Evidence map›Paper›PMID 25957525›Full record

ReviewCurrent diabetes reports2015

The evolving understanding of the contribution of lipid metabolism to diabetic kidney disease.

Krisztian Stadler, Ira J Goldberg, Katalin Susztak

Open access · greenAbstract readReview
In one paragraph

Review in Current diabetes reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
103citing papers in PubMed, 2 pooled it
7.8field-weighted citation impact, top 2% 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

103 citing papers in PubMed, 2 syntheses or guidelines pooled it, 173 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Targeting de novo lipogenesis to mitigate kidney disease.The Journal of clinical investigation · 2024
    Article

43 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

3 authors at 3 institutions in 1 country.

Krisztian StadlerOxidative Stress and Disease Laboratory, Pennington Biomedical Research Center, Baton Rouge, LA, USA.
Ira J Goldberg
Katalin Susztak
New York University · USPennington Biomedical Research Center · USUniversity of Pennsylvania · US

Funding

Role of the Notch Pathway in Kidney InjuryR01DK076077 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI KATALIN SUSZTAK · 2007 to 2026
$8.0M
Epigenetics of Chronic Kidney DiseaseR01DK087635 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI KATALIN SUSZTAK · 2009 to 2026
$7.0M
Pathways of Tissue Lipid UptakeR01HL045095 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI ABUMRAD, NADA A., GOLDBERG, IRA J · 1991 to 2024
$6.9M
Mechanisms of Fatty Acid Uptake By Cardiac MuscleR01HL073029 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI GOLDBERG, IRA J · 2003 to 2021
$6.8M
EXTRACELLULAR REGULATION OF LIPOPROTEIN LIPASE ACTIVITYR37HL045095 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GOLDBERG, IRA J · 2000 to 2009
$4.6M
Diabetes-Mediated Effects on Myeloid Precursors and Vascular ComplicationsR01DK095684 · NIDDK · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI FISHER, EDWARD A, GOLDBERG, IRA J · 2012 to 2016
$2.7M
NHLBI NIH HHS HL073029NHLBI NIH HHS HL45095NHLBI NIH HHS R01 HL045095NHLBI NIH HHS R01 HL073029NHLBI NIH HHS R37 HL045095NIDDK NIH HHS DK076077NIDDK NIH HHS DK087635NIDDK NIH HHS DK095684NIDDK NIH HHS R01 DK076077NIDDK NIH HHS R01 DK087635NIDDK NIH HHS R01 DK095684
6 · The paper itself

Abstract

Although diabetes is mainly diagnosed based on elevated glucose levels, dyslipidemia is also observed in these patients. Chronic kidney disease (CKD), a frequent occurrence in patients with diabetes, is associated with major abnormalities in circulating lipoproteins and renal lipid metabolism. At baseline, most renal epithelial cells rely on fatty acids as their energy source. CKD, including that which occurs in diabetes, is characterized by tubule epithelial lipid accumulation. Whether this is due to increased uptake or greater local fatty acid synthesis is unknown. We have recently shown that CKD also leads to decreased fatty acid oxidation, which might be an additional mechanism leading to lipid accumulation. Defective fatty acid utilization causes energy depletion resulting in increased apoptosis and dedifferentiation, which in turn contributes to fibrosis and CKD progression. Enhanced fatty acid oxidation in the kidney induced by fenofibrate, a peroxisomal proliferator-activated receptor (PPAR)-α agonist, showed benefit in mouse models of CKD. Fenofibrate treatment also reduced albuminuria in patients with diabetes in multiple clinical trials. Taken together, these findings suggest that further understanding of lipid metabolism in diabetic kidney disease may lead to novel therapeutic approaches.

Indexed as

Lipid MetabolismAnimalsDiabetic NephropathiesEnergy MetabolismEpithelial CellsFatty AcidsHumansPeroxisome Proliferator-Activated ReceptorsFatty AcidsPeroxisome Proliferator-Activated Receptors

Identifiers

PMID25957525
PMCPMC4548922
OpenAlexW812844120

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.