Evidence mapPaperPMID 26628836Full record

ArticleJournal of clinical and experimental hepatology2015

Remogliflozin Etabonate Improves Fatty Liver Disease in Diet-Induced Obese Male Mice.

Shigeru Nakano, Kenji Katsuno, Masayuki Isaji, Tatsuya Nagasawa, Benjamin Buehrer, Susan Walker, William O Wilkison, Bentley Cheatham

Abstract read
In one paragraph

Article in Journal of clinical and experimental hepatology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
field-weighted citation impact
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

40 citing papers in PubMed.

  1. Trial
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  7. The Ketogenic Effect of SGLT-2 Inhibitors-Beneficial or Harmful?Journal of cardiovascular development and disease · 2023
    Review
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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

8 authors.

Shigeru NakanoDiscovery Research R&D, Kissei Pharmaceutical Co. Ltd., Nagano 399-8304, Japan.
Kenji KatsunoDiscovery Research R&D, Kissei Pharmaceutical Co. Ltd., Nagano 399-8304, Japan.
Masayuki IsajiResearch and Development Division, Kissei Pharmaceutical Co. Ltd., Nagano 399-8304, Japan.
Tatsuya NagasawaToxicology Research Laboratory, Kissei Pharmaceutical Co. Ltd., Nagano 399-8305, Japan.
Benjamin BuehrerZenBio, Research Triangle Park, NC 27709, USA.
Susan WalkerApex Biostatistics, New Hill, NC 27562, USA.
William O WilkisonIslet Sciences, Raleigh, NC 27615, USA.
Bentley CheathamBHV Pharma, RTP, NC 27709, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNonalcoholic fatty liver disease and nonalcoholic steatohepatitis (NASH) are serious conditions and are being diagnosed at an increased rate. The etiology of these hepatic disorders is not clear but involves insulin resistance and oxidative stress. Remogliflozin etabonate (Remo) is an inhibitor of the sodium glucose-dependent renal transporter 2 (SGLT2), and improves insulin sensitivity in type 2 diabetics. In the current study, we examined the effects of Remo in a diet-induced obese mouse model of NAFLD.

methodsAfter 11-weeks on High-Fat-Diet 32 (HFD32), C57BL/6J mice were obese and displayed characteristics consistent with NAFLD. Cohorts of obese animals were continued on HFD32 for an additional 4-week treatment period with or without Remo.

resultsTreatment with Remo for 4 weeks markedly lowered both plasma alanine aminotransferase (76%) and aspartate aminotransferase (48%), and reduced both liver weight and hepatic triglyceride content by 42% and 40%, respectively. Remo also reduced hepatic mRNA content for tumor necrosis factor (TNF)-α (69%), and monocyte chemoattractant protein (MCP)-1 (69%). The diet-induced increase in thiobarbituric acid-reactive substances, a marker of oxidative stress, was reduced following treatment with Remo, as measured in both liver homogenates (22%) and serum (37%). Finally, the oxygen radical absorbance capacity (ORAC) in three different SGLT2 inhibitors was determined: remogliflozin, canagliflozin and dapagliflozin. Only remogliflozin had any significant ORAC activity.

conclusionsRemo significantly improved markers associated with NAFLD in this animal model, and may be an effective compound for the treatment of NASH and NAFLD due to its insulin-sensitizing and antioxidant properties.

Indexed as

AAPH, 2,2′-azobis-2-methyl-propanimidamide dihydrochlorideALT, Alanine aminotransferaseAST, aspartate aminotransferaseDIO, Diet-induced obesityER, Endoplasmic reticulumFFA, Free fatty acidsFXR, Farnesoid X receptorhepatic steatosisHFD32, High fat diet 32MCP-1, Monocyte chemoattractant protein-1NAFLDNAFLD, Nonalcoholic fatty liver diseaseNASHNASH, Nonalcoholic steatohepatitisobesityORAC, Oxygen radical absorbance capacityRemo, Remogliflozin etabonateROS, Reactive oxygen speciesSGLT2SGLT2, sodium glucose-dependent renal transporter 2TBARS, Thiobarbituric acid-reactive substancesTG, TriglycerideTNF-α, Tumor necrosis factor alphaTrolox, 6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid

Identifiers

PMID26628836
PMCPMC4632078

What Socratic holds

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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.