Evidence map›Paper›PMID 22829877›Full record

ArticlePloS one2012

Altered glucose homeostasis and hepatic function in obese mice deficient for both kinin receptor genes.

Carlos C Barros, Anderson Haro, Fernanda J V P Russo, Ines Schadock, Sandro S Almeida, Rosane A Ribeiro, Emerielle C Vanzela, Valeria P Lanzoni, Flavio C Barros, Milton R Moraes and 8 more

Abstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
–field-weighted citation impact
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

16 citing papers in PubMed.

  1. Bradykinin, insulin, and glycemia responses to exercise performed above and below lactate threshold in individuals with type 2 diabetes.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2017
    Trial
  2. Kinin receptors in adipose tissue: drivers of inflammation and metabolic dysfunction in obesity.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Review
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  15. Lack of kinin B₁ receptor potentiates leptin action in the liver.Journal of molecular medicine (Berlin, Germany) · 2013
    Article
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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.

Carlos C BarrosDepartment of Biophysics, Federal University of São Paulo, São Paulo, Brazil.
Anderson Haro
Fernanda J V P Russo
Ines Schadock
Sandro S Almeida
Rosane A Ribeiro
Emerielle C Vanzela
Valeria P Lanzoni
Flavio C Barros
Milton R Moraes
Marcelo A Mori
Reury F P Bacurau
Martin Wurtele
Antônio C Boschero
Everardo M Carneiro
Michael Bader
Joao B Pesquero
Ronaldo C Araujo

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Kallikrein-Kinin System (KKS) has been implicated in several aspects of metabolism, including the regulation of glucose homeostasis and adiposity. Kinins and des-Arg-kinins are the major effectors of this system and promote their effects by binding to two different receptors, the kinin B2 and B1 receptors, respectively. To understand the influence of the KKS on the pathophysiology of obesity and type 2 diabetes (T2DM), we generated an animal model deficient for both kinin receptor genes and leptin (obB1B2KO). Six-month-old obB1B2KO mice showed increased blood glucose levels. Isolated islets of the transgenic animals were more responsive to glucose stimulation releasing greater amounts of insulin, mainly in 3-month-old mice, which was corroborated by elevated serum C-peptide concentrations. Furthermore, they presented hepatomegaly, pronounced steatosis, and increased levels of circulating transaminases. This mouse also demonstrated exacerbated gluconeogenesis during the pyruvate challenge test. The hepatic abnormalities were accompanied by changes in the gene expression of factors linked to glucose and lipid metabolisms in the liver. Thus, we conclude that kinin receptors are important for modulation of insulin secretion and for the preservation of normal glucose levels and hepatic functions in obese mice, suggesting a protective role of the KKS regarding complications associated with obesity and T2DM.

Indexed as

AnimalsBlood GlucoseBody CompositionGlucoseHomeostasisHyperglycemiaInsulin ResistanceKallikrein-Kinin SystemLiverMiceMice, KnockoutMice, ObesePhosphorylationReceptor, Bradykinin B1Receptor, Bradykinin B2Blood GlucoseGlucoseReceptor, Bradykinin B1Receptor, Bradykinin B2

Identifiers

PMID22829877
PMCPMC3400662

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Registered trials

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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.