Evidence map›Paper›PMID 15710887›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2005

Concurrent suppression of hyperlipidemia and intestinal polyp formation by NO-1886, increasing lipoprotein lipase activity in Min mice.

Naoko Niho, Michihiro Mutoh, Mami Takahashi, Kazuhiko Tsutsumi, Takashi Sugimura, Keiji Wakabayashi

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
4.8field-weighted citation impact, top 5% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.

  1. Pooled it
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  11. Lipid-regulating effect of traditional chinese medicine: mechanisms of actions.Evidence-based complementary and alternative medicine : eCAM · 2012
    Article
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  19. Phenotypic reversion in analbuminemic rats due to an altered splicing mechanism.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2007
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Naoko NihoCancer Prevention Basic Research Project, National Cancer Center Research Institute, 5-1-1 Tsukiji, Chuo-ku, Tokyo 104-0045, Japan.
Michihiro Mutoh
Mami Takahashi
Kazuhiko Tsutsumi
Takashi Sugimura
Keiji Wakabayashi
Otsuka (Japan) · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We have previously reported a hyperlipidemic state in two strains of Apc-deficient mice, Min and Apc(1309), associated with low expression levels of lipoprotein lipase (LPL) in the liver and small intestine, and enforced induction of LPL mRNA by peroxisome proliferator-activated receptor (PPAR)alpha and PPARgamma agonists clearly suppressed hyperlipidemia and intestinal polyp formation in these mice. Meanwhile, a compound, NO-1886, has been shown to increase LPL mRNA and protein levels but not to possess PPARalpha and PPARgamma agonistic activity. In this study, therefore, the effects of NO-1886 on hyperlipidemia and intestinal polyp formation were investigated in Min mice. Administration of 400 and 800 ppm NO-1886 in the diet for 13 weeks from 7 weeks of age caused a reduction of serum triglycerides to 39% and 31% of the untreated value, respectively, and the values for very low-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol were improved almost to the wild-type level with a corresponding elevation of the LPL mRNA. Moreover, total numbers of intestinal polyps in the groups receiving NO-1886 at 400 and 800 ppm were decreased to 48% and 42% of the control value, respectively. We also found that NO-1886 suppressed cyclooxygenase-2 transcriptional promoter activity in a reporter gene assay and reduced cyclooxygenase-2 mRNA levels in the small intestine of Min mice. These results indicate that suppression of serum lipid levels by increasing LPL activity may contribute to a reduction of intestinal polyp formation with Apc-deficiency, and NO-1886 and its derivatives could be useful as chemopreventive agents for colon cancer.

Indexed as

AnimalsAnticarcinogenic AgentsBenzamidesCholesterol, HDLCholesterol, LDLCholesterol, VLDLCyclooxygenase 2FemaleHyperlipidemiasHypolipidemic AgentsIntestinal PolypsLipoprotein LipaseMiceMice, Inbred C57BLOrganophosphorus CompoundsProstaglandin-Endoperoxide Synthases4-diethoxyphosphorylmethyl-N-(4-bromo-2-cyanophenyl)benzamideAnticarcinogenic AgentsBenzamidesCholesterol, HDLCholesterol, LDLCholesterol, VLDLCyclooxygenase 2Hypolipidemic AgentsLipoprotein LipaseOrganophosphorus CompoundsProstaglandin-Endoperoxide SynthasesRNA, Messenger

Identifiers

PMID15710887
PMCPMC549478
OpenAlexW2045781161

What OpenQuestion holds

Textmetadata
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.