β-AR expression, β-adrenergic signaling, mitochondrial biogenesis, lipid oxidation, and lipolysis under a high fat diet, leading to elevated energy expenditure, decreased fat mass, and resistance to diet-induced obesity. Conversely, activation of ALK7 reduced β-AR-mediated signaling and lipolysis cell-autonomously in both mouse and human adipocytes. Acute inhibition of ALK7 in adult mice by a chemical-genetic approach reduced diet-induced weight gain, fat accumulation, and adipocyte size, and enhanced adipocyte lipolysis and β-adrenergic signaling. We propose that ALK7 signaling contributes to diet-induced catecholamine resistance in adipose tissue, and suggest that ALK7 inhibitors may have therapeutic value in human obesity.
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Registered trials
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.