ArticlePloS one2014
Intestinal Cgi-58 deficiency reduces postprandial lipid absorption.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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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.
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.
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Who cites it
20 citing papers in PubMed, 30 citations in OpenAlex.
- Increased fatty acid availability improves the osteo-anabolic effects of intermittent parathyroid hormone (iPTH) in murine models.Bone reports · 2025Article
- Transcriptomic Analysis of Liver in Silver sillago,Animals : an open access journal from MDPI · 2023Article
- New insights into the role of dietary triglyceride absorption in obesity and metabolic diseases.Frontiers in pharmacology · 2023Review
- Review
- When fat meets the gut-focus on intestinal lipid handling in metabolic health and disease.EMBO molecular medicine · 2022Review
- The reduction of lipid-sourced energy production caused by ATGL inhibition cannot be compensated by activation of HSL, autophagy, and utilization of other nutrients in fish.Fish physiology and biochemistry · 2021Article
- Grasp55Nature communications · 2020Article
- CGI-58: Versatile Regulator of Intracellular Lipid Droplet Homeostasis.Advances in experimental medicine and biology · 2020Review
- Intestinal basolateral lipid substrate transport is linked to chylomicron secretion and is regulated by apoC-III.Journal of lipid research · 2019Article
- Article
- Of mice and men: The physiological role of adipose triglyceride lipase (ATGL).Biochimica et biophysica acta. Molecular and cell biology of lipids · 2019Review
- Regulation of Chylomicron Secretion: Focus on Post-Assembly Mechanisms.Cellular and molecular gastroenterology and hepatology · 2019Review
- Intestinal de novo phosphatidylcholine synthesis is required for dietary lipid absorption and metabolic homeostasis.Journal of lipid research · 2018Article
- Sequence analysis and structure prediction of ABHD16A and the roles of the ABHD family members in human disease.Open biology · 2018Review
- Critical roles for α/β hydrolase domain 5 (ABHD5)/comparative gene identification-58 (CGI-58) at the lipid droplet interface and beyond.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2017Review
- Mfge8 regulates enterocyte lipid storage by promoting enterocyte triglyceride hydrolase activity.JCI insight · 2016Article
- Recent discoveries on absorption of dietary fat: Presence, synthesis, and metabolism of cytoplasmic lipid droplets within enterocytes.Biochimica et biophysica acta · 2016Review
- Intestinal triacylglycerol synthesis in fat absorption and systemic energy metabolism.Journal of lipid research · 2015Review
- Characterization of the proteome of cytoplasmic lipid droplets in mouse enterocytes after a dietary fat challenge.PloS one · 2015Article
- Loss of abhd5 promotes colorectal tumor development and progression by inducing aerobic glycolysis and epithelial-mesenchymal transition.Cell reports · 2014Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Comparative Gene Identification-58 (CGI-58), a lipid droplet (LD)-associated protein, promotes intracellular triglyceride (TG) hydrolysis in vitro. Mutations in human CGI-58 cause TG accumulation in numerous tissues including intestine. Enterocytes are thought not to store TG-rich LDs, but a fatty meal does induce temporary cytosolic accumulation of LDs. Accumulated LDs are eventually cleared out, implying existence of TG hydrolytic machinery in enterocytes. However, identities of proteins responsible for LD-TG hydrolysis remain unknown. Here we report that intestine-specific inactivation of CGI-58 in mice significantly reduces postprandial plasma TG concentrations and intestinal TG hydrolase activity, which is associated with a 4-fold increase in intestinal TG content and large cytosolic LD accumulation in absorptive enterocytes during the fasting state. Intestine-specific CGI-58 knockout mice also display mild yet significant decreases in intestinal fatty acid absorption and oxidation. Surprisingly, inactivation of CGI-58 in intestine significantly raises plasma and intestinal cholesterol, and reduces hepatic cholesterol, without altering intestinal cholesterol absorption and fecal neutral sterol excretion. In conclusion, intestinal CGI-58 is required for efficient postprandial lipoprotein-TG secretion and for maintaining hepatic and plasma lipid homeostasis. Our animal model will serve as a valuable tool to further define how intestinal fat metabolism influences the pathogenesis of metabolic disorders, such as obesity and type 2 diabetes.
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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.