Evidence map›Paper›PMID 37424591›Full record

ArticleHeliyon2023

Oral administration of kynurenic acid delays the onset of type 2 diabetes in Goto-Kakizaki rats.

Delong Zhen, Lina Ding, Bao Wang, Xiaolei Wang, Yanli Hou, Wenyu Ding, Bernard Portha, Junjun Liu

Open access · goldAbstract read
In one paragraph

Article in Heliyon, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.6field-weighted citation impact, top 39% 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

6 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Tryptophanylation of insulin receptor by WARS attenuates insulin signaling.Cellular and molecular life sciences : CMLS · 2024
    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 2 institutions in 2 countries.

Delong ZhenShandong Institute of Endocrine and Metabolic Diseases, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, China.
Lina DingShandong Institute of Endocrine and Metabolic Diseases, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, China.
Bao WangShandong Institute of Endocrine and Metabolic Diseases, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, China.
Xiaolei WangShandong Institute of Endocrine and Metabolic Diseases, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, China.
Yanli HouShandong Institute of Endocrine and Metabolic Diseases, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, China.
Wenyu DingShandong Institute of Endocrine and Metabolic Diseases, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, China.
Bernard PorthaLaboratoire B2PE (Biologie et Pathologie du Pancréas Endocrine), Unité BFA (Biologie Fonctionnelle et Adaptive), CNRS UMR 8251, Université Paris-Cité, Paris, France.
Junjun LiuShandong Institute of Endocrine and Metabolic Diseases, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, China.
Shandong First Medical University · CNCentre National de la Recherche Scientifique · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Kynurenic acid (KYNA) is an endogenous catabolite of tryptophan that has been found to demonstrate neuroprotective properties in psychiatric disorders. Recently, accumulating data have suggested that KYNA may also play a significant role in various metabolic diseases by stimulating energy metabolism in adipose tissue and muscle. However, whether KYNA can serves as an anti-diabetes agent has yet to be studied. In this study, we investigated the potential anti-diabetic effects of administering KYNA orally through drinking water in pre-diabetic Goto-Kakizaki rats and examined how this treatment may influence energy metabolism regulation within the liver. We found that hyperglycemic Goto-Kakizaki rats showed lower plasmatic KYNA levels compared to normal rats. Oral administration of KYNA significantly delayed the onset of diabetes in Goto-Kakizaki rats compared to untreated animals. Moreover, we found that KYNA treatment significantly increased respiration exchange ratio and promoted the energy expenditure by stimulating the expression of uncoupling protein (UCP). We confirmed that KYNA stimulated the UCP expression in HepG2 cells and mouse hepatocytes at mRNA and protein levels. Our study reveals that KYNA could potentially act as an anti-diabetic agent and KYNA-induced UCP upregulation is closely associated with the regulation of energy metabolism. These results provide further evidence for the therapeutic potential of KYNA in diabetes.

Indexed as

DiabetesEnergy metabolismKYNALiverUCPs

Identifiers

PMID37424591
PMCPMC10328841
OpenAlexW4382196047

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.