Evidence map›Paper›PMID 35163991›Full record

ArticleMolecules (Basel, Switzerland)2022

Sitagliptin Is More Effective Than Gliclazide in Preventing  Pro-Fibrotic and Pro-Inflammatory Changes in a Rodent Model of Diet-Induced Non-Alcoholic Fatty Liver Disease.

Jing Ren, Xiaoyu Wang, Christine Yee, Mark D Gorrell, Susan V McLennan, Stephen M Twigg

Open access · goldAbstract readComparative Study
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecules (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

7 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. Review
  3. Exploring Promising Therapies for Non-Alcoholic Fatty Liver Disease: A ClinicalTrials.gov Analysis.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024
    Review
  4. Article
  5. Review
  6. Article
  7. 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

6 authors at 1 institution in 1 country.

Jing RenGreg Brown Diabetes and Endocrinology Research Laboratories, Sydney Medical School (Central), Faculty of Medicine and Health, The University of Sydney, Camperdown, NSW 2006, Australia.
Xiaoyu WangGreg Brown Diabetes and Endocrinology Research Laboratories, Sydney Medical School (Central), Faculty of Medicine and Health, The University of Sydney, Camperdown, NSW 2006, Australia.
Christine YeeGreg Brown Diabetes and Endocrinology Research Laboratories, Sydney Medical School (Central), Faculty of Medicine and Health, The University of Sydney, Camperdown, NSW 2006, Australia.
Mark D GorrellLiver Enzymes in Metabolism and Inflammation Program, Centenary Institute, The University of Sydney, Newtown, NSW 2042, Australia.ORCID 0000-0002-0528-2604
Susan V McLennanGreg Brown Diabetes and Endocrinology Research Laboratories, Sydney Medical School (Central), Faculty of Medicine and Health, The University of Sydney, Camperdown, NSW 2006, Australia.
Stephen M TwiggGreg Brown Diabetes and Endocrinology Research Laboratories, Sydney Medical School (Central), Faculty of Medicine and Health, The University of Sydney, Camperdown, NSW 2006, Australia.
The University of Sydney · AU

Funding

China Scholarship Council 20120601005
6 · The paper itself

Abstract

A diet-induced non-alcoholic fatty liver disease (NAFLD) model causing obesity in rodents was used to examine whether sitagliptin and gliclazide therapies have similar protective effects on pathological liver change.

methodsMale mice were fed a high-fat diet (HFD) or standard chow (Chow) ad libitum for 25 weeks and randomly allocated to oral sitagliptin or gliclazide treatment for the final 10 weeks. Fasting blood glucose and circulating insulin were measured. Inflammatory and fibrotic liver markers were assessed by qPCR. The second messenger ERK and autophagy markers were examined by Western immunoblot. F4/80, collagens and CCN2 were assessed by immunohistochemistry (IHC).

resultsAt termination, HFD mice were obese, hyperinsulinemic and insulin-resistant but non-diabetic. The DPP4 inhibitor sitagliptin prevented intrahepatic induction of pro-fibrotic markers collagen-IV, collagen-VI, CCN2 and TGF-β1 and pro-inflammatory markers TNF-α and IL-1β more effectively than sulfonylurea gliclazide. By IHC, liver collagen-VI and CCN2 induction by HFD were inhibited only by sitagliptin. Sitagliptin had a greater ability than gliclazide to normalise ERK-protein liver dysregulation.

conclusionThese data indicate that sitagliptin, compared with gliclazide, exhibits greater inhibition of pro-fibrotic and pro-inflammatory changes in an HFD-induced NAFLD model. Sitagliptin therapy, even in the absence of diabetes, may have specific benefits in diet-induced NAFLD.

Indexed as

AnimalsDiet, High-FatGliclazideHypoglycemic AgentsInflammationLiver CirrhosisMaleMiceMice, Inbred C57BLNon-alcoholic Fatty Liver DiseaseSitagliptin PhosphateGliclazideHypoglycemic AgentsSitagliptin PhosphatefibrosisgliclazideinflammationNAFLDsitagliptin

Identifiers

PMID35163991
PMCPMC8838637
OpenAlexW4207073091

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.