Evidence map›Paper›PMID 26671617›Full record

ArticleMolecular neurobiology2016

Indoleamine-2,3-Dioxygenase/Kynurenine Pathway as a Potential Pharmacological Target to Treat Depression Associated with Diabetes.

Isabella Caroline da Silva Dias, Bruno Carabelli, Daniela Kaori Ishii, Helen de Morais, Milene Cristina de Carvalho, Luiz E Rizzo de Souza, Silvio M Zanata, Marcus Lira Brandão, Thiago Mattar Cunha, Anete Curte Ferraz and 2 more

Open access · greenAbstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

34 citing papers in PubMed, 88 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. TNF-α Inhibition Modulates CX3CR1, Pyroptosis-related Genes, and BDNF to Alleviate Anxiety-like Behavior in Type 2 Diabetic Rats.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025
    Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  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 2 institutions in 1 country.

Isabella Caroline da Silva DiasDepartment of Pharmacology, Federal University of Paraná, Rua Coronel H dos Santos S/N, P.O. Box 19031, Curitiba, PR, 81540-990, Brazil.
Bruno CarabelliDepartment of Physiology, Federal University of Paraná, Curitiba, PR, 81540-990, Brazil.
Daniela Kaori IshiiDepartment of Pharmacology, Federal University of Paraná, Rua Coronel H dos Santos S/N, P.O. Box 19031, Curitiba, PR, 81540-990, Brazil.
Helen de MoraisDepartment of Pharmacology, Federal University of Paraná, Rua Coronel H dos Santos S/N, P.O. Box 19031, Curitiba, PR, 81540-990, Brazil.
Milene Cristina de CarvalhoInstitute of Neurosciences and Behavior (INeC) and Laboratory of Neuropsychopharmacology of Faculty of Philosophy, Sciences and Letters of University of São Paulo, Ribeirão Preto, SP, 14040-901, Brazil.
Luiz E Rizzo de SouzaDepartment of Basic Pathology, Laboratory of Neurobiology, Federal University of Paraná, Curitiba, PR, 81531-990, Brazil.
Silvio M ZanataDepartment of Basic Pathology, Laboratory of Neurobiology, Federal University of Paraná, Curitiba, PR, 81531-990, Brazil.
Marcus Lira BrandãoInstitute of Neurosciences and Behavior (INeC) and Laboratory of Neuropsychopharmacology of Faculty of Philosophy, Sciences and Letters of University of São Paulo, Ribeirão Preto, SP, 14040-901, Brazil.
Thiago Mattar CunhaDepartment of Pharmacology, Faculty of Medicine, University of São Paulo, Ribeirão Preto, SP, 14049-900, Brazil.
Anete Curte FerrazDepartment of Physiology, Federal University of Paraná, Curitiba, PR, 81540-990, Brazil.
Joice Maria CunhaDepartment of Pharmacology, Federal University of Paraná, Rua Coronel H dos Santos S/N, P.O. Box 19031, Curitiba, PR, 81540-990, Brazil.
Janaina Menezes ZanoveliDepartment of Pharmacology, Federal University of Paraná, Rua Coronel H dos Santos S/N, P.O. Box 19031, Curitiba, PR, 81540-990, Brazil. janaina.zanoveli@ufpr.br.
Universidade Federal do Paraná · BRUniversidade de São Paulo · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetes is a chronic disease associated with depression whose pathophysiological mechanisms that associate these conditions are not fully elucidated. However, the activation of the indoleamine-2,3-dioxygenase (IDO), an enzyme that participate of the tryptophan metabolism leading to a decrease of serotonin (5-HT) levels and whose expression is associated with an immune system activation, has been proposed as a common mechanism that links depression and diabetes. To test this hypothesis, diabetic (DBT) and normoglycemic (NGL) groups had the cytokines (TNFα, IL-1β, and IL-6) and 5-HT and norepinephrine (NE) levels in the hippocampus (HIP) evaluated. Moreover, the effect of the selective serotonin reuptake inhibitor fluoxetine (FLX), IDO direct inhibitor 1-methyl-tryptophan (1-MT), anti-inflammatory and IDO indirect inhibitor minocycline (MINO), or non-selective cyclooxygenase inhibitor ibuprofen (IBU) was evaluated in DBT rats submitted to the modified forced swimming test (MFST). After the behavioral test, the HIP was obtained for IDO expression by Western blotting analysis. DBT rats exhibited a significant increase in HIP levels of TNFα, IL-1β, and IL-6 and a decrease in HIP 5-HT and NA levels. They also presented a depressive-like behavior which was reverted by all employed treatments. Interestingly, treatment with MINO, IBU, or FLX but not with 1-MT reduced the increased IDO expression in the HIP from DBT animals. Taken together, our data support our hypothesis that neuroinflammation in the HIP followed by IDO activation with a consequent decrease in the 5-HT levels can be a possible pathophysiological mechanism that links depression to diabetes.

Indexed as

Molecular Targeted TherapyAnimalsAntidepressive AgentsBehavior, AnimalBlood GlucoseCytokinesDepressionDiabetes Mellitus, ExperimentalEnzyme InhibitorsFluoxetineHippocampusIbuprofenIndoleamine-Pyrrole 2,3,-DioxygenaseInflammation MediatorsKynurenineMale1-methyltryptophanAntidepressive AgentsBlood GlucoseCytokinesEnzyme InhibitorsFluoxetineIbuprofenIndoleamine-Pyrrole 2,3,-DioxygenaseInflammation MediatorsKynurenineMinocyclineNorepinephrineSerotoninTryptophanDepressionHippocampusIndoleamine-2,3-dioxygenase inflammationSerotoninStreptozotocin

Identifiers

PMID26671617
OpenAlexW2203321050

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.