ArticleBiochemical and biophysical research communications2017
Key differences between apoC-III regulation and expression in intestine and liver.
Article in Biochemical and biophysical research communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 13 citations in OpenAlex.
- A randomized 3-way crossover study indicates that high-protein feeding induces de novo lipogenesis in healthy humans.JCI insight · 2019Trial
- Apolipoprotein C-III: Risk-factor, Regulator of Triglyceride-rich Lipoprotein Metabolism and Therapeutic Target.Current atherosclerosis reports · 2026Review
- Review
- The distinct metabolism between large and small HDL indicates unique origins of human apolipoprotein A4.JCI insight · 2023Article
- Apolipoprotein CIII Is an Important Piece in the Type-1 Diabetes Jigsaw Puzzle.International journal of molecular sciences · 2021Review
- Effects of Fructose or Glucose on Circulating ApoCIII and Triglyceride and Cholesterol Content of Lipoprotein Subfractions in Humans.Journal of clinical medicine · 2019Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
ApoC-III is a critical cardiovascular risk factor, and humans expressing null mutations in apoC-III are robustly protected from cardiovascular disease. Because of its critical role in elevating plasma lipids and CVD risk, hepatic apoC-III regulation has been studied at length. Considerably less is known about the factors that regulate intestinal apoC-III. In this work, we use primary murine enteroids, Caco-2 cells, and dietary studies in wild-type mice to show that intestinal apoC-III expression does not change in response to fatty acids, glucose, or insulin administration, in contrast to hepatic apoC-III. Intestinal apoC-III is not sensitive to changes in FoxO1 expression (which is itself very low in the intestine, as is FoxO1 target IGFBP-1), nor is intestinal apoC-III responsive to western diet, a significant contrast to hepatic apoC-III stimulation during western diet. These data strongly suggest that intestinal apoC-III is not a FoxO1 target and support the idea that apoC-III is not regulated coordinately with hepatic apoC-III, and establishes another key aspect of apoC-III that is unique in the intestine from the liver.
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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.