Evidence map›Paper›PMID 27140617›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2016

PI3K-resistant GSK3 controls adiponectin formation and protects from metabolic syndrome.

Hong Chen, Abul Fajol, Miriam Hoene, Bingbing Zhang, Erwin D Schleicher, Yun Lin, Carsten Calaminus, Bernd J Pichler, Cora Weigert, Hans U Häring and 2 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
4.3field-weighted citation impact, top 6% 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

26 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Adiponectin Resistance in Obesity: Adiponectin Leptin/Insulin Interaction.Advances in experimental medicine and biology · 2024
    Review
  10. Review
  11. Signaling pathways in obesity: mechanisms and therapeutic interventions.Signal transduction and targeted therapy · 2022
    Review
  12. Review
  13. Article
  14. Article
  15. Adiponectin Role in Neurodegenerative Diseases: Focus on Nutrition Review.International journal of molecular sciences · 2020
    Review
  16. Article
  17. Review
  18. Adiponectin and Cognitive Decline.International journal of molecular sciences · 2020
    Review
  19. Review
  20. 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

12 authors at 4 institutions in 1 country.

Hong ChenDepartment of Physiology, University of Tübingen, 72076 Tuebingen, Germany;
Abul FajolDepartment of Physiology, University of Tübingen, 72076 Tuebingen, Germany;
Miriam HoeneDivision of Clinical Chemistry and Pathobiochemistry, Department of Internal Medicine IV, University Hospital Tübingen, 72076 Tuebingen, Germany;
Bingbing ZhangDepartment of Physiology, University of Tübingen, 72076 Tuebingen, Germany;
Erwin D SchleicherDivision of Clinical Chemistry and Pathobiochemistry, Department of Internal Medicine IV, University Hospital Tübingen, 72076 Tuebingen, Germany; Institute for Diabetes Research and Metabolic Diseases of the Helmholtz-Zentrum München, University of Tübingen, 72076 Tuebingen, Germany; German Center for Diabetes Research, 85764 Neuherberg, Germany;
Yun LinWerner Siemens Imaging Center, Department of Preclinical Imaging and Radiopharmacy, University of Tübingen, 72076 Tuebingen, Germany;
Carsten CalaminusWerner Siemens Imaging Center, Department of Preclinical Imaging and Radiopharmacy, University of Tübingen, 72076 Tuebingen, Germany;
Bernd J PichlerWerner Siemens Imaging Center, Department of Preclinical Imaging and Radiopharmacy, University of Tübingen, 72076 Tuebingen, Germany;
Cora WeigertDivision of Clinical Chemistry and Pathobiochemistry, Department of Internal Medicine IV, University Hospital Tübingen, 72076 Tuebingen, Germany; Institute for Diabetes Research and Metabolic Diseases of the Helmholtz-Zentrum München, University of Tübingen, 72076 Tuebingen, Germany; German Center for Diabetes Research, 85764 Neuherberg, Germany;
Hans U HäringDivision of Clinical Chemistry and Pathobiochemistry, Department of Internal Medicine IV, University Hospital Tübingen, 72076 Tuebingen, Germany; Institute for Diabetes Research and Metabolic Diseases of the Helmholtz-Zentrum München, University of Tübingen, 72076 Tuebingen, Germany; German Center for Diabetes Research, 85764 Neuherberg, Germany;
Florian LangDepartment of Physiology, University of Tübingen, 72076 Tuebingen, Germany; Department of Internal Medicine III, University Hospital Tübingen, 72076 Tuebingen, Germany;
Michael FöllerDepartment of Physiology, University of Tübingen, 72076 Tuebingen, Germany; Institute of Agricultural and Nutritional Sciences, Martin-Luther University Halle-Wittenberg, D-06120 Halle (Saale), Germany michael.foeller@landw.uni-halle.de.
University of Tübingen · DEDeutsches Diabetes-Zentrum e.V. · DESiemens (Germany) · DEMartin Luther University Halle-Wittenberg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metabolic syndrome is characterized by insulin resistance, obesity, and dyslipidemia. It is the consequence of an imbalance between caloric intake and energy consumption. Adiponectin protects against metabolic syndrome. Insulin-induced signaling includes activation of PI3 kinase and protein kinase B (PKB)/Akt. PKB/Akt in turn inactivates glycogen synthase kinase (GSK) 3, a major regulator of metabolism. Here, we studied the significance of PI3K-dependent GSK3 inactivation for adiponectin formation in diet-induced metabolic syndrome. Mice expressing PI3K-insensitive GSK3 (gsk3(KI)) and wild-type mice (gsk3(WT)) were fed a high-fat diet. Compared with gsk3(WT) mice, gsk3(KI) mice were protected against the development of metabolic syndrome as evident from a markedly lower weight gain, lower total body and liver fat accumulation, better glucose tolerance, stronger hepatic insulin-dependent PKB/Akt phosphorylation, lower serum insulin, cholesterol, and triglyceride levels, as well as higher energy expenditure. Serum adiponectin concentration and the activity of transcription factor C/EBPα controlling the expression of adiponectin in adipose tissue was significantly higher in gsk3(KI) mice than in gsk3(WT) mice. Treatment with GSK3 inhibitor lithium significantly decreased the serum adiponectin concentration of gsk3(KI) mice and abrogated the difference in C/EBPα activity between the genotypes. Taken together, our data demonstrate that the expression of PI3K-insensitive GSK3 stimulates the production of adiponectin and protects from diet-induced metabolic syndrome.

Indexed as

AdiponectinAdipose TissueAnimalsCCAAT-Enhancer-Binding ProteinsDiet, High-FatGlucose IntoleranceGlycogen Synthase Kinase 3Insulin ResistanceLiverMaleMetabolic SyndromeMice, TransgenicPhosphatidylinositol 3-KinasesPTEN PhosphohydrolaseAdiponectinAdipoq protein, mouseCCAAT-Enhancer-Binding ProteinsCEBPA protein, mouseGlycogen Synthase Kinase 3Phosphatidylinositol 3-KinasesPTEN PhosphohydrolasePten protein, mouseinsulin resistanceleptinobesitytriglycerides

Identifiers

PMID27140617
PMCPMC4878493
OpenAlexW2345969907

What OpenQuestion holds

Textmetadata
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.