Evidence map›Paper›PMID 32253813›Full record

ArticleJournal of cellular and molecular medicine2020

Enhanced liver but not muscle OXPHOS in diabetes and reduced glucose output by complex I inhibition.

Miriayi Alimujiang, Xue-Ying Yu, Mu-Yu Yu, Wo-Lin Hou, Zhong-Hong Yan, Ying Yang, Yu-Qian Bao, Jun Yin

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

16 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Impairment of Mitochondrial Respiration in Metabolic Diseases: An Overview.International journal of molecular sciences · 2022
    Review
  10. Article
  11. Article
  12. Jabuticaba [Frontiers in physiology · 2021
    Article
  13. Article
  14. Article
  15. Review
  16. 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

8 authors at 1 institution in 1 country.

Miriayi AlimujiangDepartment of Endocrinology and Metabolism, Shanghai Clinical Center for Metabolic Diseases, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Diabetes Institute, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.ORCID 0000-0001-8759-9391
Xue-Ying YuDepartment of Endocrinology and Metabolism, Shanghai Clinical Center for Metabolic Diseases, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Diabetes Institute, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.
Mu-Yu YuDepartment of Endocrinology and Metabolism, Shanghai Clinical Center for Metabolic Diseases, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Diabetes Institute, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.
Wo-Lin HouDepartment of Endocrinology and Metabolism, Shanghai Clinical Center for Metabolic Diseases, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Diabetes Institute, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.
Zhong-Hong YanDepartment of Chemistry, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Ying YangDepartment of Endocrinology and Metabolism, Shanghai Clinical Center for Metabolic Diseases, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Diabetes Institute, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.
Yu-Qian BaoDepartment of Endocrinology and Metabolism, Shanghai Clinical Center for Metabolic Diseases, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Diabetes Institute, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.
Jun YinDepartment of Endocrinology and Metabolism, Shanghai Clinical Center for Metabolic Diseases, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Diabetes Institute, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.ORCID 0000-0002-9826-3583
Shanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial function is critical in energy metabolism. To fully capture how the mitochondrial function changes in metabolic disorders, we investigated mitochondrial function in liver and muscle of animal models mimicking different types and stages of diabetes. Type 1 diabetic mice were induced by streptozotocin (STZ) injection. The db/db mice were used as type 2 diabetic model. High-fat diet-induced obese mice represented pre-diabetic stage of type 2 diabetes. Oxidative phosphorylation (OXPHOS) of isolated mitochondria was measured with Clark-type oxygen electrode. Both in early and late stages of type 1 diabetes, liver mitochondrial OXPHOS increased markedly with complex IV-dependent OXPHOS being the most prominent. However, ATP, ADP and AMP contents in the tissue did not change. In pre-diabetes and early stage of type 2 diabetes, liver mitochondrial complex I and II-dependent OXPHOS increased greatly then declined to almost normal at late stage of type 2 diabetes, among which alteration of complex I-dependent OXPHOS was the most significant. In contrast, muscle mitochondrial OXPHOS in HFD, early-stage type 1 and 2 diabetic mice, did not change. In vitro, among inhibitors to each complex, only complex I inhibitor rotenone decreased glucose output in primary hepatocytes without cytotoxicity both in the absence and presence of oleic acid (OA). Rotenone affected cellular energy state and had no effects on cellular and mitochondrial reactive oxygen species production. Taken together, the mitochondrial OXPHOS of liver but not muscle increased in obesity and diabetes, and only complex I inhibition may ameliorate hyperglycaemia via lowering hepatic glucose production.

Indexed as

Oxidative PhosphorylationAnimalsCell DeathCells, CulturedDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 2Diet, High-FatElectron Transport Complex IEnergy MetabolismFeeding BehaviorGlucoseHepatocytesLiverMice, Inbred C57BLMitochondria, LiverMuscle, SkeletalElectron Transport Complex IGlucoseReactive Oxygen Speciesdiabeteselectron transport chaininsulin resistanceliver steatosisNAFLDobesityROS

Identifiers

PMID32253813
PMCPMC7214161
OpenAlexW3015157175

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.