Evidence map›Paper›PMID 29162604›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2018

Suppression of Hepatic FLOT1 (Flotillin-1) by Type 2 Diabetes Mellitus Impairs the Disposal of Remnant Lipoproteins via Syndecan-1.

Keyang Chen, Qingsi Wu, Kongwang Hu, Chengwei Yang, Xiangdong Wu, Peter Cheung, Kevin Jon Williams

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. The roles of FLOT1 in human diseases (Review).Molecular medicine reports · 2023
    Review
  6. Review
  7. Article
  8. Proteomic Analysis of Tear Film Obtained from Diabetic Dogs.Animals : an open access journal from MDPI · 2020
    Article
  9. Article
  10. Flotillins: At the Intersection of ProteinInternational journal of molecular sciences · 2020
    Review
  11. Review
  12. Annual Report on Sex in Preclinical Studies:Arteriosclerosis, thrombosis, and vascular biology · 2020
    Review
  13. Article
  14. Metabolism, Obesity, and Diabetes Mellitus.Arteriosclerosis, thrombosis, and vascular biology · 2019
    Article
  15. Article
  16. Review
  17. Review
  18. Article
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

7 authors at 1 institution in 1 country.

Keyang ChenFrom the School of Public Health (K.C., Q.W., C.Y.) and Department of Surgery, The First Affiliated Hospital (K.H.), Anhui Medical University, Hefei, China; Section of Endocrinology, Diabetes, & Metabolism, Department of Medicine, Lewis Katz School of Medicine at Temple University, Philadelphia, PA (K.C., X.W., P.C., K.J.W.); and Department of Molecular and Clinical Medicine, Sahlgrenska Academy of the University of Gothenburg, Sweden (K.J.W.). chenkeyang@ahmu.edu.cn kjwilliams@temple.edu kevin.jon.williams@gu.se.
Qingsi WuFrom the School of Public Health (K.C., Q.W., C.Y.) and Department of Surgery, The First Affiliated Hospital (K.H.), Anhui Medical University, Hefei, China; Section of Endocrinology, Diabetes, & Metabolism, Department of Medicine, Lewis Katz School of Medicine at Temple University, Philadelphia, PA (K.C., X.W., P.C., K.J.W.); and Department of Molecular and Clinical Medicine, Sahlgrenska Academy of the University of Gothenburg, Sweden (K.J.W.).
Kongwang HuFrom the School of Public Health (K.C., Q.W., C.Y.) and Department of Surgery, The First Affiliated Hospital (K.H.), Anhui Medical University, Hefei, China; Section of Endocrinology, Diabetes, & Metabolism, Department of Medicine, Lewis Katz School of Medicine at Temple University, Philadelphia, PA (K.C., X.W., P.C., K.J.W.); and Department of Molecular and Clinical Medicine, Sahlgrenska Academy of the University of Gothenburg, Sweden (K.J.W.).
Chengwei YangFrom the School of Public Health (K.C., Q.W., C.Y.) and Department of Surgery, The First Affiliated Hospital (K.H.), Anhui Medical University, Hefei, China; Section of Endocrinology, Diabetes, & Metabolism, Department of Medicine, Lewis Katz School of Medicine at Temple University, Philadelphia, PA (K.C., X.W., P.C., K.J.W.); and Department of Molecular and Clinical Medicine, Sahlgrenska Academy of the University of Gothenburg, Sweden (K.J.W.).
Xiangdong WuFrom the School of Public Health (K.C., Q.W., C.Y.) and Department of Surgery, The First Affiliated Hospital (K.H.), Anhui Medical University, Hefei, China; Section of Endocrinology, Diabetes, & Metabolism, Department of Medicine, Lewis Katz School of Medicine at Temple University, Philadelphia, PA (K.C., X.W., P.C., K.J.W.); and Department of Molecular and Clinical Medicine, Sahlgrenska Academy of the University of Gothenburg, Sweden (K.J.W.).
Peter CheungFrom the School of Public Health (K.C., Q.W., C.Y.) and Department of Surgery, The First Affiliated Hospital (K.H.), Anhui Medical University, Hefei, China; Section of Endocrinology, Diabetes, & Metabolism, Department of Medicine, Lewis Katz School of Medicine at Temple University, Philadelphia, PA (K.C., X.W., P.C., K.J.W.); and Department of Molecular and Clinical Medicine, Sahlgrenska Academy of the University of Gothenburg, Sweden (K.J.W.).
Kevin Jon WilliamsFrom the School of Public Health (K.C., Q.W., C.Y.) and Department of Surgery, The First Affiliated Hospital (K.H.), Anhui Medical University, Hefei, China; Section of Endocrinology, Diabetes, & Metabolism, Department of Medicine, Lewis Katz School of Medicine at Temple University, Philadelphia, PA (K.C., X.W., P.C., K.J.W.); and Department of Molecular and Clinical Medicine, Sahlgrenska Academy of the University of Gothenburg, Sweden (K.J.W.). chenkeyang@ahmu.edu.cn kjwilliams@temple.edu kevin.jon.williams@gu.se.
Temple University · US

Funding

Sulfatase-2: Key mediator of atherogenic postprandial dyslipoproteinemiaR01DK100851 · NIDDK · TEMPLE UNIV OF THE COMMONWEALTH · PI WILLIAMS, KEVIN JON · 2013 to 2017
$1.9M
NIDDK NIH HHS R01 DK100851
6 · The paper itself

Abstract

objectiveType 2 diabetes mellitus (T2DM) and the atherometabolic syndrome exhibit a deadly dyslipoproteinemia that arises in part from impaired hepatic disposal of C-TRLs (cholesterol- and triglyceride-rich remnant apoB [apolipoprotein B] lipoproteins). We previously identified syndecan-1 as a receptor for C-TRLs that directly mediates endocytosis via rafts, independent from coated pits. Caveolins and flotillins form rafts but facilitate distinct endocytotic pathways. We now investigated their participation in syndecan-1-mediated disposal of C-TRLs and their expression in T2DM liver. APPROACH AND

resultsIn cultured liver cells and nondiabetic murine livers, we found that syndecan-1 coimmunoprecipitates with FLOT1 (flotillin-1) but not with CAV1 (caveolin-1). Binding of C-TRLs to syndecan-1 on the surface of liver cells enhanced syndecan-1/FLOT1 association. The 2 molecules then trafficked together into the lysosomes, implying limited if any recycling back to the cell surface. The interaction requires the transmembrane/cytoplasmic region of syndecan-1 and the N-terminal hydrophobic domain of FLOT1. Knockdown of FLOT1 in cultured liver cells substantially inhibited syndecan-1 endocytosis. Livers from obese, T2DM KK

conclusionsFLOT1 is a novel participant in the disposal of harmful C-TRLs via syndecan-1. Low expression of FLOT1 in T2DM liver may contribute to metabolic dyslipoproteinemia.

Indexed as

AnimalsCell Line, TumorChylomicron RemnantsDiabetes Mellitus, Type 2Disease Models, AnimalDyslipidemiasEndocytosisGene Expression RegulationGenetic TherapyHepatocytesLiverMaleMembrane ProteinsProtein BindingProtein Interaction Domains and MotifsProtein TransportChylomicron RemnantsflotillinsMembrane ProteinsSdc1 protein, mouseSyndecan-1cholesteroldyslipidemiasendocytosisflotillinshypertriglyceridemiasyndecan-1type 2 diabetes mellitus

Identifiers

PMID29162604
PMCPMC5982506
OpenAlexW2770283612

What OpenQuestion holds

Textmetadata
LicenceTDM
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.