Evidence map›Paper›PMID 27042269›Full record

ArticleJournal of diabetes investigation2016

Expression profiling analysis: Uncoupling protein 2 deficiency improves hepatic glucose, lipid profiles and insulin sensitivity in high-fat diet-fed mice by modulating expression of genes in peroxisome proliferator-activated receptor signaling pathway.

Mei-Cen Zhou, Ping Yu, Qi Sun, Yu-Xiu Li

Open access · goldAbstract read
In one paragraph

Article in Journal of diabetes investigation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

15 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
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  12. PP2 Ameliorates Renal Fibrosis by Regulating the NF-Oxidative medicine and cellular longevity · 2021
    Article
  13. Article
  14. Uncoupling Protein 2 and Peroxisome Proliferator-Activated ReceptorInternational journal of endocrinology · 2018
    Article
  15. 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

4 authors at 3 institutions in 1 country.

Mei-Cen ZhouDepartment of Endocrinology Key Laboratory of Endocrinology Ministry of Health Peking Union Medical College Hospital Beijing China.
Ping YuDepartment of Pharmacy the Third People's Hospital Qinhuangdao China.
Qi SunDepartment of Endocrinology Key Laboratory of Endocrinology Ministry of Health Peking Union Medical College Hospital Beijing China.
Yu-Xiu LiDepartment of Endocrinology Key Laboratory of Endocrinology Ministry of Health Peking Union Medical College Hospital Beijing China.
Chinese Academy of Medical Sciences & Peking Union Medical College · CNFirst Hospital of Qinhuangdao · CNPeking Union Medical College Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

AIMS/

introductionUncoupling protein 2 (UCP2), which was an important mitochondrial inner membrane protein associated with glucose and lipid metabolism, widely expresses in all kinds of tissues including hepatocytes. The present study aimed to explore the impact of UCP2 deficiency on glucose and lipid metabolism, insulin sensitivity and its effect on the liver-associated signaling pathway by expression profiling analysis. MATERIALS AND

methodsFour-week-old male UCP2-/- mice and UCP2+/+ mice were randomly assigned to four groups: UCP2-/- on a high-fat diet, UCP2-/- on a normal chow diet, UCP2+/+ on a high-fat diet and UCP2+/+ on a normal chow diet. The differentially expressed genes in the four groups on the 16th week were identified by Affymetrix gene array.

resultsThe results of intraperitoneal glucose tolerance test and insulin tolerance showed that blood glucose and β-cell function were improved in the UCP2-/- group on high-fat diet. Enhanced insulin sensitivity was observed in the UCP2-/- group. The differentially expressed genes were mapped to 23 pathways (P < 0.05). We concentrated on the 'peroxisome proliferator-activated receptor (PPAR) signaling pathway' (P = 3.19 × 10(-11)), because it is closely associated with the regulation of glucose and lipid profiles. In the PPAR signaling pathway, seven genes (PPARγ, Dbi, Acsl3, Lpl, Me1, Scd1, Fads2) in the UCP2-/- mice were significantly upregulated.

conclusionsThe present study used gene arrays to show that activity of the PPAR signaling pathway involved in the improvement of glucose and lipid metabolism in the liver of UCP2-deficient mice on a long-term high-fat diet. The upregulation of genes in the PPAR signaling pathway could explain our finding that UCP2 deficiency ameliorated insulin sensitivity. The manipulation of UCP2 protein expression could represent a new strategy for the prevention and treatment of diabetes.

Indexed as

AnimalsBlood GlucoseDiet, High-FatGene Expression ProfilingGlucoseGlucose Tolerance TestInsulin ResistanceInsulin-Secreting CellsLipid MetabolismLiverMaleMicePeroxisome Proliferator-Activated ReceptorsRandom AllocationSignal TransductionUncoupling Protein 2Blood GlucoseGlucosePeroxisome Proliferator-Activated ReceptorsUcp2 protein, mouseUncoupling Protein 2Glucose and lipid metabolismPeroxisome proliferator‐activated receptor signaling pathwayUncoupling protein 2

Identifiers

PMID27042269
PMCPMC4773664
OpenAlexW1928734633

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.