Evidence map›Paper›PMID 28781340›Full record

ArticleJournal of atherosclerosis and thrombosis2018

A Novel Selective PPARα Modulator (SPPARMα), K-877 (Pemafibrate), Attenuates Postprandial Hypertriglyceridemia in Mice.

Masami Sairyo, Takuya Kobayashi, Daisaku Masuda, Koutaro Kanno, Yinghong Zhu, Takeshi Okada, Masahiro Koseki, Tohru Ohama, Makoto Nishida, Yasushi Sakata and 1 more

Erratum issuedOpen access · diamondAbstract read
In one paragraph

Article in Journal of atherosclerosis and thrombosis, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.6field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

32 citing papers in PubMed, 48 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Article
  4. Hypertriglyceridemia Therapy: Past, Present and Future Perspectives.International journal of molecular sciences · 2024
    Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Observational
  17. Review
  18. PPAROxidative medicine and cellular longevity · 2021
    Article
  19. Mechanisms of Atherosclerosis Induced by Postprandial Lipemia.Frontiers in cardiovascular medicine · 2021
    Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 3 institutions in 2 countries.

Masami SairyoDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine.
Takuya KobayashiDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine.
Daisaku MasudaDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine.
Koutaro KannoDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine.
Yinghong ZhuDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine.
Takeshi OkadaDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine.
Masahiro KosekiDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine.
Tohru OhamaDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine.
Makoto NishidaDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine.
Yasushi SakataDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine.
Shizuya YamashitaDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine.
Osaka University · JPCounseling Center · USOsaka Dental University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsFasting and postprandial hypertriglyceridemia (PHTG) are caused by the accumulation of triglyceride (TG)-rich lipoproteins and their remnants, which have atherogenic effects. Fibrates can improve fasting and PHTG; however, reduction of remnants is clinically needed to improve health outcomes. In the current study, we investigated the effects of a novel selective peroxisome proliferator-activated receptor α modulator (SPPARMα), K-877 (Pemafibrate), on PHTG and remnant metabolism.

methodsMale C57BL/6J mice were fed a high-fat diet (HFD) only, or an HFD containing 0.0005% K-877 or 0.05% fenofibrate, from 8 to 12 weeks of age. After 4 weeks of feeding, we measured plasma levels of TG, free fatty acids (FFA), total cholesterol (TC), HDL-C, and apolipoprotein (apo) B-48/B-100 during fasting and after oral fat loading (OFL). Plasma lipoprotein profiles after OFL, which were assessed by high performance liquid chromatography (HPLC), and fasting lipoprotein lipase (LPL) activity were compared among the groups.

resultsBoth K-877 and fenofibrate suppressed body weight gain and fasting and postprandial TG levels and enhanced LPL activity in mice fed an HFD. As determined by HPLC, K-877 and fenofibrate significantly decreased the abundance of TG-rich lipoproteins, including remnants, in postprandial plasma. Both K-877 and fenofibrate decreased intestinal mRNA expression of ApoB and Npc1l1; however, hepatic expression of Srebp1c and Mttp was increased by fenofibrate but not by K-877.Hepatic mRNA expression of apoC-3 was decreased by K-877 but not by fenofibrate.

conclusionK-877 may attenuate PHTG by suppressing the postprandial increase of chylomicrons and the accumulation of chylomicron remnants more effectively than fenofibrate.

Indexed as

AnimalsChylomicronsDiet, High-FatFenofibrateHypertriglyceridemiaHypolipidemic AgentsMaleMiceMice, Inbred C57BLPostprandial PeriodPPAR gammaChylomicronsFenofibrateHypolipidemic AgentsPPAR gammaChylomicron remnantsFenofibrateK-877 (Pemafibrate)Postprandial hypertriglyceridemiaSPPARMα

Identifiers

PMID28781340
PMCPMC5827084
OpenAlexW2744310085

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

None linked

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.