Evidence map›Paper›PMID 26927057›Full record

ArticleMolecules (Basel, Switzerland)2016

1-Deoxynojirimycin Alleviates Liver Injury and Improves Hepatic Glucose Metabolism in db/db Mice.

Qingpu Liu, Xuan Li, Cunyu Li, Yunfeng Zheng, Fang Wang, Hongyang Li, Guoping Peng

Open access · goldAbstract read
In one paragraph

Article in Molecules (Basel, Switzerland), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
6.8field-weighted citation impact, top 4% 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

24 citing papers in PubMed, 61 citations in OpenAlex.

  1. Review
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  8. 1-Deoxynojirimycin attenuates pathological markers of Alzheimer's disease in the in vitro model of neuronal insulin resistance.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Article
  9. Article
  10. Article
  11. Metabolic engineering ofSynthetic and systems biotechnology · 2023
    Article
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  17. Article
  18. 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

7 authors at 1 institution in 1 country.

Qingpu LiuCollege of Pharmacy, Nanjing University of Chinese Medicine, Nanjing 210023, China. lqpcy1224@163.com.
Xuan LiCollege of Pharmacy, Nanjing University of Chinese Medicine, Nanjing 210023, China. xuanli@njutcm.edu.cn.
Cunyu LiCollege of Pharmacy, Nanjing University of Chinese Medicine, Nanjing 210023, China. licunyuok@163.com.
Yunfeng ZhengCollege of Pharmacy, Nanjing University of Chinese Medicine, Nanjing 210023, China. zyunfeng88@126.com.
Fang WangCollege of Pharmacy, Nanjing University of Chinese Medicine, Nanjing 210023, China. wangfa8875@163.com.
Hongyang LiCollege of Pharmacy, Nanjing University of Chinese Medicine, Nanjing 210023, China. lihongyang@sina.com.
Guoping PengCollege of Pharmacy, Nanjing University of Chinese Medicine, Nanjing 210023, China. guopingpeng@sohu.com.
Nanjing University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The present study investigated the effect of 1-Deoxynojirimycin (DNJ) on liver injury and hepatic glucose metabolism in db/db mice. Mice were divided into five groups: normal control, db/db control, DNJ-20 (DNJ 20 mg·kg(-1)·day(-1)), DNJ-40 (DNJ 40 mg·kg(-1)·day(-1)) and DNJ-80 (DNJ 80 mg·kg(-1)·day(-1)). All doses were treated intravenously by tail vein for four weeks. DNJ was observed to significantly reduce the levels of serum triglyceride (TG), total cholesterol (TC), low density lipoprotein cholesterol (LDL-C) and liver TG, as well as activities of serum alanine aminotransferase (ALT), and aspartate transaminase (AST); DNJ also alleviated macrovesicular steatosis and decreased tumor necrosis factor α (TNF-α), interleukin-1 (IL-1), interleukin-6 (IL-6) levels in liver tissue. Furthermore, DNJ treatment significantly increased hepatic glycogen content, the activities of hexokinase (HK), pyruvate kinase (PK) in liver tissue, and decreased the activities of glucose-6-phosphatase (G6Pase), glycogen phosphorylase (GP), and phosphoenolpyruvate carboxykinase (PEPCK). Moreover, DNJ increased the phosphorylation of phosphatidylinositol 3 kinase (PI3K) on p85, protein kinase B (PKB) on Ser473, glycogen synthase kinase 3β (GSK-3β) on Ser9, and inhibited phosphorylation of glycogen synthase (GS) on Ser645 in liver tissue of db/db mice. These results demonstrate that DNJ can increase hepatic insulin sensitivity via strengthening of the insulin-stimulated PKB/GSK-3β signal pathway and by modulating glucose metabolic enzymes in db/db mice. Moreover, DNJ also can improve lipid homeostasis and attenuate hepatic steatosis in db/db mice.

Indexed as

1-DeoxynojirimycinAnimalsDose-Response Relationship, DrugFatty LiverGlucoseHypoglycemic AgentsInjections, IntravenousInsulin ResistanceLipid MetabolismLiverMaleMiceMice, TransgenicMolecular StructureSignal Transduction1-DeoxynojirimycinGlucoseHypoglycemic Agents1-Deoxynojirimycindb/db miceglucose metabolic enzymeshepatic glucose metabolismhepatic glycogenhepatic insulin sensitivitylipid metabolismliverPKB/GSK-3β

Identifiers

PMID26927057
PMCPMC6274115
OpenAlexW2280443532

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.