ArticleJournal of lipid research2009
Glucosamine-induced endoplasmic reticulum stress attenuates apolipoprotein B100 synthesis via PERK signaling.
Article in Journal of lipid research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 49 citations in OpenAlex.
- Glucosamine as a regulator of O-GlcNAc signaling: linking metabolism to disease pathogenesis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Current and Emerging Issues in Familial Hypobetalipoproteinemia-related Steatotic Liver Diseases.Journal of clinical and translational hepatology · 2025Review
- Dietary Choline Mitigates High-Fat Diet-Impaired Chylomicrons Assembly via UPRer Modulated byCells · 2022Article
- The Pathogenesis of HCC Driven by NASH and the Preventive and Therapeutic Effects of Natural Products.Frontiers in pharmacology · 2022Review
- Drug-induced hepatic steatosis in absence of severe mitochondrial dysfunction in HepaRG cells: proof of multiple mechanism-based toxicity.Cell biology and toxicology · 2021Article
- Protective Effect of Patchouli Alcohol Against High-Fat Diet Induced Hepatic Steatosis by Alleviating Endoplasmic Reticulum Stress and Regulating VLDL Metabolism in Rats.Frontiers in pharmacology · 2019Article
- Vildagliptin Can Alleviate Endoplasmic Reticulum Stress in the Liver Induced by a High Fat Diet.BioMed research international · 2018Article
- CREBH mediates metabolic inflammation to hepatic VLDL overproduction and hyperlipoproteinemia.Journal of molecular medicine (Berlin, Germany) · 2017Article
- Effect of BI-1 on insulin resistance through regulation of CYP2E1.Scientific reports · 2016Article
- Glucosamine induces REDD1 to suppress insulin action in retinal Müller cells.Cellular signalling · 2016Article
- Autophagy regulates insulin resistance following endoplasmic reticulum stress in diabetes.Journal of physiology and biochemistry · 2015Review
- Hepatic mitochondrial and ER stress induced by defective PPARα signaling in the pathogenesis of hepatic steatosis.American journal of physiology. Endocrinology and metabolism · 2014Article
- Apolipoprotein B100 quality control and the regulation of hepatic very low density lipoprotein secretion.Journal of biomedical research · 2014Article
- Up-regulation of endoplasmic reticulum stress induced genes of the unfolded protein response in the liver of periparturient dairy cows.BMC veterinary research · 2014Article
- The novel IGF-IR/Akt-dependent anticancer activities of glucosamine.BMC cancer · 2014Article
- Endoplasmic reticulum stress in cardiometabolic disorders.Current atherosclerosis reports · 2012Review
- Increased very low density lipoprotein (VLDL) secretion, hepatic steatosis, and insulin resistance.Trends in endocrinology and metabolism: TEM · 2011Review
- Autophagy and cartilage homeostasis mechanisms in joint health, aging and OA.Nature reviews. Rheumatology · 2011Review
- Endoplasmic reticulum stress and the unfolded protein response in nonalcoholic fatty liver disease.Antioxidants & redox signaling · 2011Review
- The unfolded protein response transducer IRE1α prevents ER stress-induced hepatic steatosis.The EMBO journal · 2011Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glucosamine impairs hepatic apolipoprotein B100 (apoB100) production by inducing endoplasmic reticulum (ER) stress and enhancing cotranslational and posttranslational apoB100 degradation (Qiu, W., R. K. Avramoglu, A. C. Rutledge, J. Tsai, and K. Adeli. Mechanisms of glucosamine-induced suppression of the hepatic assembly and secretion of apolipoprotein B-100-containing lipoproteins. J. Lipid Res. 2006. 47: 1749-1761). Here, we report that glucosamine also regulates apoB100 protein synthesis via ER-stress-induced PERK activation. Short-term (4 h) glucosamine treatment of HepG2 cells reduced both cellular (by 62%) and secreted apoB100 (by 43%) without altering apoB100 mRNA. Treatment with proteasomal inhibitors only partially prevented the suppressive effects of glucosamine, suggesting that mechanisms other than proteasomal degradation may also be involved. Glucosamine-induced ER stress was associated with a significantly reduced apoB100 synthesis with no significant change in posttranslational decay rates, suggesting that glucosamine exerted its effect early during apoB biosynthesis. The role of PERK and its substrate, alpha-subunit of eukaryotic initiation factor 2 (eIF2alpha), in the suppressive effects of glucosamine on apoB synthesis was then investigated. Coexpression of apoB15 (normally resistant to intracellular degradation) with wild-type double stranded (ds) RNA activated protein kinase (PKR)-like endoplasmic reticulum kinase (PERK) in COS-7 cells resulted in a dramatic reduction in the levels of newly synthesized apoB15. Interestingly, cotransfection with apoB15 and a kinase inactive PERK mutant (K618A) increased apoB15 expression. In addition, short-term glucosamine treatment stimulated an increase in phosphorylation of PERK and eIF2alpha. Taken together, these data suggest that in addition to the induction of ER-associated degradation and other degradative pathways, ER stress is associated with suppression of apoB synthesis via a PERK-dependent mechanism.
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