Evidence map›Paper›PMID 27827363›Full record

ArticleNature communications2016

Control of diabetic hyperglycaemia and insulin resistance through TSC22D4.

Bilgen Ekim Üstünel, Kilian Friedrich, Adriano Maida, Xiaoyue Wang, Anja Krones-Herzig, Oksana Seibert, Anke Sommerfeld, Allan Jones, Tjeerd P Sijmonsma, Carsten Sticht and 8 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 18% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. Pooled it
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  6. RNA Therapies in Cardio-Kidney-Metabolic Syndrome: Advancing Disease Management.Journal of cardiovascular translational research · 2025
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  12. Identification, characterization and expression analysis ofActa biochimica et biophysica Sinica · 2023
    Article
  13. The role of hepatokines in NAFLD.Cell metabolism · 2023
    Review
  14. Article
  15. Article
  16. Emerging Targets in Type 2 Diabetes and Diabetic Complications.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021
    Review
  17. Article
  18. Review
  19. 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

18 authors at 4 institutions in 1 country.

Bilgen Ekim ÜstünelInstitute for Diabetes and Cancer (IDC), Helmholtz Center Munich, and Joint Heidelberg-IDC Translational Diabetes Program, Internal Medicine I, 85764 Neuherberg, Germany.
Kilian FriedrichInstitute for Diabetes and Cancer (IDC), Helmholtz Center Munich, and Joint Heidelberg-IDC Translational Diabetes Program, Internal Medicine I, 85764 Neuherberg, Germany.
Adriano MaidaInstitute for Diabetes and Cancer (IDC), Helmholtz Center Munich, and Joint Heidelberg-IDC Translational Diabetes Program, Internal Medicine I, 85764 Neuherberg, Germany.
Xiaoyue WangInstitute for Diabetes and Cancer (IDC), Helmholtz Center Munich, and Joint Heidelberg-IDC Translational Diabetes Program, Internal Medicine I, 85764 Neuherberg, Germany.
Anja Krones-HerzigInstitute for Diabetes and Cancer (IDC), Helmholtz Center Munich, and Joint Heidelberg-IDC Translational Diabetes Program, Internal Medicine I, 85764 Neuherberg, Germany.
Oksana SeibertInstitute for Diabetes and Cancer (IDC), Helmholtz Center Munich, and Joint Heidelberg-IDC Translational Diabetes Program, Internal Medicine I, 85764 Neuherberg, Germany.
Anke SommerfeldInstitute for Diabetes and Cancer (IDC), Helmholtz Center Munich, and Joint Heidelberg-IDC Translational Diabetes Program, Internal Medicine I, 85764 Neuherberg, Germany.
Allan JonesInstitute for Diabetes and Cancer (IDC), Helmholtz Center Munich, and Joint Heidelberg-IDC Translational Diabetes Program, Internal Medicine I, 85764 Neuherberg, Germany.
Tjeerd P SijmonsmaInstitute for Diabetes and Cancer (IDC), Helmholtz Center Munich, and Joint Heidelberg-IDC Translational Diabetes Program, Internal Medicine I, 85764 Neuherberg, Germany.
Carsten StichtCenter for Clinical Research, Medical Faculty Mannheim, 68167 Mannheim, Germany.
Norbert GretzCenter for Clinical Research, Medical Faculty Mannheim, 68167 Mannheim, Germany.
Thomas FlemingDepartment of Medicine I and Clinical Chemistry, Heidelberg University, 69120 Heidelberg, Germany.
Peter P NawrothDepartment of Medicine I and Clinical Chemistry, Heidelberg University, 69120 Heidelberg, Germany.
Wolfgang StremmelDepartment of Internal Medicine IV, Heidelberg University Hospital, 69120 Heidelberg, Germany.
Adam J RoseInstitute for Diabetes and Cancer (IDC), Helmholtz Center Munich, and Joint Heidelberg-IDC Translational Diabetes Program, Internal Medicine I, 85764 Neuherberg, Germany.
Mauricio Berriel-DiazInstitute for Diabetes and Cancer (IDC), Helmholtz Center Munich, and Joint Heidelberg-IDC Translational Diabetes Program, Internal Medicine I, 85764 Neuherberg, Germany.
Matthias BlüherDepartment of Medicine, University of Leipzig, 04103 Leipzig, Germany.
Stephan HerzigInstitute for Diabetes and Cancer (IDC), Helmholtz Center Munich, and Joint Heidelberg-IDC Translational Diabetes Program, Internal Medicine I, 85764 Neuherberg, Germany.
German Center for Diabetes Research · DEHeidelberg University · DEUniversity Hospital Heidelberg · DELeipzig University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Obesity-related insulin resistance represents the core component of the metabolic syndrome, promoting glucose intolerance, pancreatic beta cell failure and type 2 diabetes. Efficient and safe insulin sensitization and glucose control remain critical therapeutic aims to prevent diabetic late complications Here, we identify transforming growth factor beta-like stimulated clone (TSC) 22 D4 as a molecular determinant of insulin signalling and glucose handling. Hepatic TSC22D4 inhibition both prevents and reverses hyperglycaemia, glucose intolerance and insulin resistance in diabetes mouse models. TSC22D4 exerts its effects on systemic glucose homeostasis-at least in part-through the direct transcriptional regulation of the small secretory protein lipocalin 13 (LCN13). Human diabetic patients display elevated hepatic TSC22D4 expression, which correlates with decreased insulin sensitivity, hyperglycaemia and LCN13 serum levels. Our results establish TSC22D4 as a checkpoint in systemic glucose metabolism in both mice and humans, and propose TSC22D4 inhibition as an insulin sensitizing option in diabetes therapy.

Indexed as

AnimalsBlood GlucoseCell LineDiabetes Mellitus, Type 2FemaleGene Expression RegulationHumansHyperglycemiaInsulin ResistanceLipocalinsLiverMaleMice, Inbred C57BLMice, KnockoutTranscription FactorsBlood GlucoseLipocalinsTranscription FactorsTSC22D4 protein, human

Identifiers

PMID27827363
PMCPMC5105165
OpenAlexW2551870514

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.