Evidence map›Paper›PMID 32347024›Full record

ReviewDiabetes & metabolism journal2020

The Role of CD36 in Type 2 Diabetes Mellitus: β-Cell Dysfunction and Beyond.

Jun Sung Moon, Udayakumar Karunakaran, Elumalai Suma, Seung Min Chung, Kyu Chang Won

Open access · goldAbstract readReview
In one paragraph

Review in Diabetes & metabolism journal, 2020. 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
3.3field-weighted citation impact, top 7% 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, 39 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Defective efferocytosis in diabetes: molecular mechanisms and emerging therapeutic strategies.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
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  5. Article
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  7. Article
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  9. Observational
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  11. Article
  12. The role of candidate transport proteins in β-cell long-chain fatty acid uptake: Where are we now?Diabetic medicine : a journal of the British Diabetic Association · 2023
    Review
  13. Review
  14. Review
  15. Article
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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

5 authors at 1 institution in 1 country.

Jun Sung Moon *Department of Internal Medicine, Yeungnam University College of Medicine, Daegu, Korea.ORCID 0000-0003-1569-3068
Udayakumar Karunakaran *Department of Internal Medicine, Yeungnam University College of Medicine, Daegu, Korea.ORCID 0000-0002-7049-9105
Elumalai SumaDepartment of Internal Medicine, Yeungnam University College of Medicine, Daegu, Korea.
Seung Min ChungDepartment of Internal Medicine, Yeungnam University College of Medicine, Daegu, Korea.
Kyu Chang WonDepartment of Internal Medicine, Yeungnam University College of Medicine, Daegu, Korea. kcwon@med.yu.ac.kr.ORCID 0000-0001-5945-3395
Yeungnam University College

Funding

NRF NRF-2020R1A2C1003649YU
6 · The paper itself

Abstract

Impaired β-cell function is the key pathophysiology of type 2 diabetes mellitus, and chronic exposure of nutrient excess could lead to this tragedy. For preserving β-cell function, it is essential to understand the cause and mechanisms about the progression of β-cells failure. Glucotoxicity, lipotoxicity, and glucolipotoxicity have been suggested to be a major cause of β-cell dysfunction for decades, but not yet fully understood. Fatty acid translocase cluster determinant 36 (CD36), which is part of the free fatty acid (FFA) transporter system, has been identified in several tissues such as muscle, liver, and insulin-producing cells. Several studies have reported that induction of CD36 increases uptake of FFA in several cells, suggesting the functional interplay between glucose and FFA in terms of insulin secretion and oxidative metabolism. However, we do not currently know the regulating mechanism and physiological role of CD36 on glucolipotoxicity in pancreatic β-cells. Also, the downstream and upstream targets of CD36 related signaling have not been defined. In the present review, we will focus on the expression and function of CD36 related signaling in the pancreatic β-cells in response to hyperglycemia and hyperlipidemia (ceramide) along with the clinical studies on the association between CD36 and metabolic disorders.

Indexed as

CD36 AntigensCeramidesDiabetes Mellitus, Type 2Fatty Acids, NonesterifiedFemaleGlucoseHumansHyperglycemiaInflammationInsulin-Secreting CellsInsulin SecretionLipidsMaleMetabolic SyndromeOxidative StressReactive Oxygen SpeciesCD36 AntigensCeramidesFatty Acids, NonesterifiedGlucoseLipidsReactive Oxygen SpeciesCD36 antigensCeramidesDiabetes mellitus, type 2Fatty acidsHyperglycemiaInflammationInsulin-secreting cellsOxidative stressReactive oxygen species

Identifiers

PMID32347024
PMCPMC7188969
OpenAlexW3019427568

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.