Evidence map›Paper›PMID 29998913›Full record

ReviewJournal of atherosclerosis and thrombosis2018

Pathophysiology of Diabetic Dyslipidemia.

Tsutomu Hirano

Open access · diamondAbstract readReview
In one paragraph

Review 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 267 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
267citing papers in PubMed, 3 pooled it
24.6field-weighted citation impact, top 1% 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

267 citing papers in PubMed, 3 syntheses or guidelines pooled it, 514 citations in OpenAlex.

  1. Pooled it
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  4. Effect ofNutrients · 2026
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  12. Binaphthoquinone attenuates myofibroblast transition of human ventricular cardiac fibroblastsThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026
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207 more citing papers are in PubMed but not listed here.

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

1 author at 1 institution in 1 country.

Tsutomu HiranoDepartment of Medicine, Division of Diabetes, Metabolism, and Endocrinology, Showa University School of Medicine.
Showa University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Accumulating clinical evidence has suggested serum triglyceride (TG) is a leading predictor of atherosclerotic cardiovascular disease, comparable to low-density lipoprotein (LDL)-cholesterol (C) in populations with type 2 diabetes, which exceeds the predictive power of hemoglobinA1c. Atherogenic dyslipidemia in diabetes consists of elevated serum concentrations of TG-rich lipoproteins (TRLs), a high prevalence of small dense low-density lipoprotein (LDL), and low concentrations of cholesterol-rich high-density lipoprotein (HDL)2-C. A central lipoprotein abnormality is an increase in large TG-rich very-low-density lipoprotein (VLDL)1, and other lipoprotein abnormalities are metabolically linked to increased TRLs. Insulin critically regulates serum VLDL concentrations by suppressing hepatic VLDL production and stimulating VLDL removal by activation of lipoprotein lipase. It is still debated whether hyperinsulinemia compensatory for insulin resistance is causally associated with the overproduction of VLDL. This review introduces experimental and clinical observations revealing that insulin resistance, but not hyperinsulinemia stimulates hepatic VLDL production. LDL and HDL consist of heterogeneous particles with different size and density. Cholesterol-depleted small dense LDL and cholesterol-rich HDL2 subspecies are particularly affected by insulin resistance and can be named "Metabolic LDL and HDL," respectively. We established the direct assays for quantifying small dense LDL-C and small dense HDL(HDL3)-C, respectively. Subtracting HDL3-C from HDL-C gives HDL2-C. I will explain clinical relevance of measurements of LDL and HDL subspecies determined by our assays. Diabetic kidney disease (DKD) substantially worsens plasma lipid profile thereby potentiated atherogenic risk. Finally, I briefly overview pathophysiology of dyslipidemia associated with DKD, which has not been so much taken up by other review articles.

Indexed as

AnimalsCholesterolCholesterol, HDLCholesterol, LDLCholesterol, VLDLChylomicronsDiabetes Mellitus, Type 2Diabetic NephropathiesDyslipidemiasFatty Acids, NonesterifiedGlycated HemoglobinHumansInsulinInsulin ResistanceLipoproteinsLipoproteins, VLDLCholesterolCholesterol, HDLCholesterol, LDLCholesterol, VLDLChylomicronsFatty Acids, NonesterifiedGlycated Hemoglobinhemoglobin A1c protein, humanInsulinLipoproteinsLipoproteins, VLDLlipoprotein triglyceridePioglitazoneTriglyceridesDiabetesHDL subspeciesInsulin resistanceSmall dense LDLTriglyceride-rich lipoproteins

Identifiers

PMID29998913
PMCPMC6143775
OpenAlexW2820707192

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.