Evidence map›Paper›PMID 26984517›Full record

Trial reportLipids in health and disease2016

Serum CETP status is independently associated with reduction rates in LDL-C in pitavastatin-treated diabetic patients and possible involvement of LXR in its association.

Akihiro Shimada, Hideki Kimura, Koji Oida, Hideo Kanehara, Yukihiro Bando, Shinobu Sakamoto, Takanobu Wakasugi, Takashi Saga, Yasuki Ito, Kazuko Kamiyama and 4 more

Open access · goldFull text readClinical TrialMulticenter Study
In one paragraph

Trial report in Lipids in health and disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

6 citing papers in PubMed, 12 citations in OpenAlex.

  1. 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

14 authors at 7 institutions in 1 country.

Akihiro ShimadaDepartment of Clinical Laboratory and Nephrology, University of Fukui Hospital, 23-3 Matsuoka-shimoaizuki, Eiheiji, Yoshida, Fukui, 910-1193, Japan.
Hideki KimuraDepartment of Clinical Laboratory and Nephrology, University of Fukui Hospital, 23-3 Matsuoka-shimoaizuki, Eiheiji, Yoshida, Fukui, 910-1193, Japan. hkimura@u-fukui.ac.jp.
Koji OidaDivision of Internal Medicine, Fukui Chuo Clinic, 4-5-10, Matsumoto, Fukui, 910-0003, Japan.
Hideo KaneharaDivision of Endocrinology, Fukui-ken Saiseikai Hospital, 7-1, Funahashi, Wadanaka, 918-8503, Japan.
Yukihiro BandoDivision of Endocrinology, Fukui-ken Saiseikai Hospital, 7-1, Funahashi, Wadanaka, 918-8503, Japan.
Shinobu SakamotoDivision of Internal Medicine, Yasukawa Hospital, 2-108, Owada, Fukui, 910-0005, Japan.
Takanobu WakasugiDivision of Endocrinology, Fukui Prefectural Hospital, 2-8-1, Yotsui, Fukui, 910-8526, Japan.
Takashi SagaDivision of Internal Medicine, Tanaka Hospital, 2-3-1 Ohte, Fukui, Fukui, 910-0005, Japan.
Yasuki ItoResearch and Development Department, Denka Seiken Co. Ltd, Tokyo, Japan.
Kazuko KamiyamaDivision of Nephrology, Department of Medicine, School of Medicine, Faculty of Medical Sciences, University of Fukui, 23-3 Matsuoka-shimoaizuki, Eiheiji, Yoshida, Fukui, 910-1193, Japan.
Daisuke MikamiDivision of Nephrology, Department of Medicine, School of Medicine, Faculty of Medical Sciences, University of Fukui, 23-3 Matsuoka-shimoaizuki, Eiheiji, Yoshida, Fukui, 910-1193, Japan.
Masayuki IwanoDivision of Nephrology, Department of Medicine, School of Medicine, Faculty of Medical Sciences, University of Fukui, 23-3 Matsuoka-shimoaizuki, Eiheiji, Yoshida, Fukui, 910-1193, Japan.
Tsutomu HiranoDepartment of Medicine, Division of Diabetes, Metabolism, and Endocrinology, Showa University School of Medicine, Tokyo, Japan.
Haruyoshi YoshidaDivision of Nephrology, Department of Medicine, School of Medicine, Faculty of Medical Sciences, University of Fukui, 23-3 Matsuoka-shimoaizuki, Eiheiji, Yoshida, Fukui, 910-1193, Japan.
University of Fukui · JPUniversity of Fukui Hospital · JPFukui-ken Saiseikai Hospital · JPDenka (Japan) · JPFukui CardioVascular Center · JPFukui Prefectural Hospital · JPShowa University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundStatins decrease cholesteryl ester transfer protein (CETP) levels, which have been positively associated with hepatic lipid content as well as serum low density lipoproteins-cholesterol (LDL-C) levels. However, the relationship between the CETP status and statin-induced reductions in LDL-C levels has not yet been elucidated in detail. We herein examined the influence of the CETP status on the lipid-reducing effects of pitavastatin in hypercholesterolemic patients with type 2 diabetes mellitus as well as the molecular mechanism underlying pitavastatin-induced modifications in CETP levels.

methodsFifty-three patients were treated with 2 mg of pitavastatin for 3 months. Serum levels of LDL-C, small dense (sd) LDL-C, and CETP were measured before and after the pitavastatin treatment. The effects of pitavastatin, T0901317, a specific agonist for liver X receptor (LXR) that reflects hepatic cholesterol contents, and LXR silencing on CETP mRNA expression in HepG2 cells were also examined by a real-time PCR assay.

resultsThe pitavastatin treatment decreased LDL-C, sdLDL-C, and CETP levels by 39, 42, and 23%, respectively. Despite the absence of a significant association between CETP and LDL-C levels at baseline, baseline CETP levels and its percentage change were an independent positive determinant for the changes observed in LDL-C and sdLDL-C levels. The LXR activation with T0901317 (0.5 μM), an in vitro condition analogous to hepatic cholesterol accumulation, increased CETP mRNA levels in HepG2 cells by approximately 220%, while LXR silencing markedly diminished the increased expression of CETP. Pitavastatin (5 μM) decreased basal CETP mRNA levels by 21%, and this was completely reversed by T0901317.

conclusionBaseline CETP levels may predict the lipid-reducing effects of pitavastatin. Pitavastatin-induced CETP reductions may be partially attributed to decreased LXR activity, predictable by the ensuing decline in hepatic cholesterol synthesis.

trial registrationUMIN Clinical Trials Registry ID UMIN000019020.

Indexed as

AgedBenzenesulfonamidesCholesterol Ester Transfer ProteinsCholesterol, LDLDiabetes Mellitus, Type 2FemaleFluorocarbonsGene Expression RegulationHep G2 CellsHumansHydrocarbons, FluorinatedHydroxymethylglutaryl-CoA Reductase InhibitorsHypercholesterolemiaLiver X ReceptorsMaleMiddle AgedBenzenesulfonamidesCETP protein, humanCholesterol Ester Transfer ProteinsCholesterol, LDLFluorocarbonsHydrocarbons, FluorinatedHydroxymethylglutaryl-CoA Reductase InhibitorsLiver X ReceptorsNR1H3 protein, humanpitavastatinQuinolinesSulfonamidesT0901317CETPLiver X receptorPitavastatinSmall dense LDL-CT0901317

Identifiers

PMID26984517
PMCPMC4794860
OpenAlexW2301152712

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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.