Evidence mapPaperPMID 28196866Full record

ArticleThe Journal of biological chemistry2017

SGLT2 Protein Expression Is Increased in Human Diabetic Nephropathy: SGLT2 PROTEIN INHIBITION DECREASES RENAL LIPID ACCUMULATION, INFLAMMATION, AND THE DEVELOPMENT OF NEPHROPATHY IN DIABETIC MICE.

Xiaoxin X Wang, Jonathan Levi, Yuhuan Luo, Komuraiah Myakala, Michal Herman-Edelstein, Liru Qiu, Dong Wang, Yingqiong Peng, Almut Grenz, Scott Lucia and 6 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 172 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
172citing papers in PubMed, 3 pooled it
19.7field-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

172 citing papers in PubMed, 3 syntheses or guidelines pooled it, 296 citations in OpenAlex.

  1. Pooled it
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  9. Salt and chronic kidney disease.Nature reviews. Nephrology · 2026
    Review
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112 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

16 authors at 7 institutions in 3 countries.

Xiaoxin X WangFrom the Departments of Medicine, Anesthesiology, and Pathology, University of Colorado Anschutz Medical Campus, Aurora, Colorado 80220.
Jonathan Levithe NIDDK, National Institutes of Health, Bethesda, Maryland 20892.
Yuhuan LuoFrom the Departments of Medicine, Anesthesiology, and Pathology, University of Colorado Anschutz Medical Campus, Aurora, Colorado 80220.
Komuraiah MyakalaFrom the Departments of Medicine, Anesthesiology, and Pathology, University of Colorado Anschutz Medical Campus, Aurora, Colorado 80220.
Michal Herman-Edelsteinthe Rabin Medical Center, Department of Nephrology and Hypertension, Felsenstein Medical Research Center, Sackler School of Medicine, Tel Aviv University, 6997801 Tel Aviv, Israel.
Liru QiuFrom the Departments of Medicine, Anesthesiology, and Pathology, University of Colorado Anschutz Medical Campus, Aurora, Colorado 80220.
Dong WangFrom the Departments of Medicine, Anesthesiology, and Pathology, University of Colorado Anschutz Medical Campus, Aurora, Colorado 80220.
Yingqiong PengFrom the Departments of Medicine, Anesthesiology, and Pathology, University of Colorado Anschutz Medical Campus, Aurora, Colorado 80220.
Almut GrenzFrom the Departments of Medicine, Anesthesiology, and Pathology, University of Colorado Anschutz Medical Campus, Aurora, Colorado 80220.
Scott LuciaFrom the Departments of Medicine, Anesthesiology, and Pathology, University of Colorado Anschutz Medical Campus, Aurora, Colorado 80220.
Evgenia DobrinskikhFrom the Departments of Medicine, Anesthesiology, and Pathology, University of Colorado Anschutz Medical Campus, Aurora, Colorado 80220.
Vivette D D'Agatithe Department of Pathology, Columbia University, College of Physicians and Surgeons, New York, New York 10027.
Hermann Koepsellthe Department of Molecular Plant Physiology and Biophysics, Julius-von-Sachs-Institute, University of Würzburg, D-97082 Würzburg, Germany, and.
Jeffrey B Koppthe NIDDK, National Institutes of Health, Bethesda, Maryland 20892.
Avi Z Rosenbergthe Department of Pathology, The Johns Hopkins University, Baltimore, Maryland 21218.
Moshe LeviFrom the Departments of Medicine, Anesthesiology, and Pathology, University of Colorado Anschutz Medical Campus, Aurora, Colorado 80220, moshe.levi@ucdenver.edu MMJJL@aol.com.
University of Colorado Anschutz Medical Campus · USNational Institutes of Health · USColumbia University · USJohns Hopkins University · USTel Aviv University · ILUniversity of Würzburg · DEVA Eastern Colorado Health Care System · US

Funding

NIDDK NIH HHS R01 DK098336
6 · The paper itself

Abstract

There is very limited human renal sodium gradient-dependent glucose transporter protein (SGLT2) mRNA and protein expression data reported in the literature. The first aim of this study was to determine SGLT2 mRNA and protein levels in human and animal models of diabetic nephropathy. We have found that the expression of SGLT2 mRNA and protein is increased in renal biopsies from human subjects with diabetic nephropathy. This is in contrast to db-db mice that had no changes in renal SGLT2 protein expression. Furthermore, the effect of SGLT2 inhibition on renal lipid content and inflammation is not known. The second aim of this study was to determine the potential mechanisms of beneficial effects of SGLT2 inhibition in the progression of diabetic renal disease. We treated db/db mice with a selective SGLT2 inhibitor JNJ 39933673. We found that SGLT2 inhibition caused marked decreases in systolic blood pressure, kidney weight/body weight ratio, urinary albumin, and urinary thiobarbituric acid-reacting substances. SGLT2 inhibition prevented renal lipid accumulation via inhibition of carbohydrate-responsive element-binding protein-β, pyruvate kinase L, SCD-1, and DGAT1, key transcriptional factors and enzymes that mediate fatty acid and triglyceride synthesis. SGLT2 inhibition also prevented inflammation via inhibition of CD68 macrophage accumulation and expression of p65, TLR4, MCP-1, and osteopontin. These effects were associated with reduced mesangial expansion, accumulation of the extracellular matrix proteins fibronectin and type IV collagen, and loss of podocyte markers WT1 and synaptopodin, as determined by immunofluorescence microscopy. In summary, our study showed that SGLT2 inhibition modulates renal lipid metabolism and inflammation and prevents the development of nephropathy in db/db mice.

Indexed as

Sodium-Glucose Transporter 2 InhibitorsAnimalsDiabetes Mellitus, ExperimentalDiabetic NephropathiesHumansInflammationKidney DiseasesLipid MetabolismMiceRNA, MessengerSodium-Glucose Transporter 2RNA, MessengerSodium-Glucose Transporter 2Sodium-Glucose Transporter 2 Inhibitorsdiabetesdiabetic nephropathyglucose transportimmunochemistryinflammationlipid synthesismicroscopic imaging

Identifiers

PMID28196866
PMCPMC5392679
OpenAlexW2588592529

What Socratic 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 Socratic graph.