Evidence map›Paper›PMID 27752755›Full record

ArticleEuropean journal of nutrition2018

Methylglyoxal treatment in lactating mothers leads to type 2 diabetes phenotype in male rat offspring at adulthood.

Flávio Andrade Francisco, Luiz Felipe Barella, Sandra da Silva Silveira, Lucas Paulo Jacinto Saavedra, Kelly Valério Prates, Vander Silva Alves, Claudinéia Conationi da Silva Franco, Rosiane Aparecida Miranda, Tatiane Aparecida Ribeiro, Laize Peron Tófolo and 9 more

Abstract read
PubMed Publisher
In one paragraph

Article in European journal of nutrition, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

5 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. 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

19 authors at 5 institutions in 2 countries.

Flávio Andrade FranciscoDepartment of Biotechnology, Genetics, and Cellular Biology, State University of Maringá, Maringá, PR, Brazil.
Luiz Felipe BarellaNational Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA.
Sandra da Silva SilveiraDepartment of Biotechnology, Genetics, and Cellular Biology, State University of Maringá, Maringá, PR, Brazil.
Lucas Paulo Jacinto SaavedraDepartment of Biotechnology, Genetics, and Cellular Biology, State University of Maringá, Maringá, PR, Brazil.
Kelly Valério PratesDepartment of Biotechnology, Genetics, and Cellular Biology, State University of Maringá, Maringá, PR, Brazil.
Vander Silva AlvesDepartment of Biotechnology, Genetics, and Cellular Biology, State University of Maringá, Maringá, PR, Brazil.
Claudinéia Conationi da Silva FrancoDepartment of Biotechnology, Genetics, and Cellular Biology, State University of Maringá, Maringá, PR, Brazil.
Rosiane Aparecida MirandaCarlos Chagas Filho Institute, Federal University of Rio de Janeiro, Rio de Janeiro, RJ, Brazil.
Tatiane Aparecida RibeiroDepartment of Biotechnology, Genetics, and Cellular Biology, State University of Maringá, Maringá, PR, Brazil.
Laize Peron TófoloDepartment of Biotechnology, Genetics, and Cellular Biology, State University of Maringá, Maringá, PR, Brazil.
Ananda MaltaDepartment of Biotechnology, Genetics, and Cellular Biology, State University of Maringá, Maringá, PR, Brazil.
Elaine VieiraDepartment of Biotechnology, Genetics, and Cellular Biology, State University of Maringá, Maringá, PR, Brazil.
Kesia Palma-RigoDepartment of Biotechnology, Genetics, and Cellular Biology, State University of Maringá, Maringá, PR, Brazil.
Audrei PavanelloDepartment of Biotechnology, Genetics, and Cellular Biology, State University of Maringá, Maringá, PR, Brazil.
Isabela Peixoto MartinsDepartment of Biotechnology, Genetics, and Cellular Biology, State University of Maringá, Maringá, PR, Brazil.
Veridiana Mota MoreiraDepartment of Biotechnology, Genetics, and Cellular Biology, State University of Maringá, Maringá, PR, Brazil.
Júlio Cezar de OliveiraInstitute of Health Sciences, Federal University of Mato Grosso, Sinop, MT, Brazil.
Paulo Cezar de Freitas MathiasDepartment of Biotechnology, Genetics, and Cellular Biology, State University of Maringá, Maringá, PR, Brazil.
Rodrigo Mello GomesDepartment of Physiological Sciences (DCiF) - Biological Science Institute II (ICB-II), Room 220, Federal University of Goiás (UFG) - Campus II, Esperança Avenue s/n, CEP 74690-900, Goiânia, GO, Brazil. rodrigomellogomes@hotmail.com.
Universidade Estadual de Maringá · BRFundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro · BRNational Institute of Diabetes and Digestive and Kidney Diseases · USUniversidade Federal de Goiás · BRUniversidade Federal de Mato Grosso · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeEnvironmental and nutritional disorders during perinatal period cause metabolic dysfunction in the progeny and impair human health. Advanced glycation end products (AGEs) are primarily produced during metabolism of excess blood glucose, which is observed in diabetes. Methylglyoxal (MG) is a precursor for the generation of endogenous AGEs, which disturbs the metabolism. This work aimed to investigate whether the maternal MG treatment during lactation programs the progeny to metabolic dysfunction later in life.

methodsFemale Wistar rats were divided into two groups: control group (C) treated with saline and MG group treated with MG (60 mg/kg/day) by gavage throughout the lactation period. Both mothers and offspring were fed a standard chow. At weaning, breast milk composition was analyzed and mothers euthanized for blood and tissue sample collections. At 90 days of age, offspring were submitted to glucose tolerance test (ivGTT) and euthanized for blood and tissue samples collection.

resultsMG mothers showed increase in glucose and fructosamine levels; however, they showed low insulin levels and failure in β-cell function (p < 0.05). MG mothers also showed dyslipidemia (p < 0.05). Moreover, breast milk had elevated levels of glucose, triglycerides, cholesterol and fructosamine and low insulin (p < 0.05). Interestingly, MG offspring had increased body weight and adipose tissue at adulthood, and they also showed glucose intolerance and failure in β-cell function (p < 0.05). Besides, MG offspring showed dyslipidemia (p < 0.05) increasing cardiovascular diseases risk.

conclusionsMaternal MG treatment negatively affects the male rat offspring, leading to type 2 diabetes and dyslipidemia in later life, possibly by changes in breast milk composition.

Indexed as

AdiposityAdministration, OralAnimalsDiabetes Mellitus, Type 2DyslipidemiasEnvironmental PollutantsFemaleInsulinInsulin ResistanceInsulin-Secreting CellsInsulin SecretionIntra-Abdominal FatLactationMaleMaternal ExposureMilkEnvironmental PollutantsInsulinPyruvaldehydeAGEsDiabetesDyslipidemiaLactationMetabolic programmingMethylglyoxal

Identifiers

PMID27752755
OpenAlexW2536218646

What Socratic 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 Socratic graph.