Evidence map›Paper›PMID 31309261›Full record

ArticleDiabetologia2019

Antioxidants protect against diabetes by improving glucose homeostasis in mouse models of inducible insulin resistance and obesity.

Leon G Straub, Vissarion Efthymiou, Gerald Grandl, Miroslav Balaz, Tenagne Delessa Challa, Luca Truscello, Carla Horvath, Caroline Moser, Yael Rachamin, Myrtha Arnold and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Diabetologia, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

20 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Review
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  4. Article
  5. Current drug discovery technologies · 2025
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  9. Does Iodine Influence the Metabolism of Glucose?Medicina (Kaunas, Lithuania) · 2023
    Review
  10. Article
  11. Article
  12. Antioxidants (Basel, Switzerland) · 2022
    Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  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

13 authors at 3 institutions in 3 countries.

Leon G StraubLaboratory of Translational Nutrition Biology, Institute of Food, Nutrition and Health, Swiss Federal Institute of Technology, ETH Zürich, CH-8603, Schwerzenbach, Switzerland.
Vissarion EfthymiouLaboratory of Translational Nutrition Biology, Institute of Food, Nutrition and Health, Swiss Federal Institute of Technology, ETH Zürich, CH-8603, Schwerzenbach, Switzerland.
Gerald GrandlLaboratory of Translational Nutrition Biology, Institute of Food, Nutrition and Health, Swiss Federal Institute of Technology, ETH Zürich, CH-8603, Schwerzenbach, Switzerland.
Miroslav BalazLaboratory of Translational Nutrition Biology, Institute of Food, Nutrition and Health, Swiss Federal Institute of Technology, ETH Zürich, CH-8603, Schwerzenbach, Switzerland.
Tenagne Delessa ChallaLaboratory of Translational Nutrition Biology, Institute of Food, Nutrition and Health, Swiss Federal Institute of Technology, ETH Zürich, CH-8603, Schwerzenbach, Switzerland.
Luca TruscelloLaboratory of Translational Nutrition Biology, Institute of Food, Nutrition and Health, Swiss Federal Institute of Technology, ETH Zürich, CH-8603, Schwerzenbach, Switzerland.
Carla HorvathLaboratory of Translational Nutrition Biology, Institute of Food, Nutrition and Health, Swiss Federal Institute of Technology, ETH Zürich, CH-8603, Schwerzenbach, Switzerland.
Caroline MoserLaboratory of Translational Nutrition Biology, Institute of Food, Nutrition and Health, Swiss Federal Institute of Technology, ETH Zürich, CH-8603, Schwerzenbach, Switzerland.
Yael RachaminLaboratory of Translational Nutrition Biology, Institute of Food, Nutrition and Health, Swiss Federal Institute of Technology, ETH Zürich, CH-8603, Schwerzenbach, Switzerland.
Myrtha ArnoldLaboratory of Translational Nutrition Biology, Institute of Food, Nutrition and Health, Swiss Federal Institute of Technology, ETH Zürich, CH-8603, Schwerzenbach, Switzerland.
Wenfei SunLaboratory of Translational Nutrition Biology, Institute of Food, Nutrition and Health, Swiss Federal Institute of Technology, ETH Zürich, CH-8603, Schwerzenbach, Switzerland.
Salvatore ModicaLaboratory of Translational Nutrition Biology, Institute of Food, Nutrition and Health, Swiss Federal Institute of Technology, ETH Zürich, CH-8603, Schwerzenbach, Switzerland.
Christian WolfrumLaboratory of Translational Nutrition Biology, Institute of Food, Nutrition and Health, Swiss Federal Institute of Technology, ETH Zürich, CH-8603, Schwerzenbach, Switzerland. christian-wolfrum@ethz.ch.
École Polytechnique Fédérale de Lausanne · CHETH Zurich · CHSouthwestern Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aims/hypothesisIn the context of diabetes, the health benefit of antioxidant treatment has been widely debated. In this study, we investigated the effect of antioxidant treatment during the development of insulin resistance and hyperphagia in obesity and partial lipodystrophy.

methodsWe studied the role of antioxidants in the regulation of insulin resistance using the tamoxifen-inducible fat-specific insulin receptor knockout (iFIRKO) mouse model, which allowed us to analyse the antioxidant's effect in a time-resolved manner. In addition, leptin-deficient ob/ob mice were used as a hyperphagic, chronically obese and diabetic mouse model to validate the beneficial effect of antioxidants on metabolism.

resultsAcute induction of insulin receptor knockout in adipocytes changed the substrate preference to fat before induction of a diabetic phenotype including hyperinsulinaemia and hyperglycaemia. In healthy chow-fed animals as well as in morbidly obese mice, this diabetic phase could be reversed within a few weeks. Furthermore, after the induction of insulin receptor knockout in mature adipocytes, iFIRKO mice were protected from subsequent obesity development through high-fat diet feeding. By genetic tracing we show that the persistent fat mass loss in mice after insulin receptor knockout in adipocytes is not caused by the depletion of adipocytes. Treatment of iFIRKO mice with antioxidants postponed and reduced hyperglycaemia by increasing insulin sensitivity. In ob/ob mice, antioxidants rescued both hyperglycaemia and hyperphagia. CONCLUSIONS/

interpretationWe conclude that fat mass reduction through insulin resistance in adipocytes is not reversible. Furthermore, it seems unlikely that adipocytes undergo apoptosis during the process of extreme lipolysis, as a consequence of insulin resistance. Antioxidants have a beneficial health effect not only during the acute phase of diabetes development, but also in a temporary fashion once chronic obesity and diabetes have been established.

Indexed as

Insulin ResistanceAdipocytesAdipose Tissue, BrownAnimalsAntioxidantsBlood GlucoseCalorimetryDiabetes MellitusDisease Models, AnimalGlucoseHomeostasisHyperinsulinismHyperphagiaInsulinLeptinLipodystrophyAntioxidantsBlood GlucoseGlucoseInsulinLeptinReceptor, InsulinAcetovanilloneAdipocyteAdipocyte quantificationAdipocyte-specificAdipose tissueAntioxidantsApocyninCreERT2Diet-induced obesityFatHyperglycaemiaHyperinsulinaemic–euglycaemic clampHyperphagiaiFIRKOInsulin receptorInsulin resistanceLeptin deficiencyLipolysisN-acetylcysteineObesity resistanceob/obPolydipsia obesityTamoxifenType 2 diabetes

Identifiers

PMID31309261
PMCPMC6805816
OpenAlexW2957327850

What OpenQuestion holds

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LicenceCC BY
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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.