ArticlePloS one2013
Insulin-stimulated degradation of apolipoprotein B100: roles of class II phosphatidylinositol-3-kinase and autophagy.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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.
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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
17 citing papers in PubMed, 30 citations in OpenAlex.
- DIAPH1 mediates progression of atherosclerosis and regulates hepatic lipid metabolism in mice.Communications biology · 2023Article
- Sortilin restricts secretion of apolipoprotein B-100 by hepatocytes under stressed but not basal conditions.The Journal of clinical investigation · 2022Article
- Multi-organ Coordination of Lipoprotein Secretion by Hormones, Nutrients and Neural Networks.Endocrine reviews · 2021Review
- GCA links TRAF6-ULK1-dependent autophagy activation in resistant chronic myeloid leukemia.Autophagy · 2019Article
- Can modulators of apolipoproteinB biogenesis serve as an alternate target for cholesterol-lowering drugs?Biochimica et biophysica acta. Molecular and cell biology of lipids · 2018Review
- Autophagy Is Required for Sortilin-Mediated Degradation of Apolipoprotein B100.Circulation research · 2018Article
- Complex role of autophagy in regulation of hepatic lipid and lipoprotein metabolism.Journal of biomedical research · 2017Article
- Prosteatotic and Protective Components in a Unique Model of Fatty Liver: Gut Microbiota and Suppressed Complement System.Scientific reports · 2016Article
- Regression of Atherosclerosis: The Journey From the Liver to the Plaque and Back.Arteriosclerosis, thrombosis, and vascular biology · 2016Review
- Insulin dependent apolipoprotein B degradation and phosphatidylinositide 3-kinase activation with microsomal translocation are restored in McArdle RH7777 cells following serum deprivation.Biochemical and biophysical research communications · 2016Article
- Class II but Not Second Class-Prospects for the Development of Class II PI3K Inhibitors.ACS medicinal chemistry letters · 2015Article
- Emerging regulation and function of betatrophin.International journal of molecular sciences · 2014Review
- Hyperlipoproteinemia type 3: the forgotten phenotype.Current atherosclerosis reports · 2014Review
- Apolipoprotein B100 quality control and the regulation of hepatic very low density lipoprotein secretion.Journal of biomedical research · 2014Article
- Docosahexaenoic acid impairs the maturation of very low density lipoproteins in rat hepatic cells.Journal of lipid research · 2014Article
- The regulation of ApoB metabolism by insulin.Trends in endocrinology and metabolism: TEM · 2013Review
- Insulin-dependent apolipoprotein B degradation is mediated by autophagy and involves class I and class III phosphatidylinositide 3-kinases.Biochemical and biophysical research communications · 2013Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Both in humans and animal models, an acute increase in plasma insulin levels, typically following meals, leads to transient depression of hepatic secretion of very low density lipoproteins (VLDL). One contributing mechanism for the decrease in VLDL secretion is enhanced degradation of apolipoprotein B100 (apoB100), which is required for VLDL formation. Unlike the degradation of nascent apoB100, which occurs in the endoplasmic reticulum (ER), insulin-stimulated apoB100 degradation occurs post-ER and is inhibited by pan-phosphatidylinositol (PI)3-kinase inhibitors. It is unclear, however, which of the three classes of PI3-kinases is required for insulin-stimulated apoB100 degradation, as well as the proteolytic machinery underlying this response. Class III PI3-kinase is not activated by insulin, but the other two classes are. By using a class I-specific inhibitor and siRNA to the major class II isoform in liver, we now show that it is class II PI3-kinase that is required for insulin-stimulated apoB100 degradation in primary mouse hepatocytes. Because the insulin-stimulated process resembles other examples of apoB100 post-ER proteolysis mediated by autophagy, we hypothesized that the effects of insulin in autophagy-deficient mouse primary hepatocytes would be attenuated. Indeed, apoB100 degradation in response to insulin was significantly impaired in two types of autophagy-deficient hepatocytes. Together, our data demonstrate that insulin-stimulated apoB100 degradation in the liver requires both class II PI3-kinase activity and autophagy.
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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.