Evidence map›Paper›PMID 29199201›Full record

ArticleJournal of atherosclerosis and thrombosis2018

Effects of a Dipeptidyl Peptidase 4 Inhibitor Sitagliptin on Glycemic Control and Lipoprotein Metabolism in Patients with Type 2 Diabetes Mellitus (GLORIA Trial).

Daisaku Masuda, Takuya Kobayashi, Masami Sairyou, Hiroyuki Hanada, Tohru Ohama, Masahiro Koseki, Makoto Nishida, Norikazu Maeda, Shinji Kihara, Tatsuya Minami and 3 more

Abstract 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. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

13 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  12. Anti-atherosclerotic effect of incretin mimetics: a meta-analysis of randomized controlled trials.Journal of community hospital internal medicine perspectives · 2018
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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

13 authors.

Daisaku MasudaDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine.
Takuya KobayashiDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine.
Masami SairyouDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine.
Hiroyuki HanadaDivision of Laboratory for Clinical Investigation, Department of Medical Technology, Osaka University Hospital.
Tohru OhamaDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine.
Masahiro KosekiDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine.
Makoto NishidaDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine.
Norikazu MaedaDepartment of Metabolism and Atherosclerosis, Osaka University Graduate School of Medicine.
Shinji KiharaDepartment of Metabolism and Atherosclerosis, Osaka University Graduate School of Medicine.
Tatsuya MinamiSouseikai Sousei Hospital.
Koji YanagiOsaka Central Hospital.
Yasushi SakataDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine.
Shizuya YamashitaDepartment of Community Medicine, Osaka University Graduate School of Medicine.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimThe morbidity of cardiovascular disease in patients with type 2 diabetes mellitus (DM) deteriorates in combination with dyslipidemia. The accumulation of remnant lipoproteins in patients with fasting and postprandial hypertriglyceridemia is highly atherogenic. The current study investigated whether the dipeptidyl peptidase-4 inhibitor sitagliptin ameliorates dyslipidemia and hyperglycemia.

methodsWe enrolled 38 patients with type 2 DM (20 males and 18 females, 65.7±9.9 years old, HbA1c levels <8.4%), and all patients gave written informed consent. Sitagliptin (50 mg/day) was added to current antidiabetic treatments and increased to 100 mg/day to achieve low HbA1c levels (<7.4%). Glucose and lipoprotein metabolism profiles were analyzed at 0, 4, and 12 weeks after sitagliptin administration.

resultsSitagliptin significantly decreased fasting levels of triglyceride (TG) (161±90 vs. 130±66 mg/dl, p<0.01) and non-HDL-C (129±29 vs. 116±20 mg/dl, p<0.01) in combination with glucose (150±47 vs. 129±27 mg/dl, p<0.01) and HbA1c (7.1±0.6 vs. 6.6±0.7 mg/dl, p<0.001). Sitagliptin also significantly decreased the fasting levels of apolipoprotein (apo) B-48 (7.8±6.7 vs. 5.6±4.0 µg/ml, p<0.01), remnant lipoprotein cholesterol (15.3±9.5 vs. 12.0±7.9 mg/dl, p<0.05) and other apolipoproteins, such as apoB, apoC-II, apoC-III, and apoE. Analyses of the lipoprotein profiles of fasting sera revealed that sitagliptin significantly decreased cholesterol and TG levels of lipoprotein fractions in the size of very low density lipoprotein and low density lipoprotein.

conclusionsThese findings indicated that sitagliptin administration ameliorated the lipid and lipoprotein profiles in patients with diabetes, which may be due to the decrease in atherogenic remnant lipoproteins (UMIN#000013218).

Indexed as

AgedBiomarkersDiabetes Mellitus, Type 2Dipeptidyl-Peptidase IV InhibitorsFemaleFollow-Up StudiesHumansHyperglycemiaHypoglycemiaLipoproteinsMalePrognosisProspective StudiesSitagliptin PhosphateBiomarkersDipeptidyl-Peptidase IV InhibitorsLipoproteinsSitagliptin PhosphateDPP-4Lipoprotein ProfilePostprandial hypertriglyceridemiaRemnantsSitagliptin

Identifiers

PMID29199201
PMCPMC6005231

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Registered trials

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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.