ArticleThe EMBO journal2025
Hepatic ASPG-mediated lysophosphatidylinositol catabolism impairs insulin signal transduction.
Article in The EMBO journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
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Who cites it
5 citing papers in PubMed.
- Fatty Acid Metabolism in Health and Cancer: From Fundamental Mechanisms to Therapeutic Application.MedComm · 2026Review
- A comprehensive landscape of mechanical stress-mediated lipid metabolism in human cavernous fibroblasts.Communications biology · 2026Article
- Appropriate Dietary Levels of Soybean Lecithin and Krill Oil Phospholipids Promote Growth, Antioxidant Capacity, and Lipid Metabolism While Reducing Lipid Deposition in Atlantic Salmon (Animals : an open access journal from MDPI · 2026Article
- Effects of a Reprometabolic Syndrome-Inducing Eucaloric High-Fat Diet on Insulin Sensitivity, Body Composition, the Lipidome, and the Microbiome.Metabolites · 2026Article
- Dysregulation of the AMPK-SREBP1-FASN axis in MASLD: driving a vicious cycle of lipotoxicity and metabolic-immune crosstalk.Lipids in health and disease · 2026Review
Corrections and comments
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Authors and funding
14 authors.
Funding
Abstract
Bioactive glycerolysophospholipids (GLPs) are implicated in the pathogenesis of metabolic dysfunction-associated steatotic liver disease (MASLD) and obesity; however, the mechanisms underlying glycerolysophospholipid-mediated changes in insulin signaling remain poorly understood. Here, we identify the amino acid-metabolism enzyme asparaginase (ASPG) as a critical regulator of systemic fatty acid handling and insulin signal transduction. Hepatic ASPG expression levels negatively correlate with insulin sensitivity in humans. Loss of Aspg in MASLD mice modifies the liver hepatokine secretome, enhancing systemic insulin sensitivity. Notably, ASPG bears lysophospholipase activity towards the bioactive lipid lysophosphatidylinositol (LPI) in vitro and in vivo. Mechanistically, Aspg deficiency results in accumulation of intracellular LPIs and consequently in suppression of tyrosine phosphatase PTP1B activity. This in turn decreases FOXO1-dependent expression of the hepatokine Sepp1, leading to reduced SEPP1 secretion and extrahepatic insulin-sensitization. In summary, this study uncovers a novel biological mechanism whereby ASPG-controlled bioactive lipid levels modulate insulin resistance and insulin secretion, suggesting complementary therapeutic strategies for the improvement of systemic glucose homeostasis.
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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 Socratic graph.