Evidence map›Paper›PMID 32614804›Full record

ArticleJCI insight2020

Fatty acid transport protein-2 regulates glycemic control and diabetic kidney disease progression.

Shenaz Khan, Robert Gaivin, Caroline Abramovich, Michael Boylan, Jorge Calles, Jeffrey R Schelling

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
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

49 citing papers in PubMed, 78 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. Insulin Resistance and Inflammation.International journal of molecular sciences · 2026
    Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Differential effects of deleting the angiotensin receptor ATAmerican journal of physiology. Regulatory, integrative and comparative physiology · 2025
    Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Crosstalk between glomeruli and tubules.Nature reviews. Nephrology · 2025
    Review
  20. Review
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

6 authors at 3 institutions in 1 country.

Shenaz KhanDepartment of Medicine, Division of Nephrology.
Robert GaivinDepartment of Medicine, Division of Nephrology.
Caroline AbramovichDepartment of Pathology.
Michael BoylanDepartment of Medicine, Division of Gastroenterology.
Jorge CallesDepartment of Medicine, Division of Endocrinology, MetroHealth Campus, and.
Jeffrey R SchellingDepartment of Medicine, Division of Nephrology.
Case Western Reserve University · USMetroHealth · USUniversity Gastroenterology · US

Funding

Mechanisms of tubular atrophy in renal diseaseR01DK067528 · NIDDK · CASE WESTERN RESERVE UNIVERSITY · PI SCHELLING, JEFFREY R · 2005 to 2025
$7.1M
Identification of CKD and CVD BiomarkersU01DK106965 · NIDDK · CASE WESTERN RESERVE UNIVERSITY · PI BRUNENGRABER, HENRI, HOSTETTER, THOMAS HEARD · 2015 to 2019
$1.6M
NIDDK NIH HHS R01 DK067528NIDDK NIH HHS U01 DK106965
6 · The paper itself

Abstract

Kidney disease is one of the most devastating complications of diabetes, and tubular atrophy predicts diabetic kidney disease (DKD) progression to end-stage renal disease. We have proposed that fatty acids bound to albumin contribute to tubular atrophy by inducing lipotoxicity, after filtration across damaged glomeruli, and subsequent proximal tubule reabsorption by a fatty acid transport protein-2-dependent (FATP2-dependent) mechanism. To address this possibility, genetic (Leprdb/db eNOS-/-) and induced (high-fat diet plus low-dose streptozotocin) mouse models of obesity and DKD were bred with global FATP2 gene-deleted mice (Slc27a2) and then phenotyped. DKD-prone mice with the Slc27a2-/- genotype demonstrated normalization of glomerular filtration rate, reduced albuminuria, improved kidney histopathology, and longer life span compared with diabetic Slc27a2+/+ mice. Genetic and induced DKD-prone Slc27a2-/- mice also exhibited markedly reduced fasting plasma glucose, with mean values approaching euglycemia, despite increased obesity and decreased physical activity. Glucose lowering in DKD-prone Slc27a2-/- mice was accompanied by β cell hyperplasia and sustained insulin secretion. Together, our data indicate that FATP2 regulates DKD pathogenesis by a combined lipotoxicity and glucotoxicity (glucolipotoxicity) mechanism.

Indexed as

Glycemic ControlAlbuminuriaAnimalsBiomarkersCoenzyme A LigasesDiabetes Mellitus, ExperimentalDiabetic NephropathiesDisease ProgressionFemaleGlomerular Filtration RateMaleMiceMice, Inbred C57BLMice, KnockoutMice, ObeseNitric Oxide Synthase Type IIIBiomarkersCoenzyme A LigasesFATP2 protein, mouseleptin receptor, mouseNitric Oxide Synthase Type IIINos3 protein, mouseReceptors, LeptinDiabetesFatty acid oxidationMetabolismNephrologyObesity

Identifiers

PMID32614804
PMCPMC7455077
OpenAlexW3039517774

What OpenQuestion holds

Textmetadata
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.