ArticleArteriosclerosis, thrombosis, and vascular biology2014
Acceleration of biliary cholesterol secretion restores glycemic control and alleviates hypertriglyceridemia in obese db/db mice.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 26 citations in OpenAlex.
- Liver-specific delivery of MDM2 antisense oligonucleotides counteracts diet-induced metabolic-dysfunction-associated steatotic liver diseases.Molecular therapy. Nucleic acids · 2026Article
- Differential Effects ofGenes · 2023Article
- The Adaptive Characteristics of Cholesterol and Bile Acid Metabolism in Nile Tilapia Fed a High-Fat Diet.Aquaculture nutrition · 2022Article
- Sitosterolemia: Twenty Years of Discovery of the Function ofInternational journal of molecular sciences · 2021Review
- Article
- ABCG5 and ABCG8: more than a defense against xenosterols.Journal of lipid research · 2018Review
- Ultrasonographic Characterization of theJournal of diabetes research · 2018Article
- GRP78 rescues the ABCG5 ABCG8 sterol transporter in db/db mice.Metabolism: clinical and experimental · 2015Article
- The growing problem of obesity: mechanisms, consequences, and therapeutic approaches.Arteriosclerosis, thrombosis, and vascular biology · 2015Review
- The combination of ezetimibe and ursodiol promotes fecal sterol excretion and reveals a G5G8-independent pathway for cholesterol elimination.Journal of lipid research · 2015Article
- Cholesterol and lipoprotein metabolism: Early Career Committee contribution.Arteriosclerosis, thrombosis, and vascular biology · 2014Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
objectiveRecent studies support a role for cholesterol in the development of obesity and nonalcoholic fatty liver disease. Mice lacking the ABCG5 ABCG8 (G5G8) sterol transporter have reduced biliary cholesterol secretion and are more susceptible to steatosis, hepatic insulin resistance, and loss of glycemic control when challenged with a high-fat diet. We hypothesized that accelerating G5G8-mediated biliary cholesterol secretion would correct these phenotypes in obese mice. APPROACH AND
resultsObese (db/db) male and their lean littermates were administered a cocktail of control adenovirus or adenoviral vectors encoding ABCG5 and ABCG8 (AdG5G8). Three days after viral administration, measures of lipid and glucose homeostasis were determined, and tissues were collected for biochemical analyses. AdG5G8 increased biliary cholesterol and fecal sterol elimination. Fasting glucose and triglycerides declined, and glucose tolerance improved in obese mice expressing G5G8 compared with mice receiving control adenovirus. These changes were associated with a reduction in phosphorylated eukaryotic initiation factor 2α and c-Jun N-terminal kinase in liver, suggesting alleviation of endoplasmic reticulum stress. Phosphorylated insulin receptor and protein kinase B were increased, indicating restored hepatic insulin signaling. However, there was no reduction in hepatic triglycerides after the 3-day treatment period.
conclusionsAccelerating biliary cholesterol secretion restores glycemic control and reduces plasma triglycerides in obese db/db mice.
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