Evidence map›Paper›PMID 28777337›Full record

ArticleInternational journal of molecular sciences2017

Endoplasmic Reticulum Stress Inducer Tunicamycin Alters Hepatic Energy Homeostasis in Mice.

Bin Feng, Xiaohua Huang, Dandan Jiang, Lun Hua, Yong Zhuo, De Wu

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

34 citing papers in PubMed, 81 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Oxysterol binding protein regulates the resolution of TLR-induced cytokine production in macrophages.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. eIF2A-knockout mice reveal decreased life span and metabolic syndrome.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    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.

Bin FengAnimal Nutrition Institute, Sichuan Agricultural University, Chengdu 611130, China. fengbin@sicau.edu.cn.
Xiaohua HuangAnimal Nutrition Institute, Sichuan Agricultural University, Chengdu 611130, China. hxh3028@163.com.
Dandan JiangAnimal Nutrition Institute, Sichuan Agricultural University, Chengdu 611130, China. dandanjiang@163.com.
Lun HuaAnimal Nutrition Institute, Sichuan Agricultural University, Chengdu 611130, China. hualun0516@163.com.
Yong ZhuoAnimal Nutrition Institute, Sichuan Agricultural University, Chengdu 611130, China. zhuoyong2003@163.com.
De WuAnimal Nutrition Institute, Sichuan Agricultural University, Chengdu 611130, China. wude@sicau.edu.cn.
Sichuan Agricultural University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Disorders of hepatic energy metabolism, which can be regulated by endoplasmic reticulum (ER) stress, lead to metabolic diseases such as hepatic steatosis and hypoglycemia. Tunicamycin, a pharmacological ER stress inducer, is used to develop an anti-cancer drug. However, the effects of tunicamycin on hepatic energy metabolism have not been well elucidated. Mice were intraperitoneally injected with tunicamycin or vehicle. Twenty-four hours later, hepatic triglyceride and glycogen content and serum lipids profiles were analyzed, as well as the expression of lipogenic and gluconeogenic genes. Tunicamycin significantly induced hepatic a yellowish color and ER stress, as well as increasing serum levels of aspartate transaminase and alanine transaminase. Besides, tunicamycin remarkably increased hepatic triglyceride content and suppressed the expression of apolipoprotein B100. In addition, tunicamycin-treated mice had lower serum levels of triglyceride, apolipoprotein B, low-density lipoprotein cholesterol and high-density lipoprotein cholesterol. Gene expression of peroxisome proliferator-activated receptor α was decreased by tunicamycin, but the protein level was increased. Furthermore, blood glucose level and hepatic glycogen content were decreased in tunicamycin-treated mice. Protein kinase B signaling was attenuated in the tunicamycin-treated liver, but the expression and activities of phosphoenolpyruvate carboxykinase and glucose-6-phosphatase were unchanged. Tunicamycin alters hepatic energy homeostasis by increasing triglyceride accumulation and decreasing glycogen content.

Indexed as

AnimalsBlood GlucoseEndoplasmic Reticulum StressEnergy MetabolismGene Expression RegulationGlycogenHomeostasisLipogenesisLipoproteinsLiverMaleMice, Inbred C57BLTriglyceridesTunicamycinBlood GlucoseGlycogenLipoproteinsTriglyceridesTunicamycinAktblood glucoseER stressglycogenlipoproteinlivertriglyceridetunicamycin

Identifiers

PMID28777337
PMCPMC5578100
OpenAlexW2743837016

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.