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Early postnatal exposure of rat pups to methylglyoxal induces oxidative stress, inflammation and dysmetabolism at adulthood

Published online by Cambridge University Press:  21 January 2022

Flávio A. Francisco
Affiliation:
Department of Biotechnology, Genetics, and Cellular Biology, State University of Maringá, Maringá, Brazil
Lucas P. J. Saavedra
Affiliation:
Department of Biotechnology, Genetics, and Cellular Biology, State University of Maringá, Maringá, Brazil
Marcos D. Ferreira-Junior
Affiliation:
Department of Physiological Sciences, Federal University of Goiás, Goiânia, Brazil
Keilah V. N. Cavalcante
Affiliation:
Department of Physiological Sciences, Federal University of Goiás, Goiânia, Brazil
Veridiana M. Moreira
Affiliation:
Department of Biotechnology, Genetics, and Cellular Biology, State University of Maringá, Maringá, Brazil Department of Physiology, Federal University of Sergipe, São Cristóvão, Brazil
Kelly V. Prates
Affiliation:
Department of Biotechnology, Genetics, and Cellular Biology, State University of Maringá, Maringá, Brazil
Stephanie C. Borges
Affiliation:
Department of Morphological Sciences, State University of Maringá, Maringá, Brazil
Nilza C. Buttow
Affiliation:
Department of Morphological Sciences, State University of Maringá, Maringá, Brazil
Tatiane A. Ribeiro
Affiliation:
Department of Biochemistry and Biomedical Sciences, McMaster University, Hamilton, ON, Canada
Gustavo R. Pedrino
Affiliation:
Department of Physiological Sciences, Federal University of Goiás, Goiânia, Brazil
Carlos H. Xavier
Affiliation:
Department of Physiological Sciences, Federal University of Goiás, Goiânia, Brazil
Paulo Matafome
Affiliation:
Coimbra Institute of Clinical and Biomedical Research (iCBR), Faculty of Medicine and Center for Innovative Biomedicine and Biotechnology (CIBB), University of Coimbra, Coimbra, Portugal Clinical Academic Center of Coimbra, Coimbra, Portugal Department of Complementary Sciences, Instituto Politécnico de Coimbra, Coimbra Health School (ESTeSC), Coimbra, Portugal
Paulo C. de Freitas Mathias
Affiliation:
Department of Biotechnology, Genetics, and Cellular Biology, State University of Maringá, Maringá, Brazil
Rodrigo M. Gomes*
Affiliation:
Department of Physiological Sciences, Federal University of Goiás, Goiânia, Brazil
*
Address for correspondence: Rodrigo M. Gomes, Laboratory of Endocrine Physiology and Metabolism (LabFEM), Department of Physiological Sciences (DCiF) – Biological Science Institute II (ICB-II), room 101, Federal University of Goiás (UFG) – Campus II, Esperança Avenue s/n, Goiânia, GO 74690-900, Brazil. Email: [email protected]

Abstract

This work aimed to investigate the effects of early progeny exposure to methylglyoxal (MG), programming for metabolic dysfunction and diabetes-like complications later in life. At delivery (PN1), the animals were separated into two groups: control group (CO), treated with saline, and MG group, treated with MG (20 mg/kg of BW; i.p.) during the first 2 weeks of the lactation period. In vivo experiments and tissue collection were done at PN90. Early MG exposure decreased body weight, adipose tissue, liver and kidney weight at adulthood. On the other hand, MG group showed increased relative food intake, blood fructosamine, blood insulin and HOMA-IR, which is correlated with insulin resistance. Besides, MG-treated animals presented dyslipidaemia, increased oxidative stress and inflammation. Likewise, MG group showed steatosis and perivascular fibrosis in the liver, pancreatic islet hypertrophy, increased glomerular area and pericapsular fibrosis, but reduced capsular space. This study shows that early postnatal exposure to MG induces oxidative stress, inflammation and fibrosis markers in pancreas, liver and kidney, which are related to metabolic dysfunction features. Thus, nutritional disruptors during lactation period may be an important risk factor for metabolic alterations at adulthood.

Type
Original Article
Copyright
© The Author(s), 2022. Published by Cambridge University Press in association with International Society for Developmental Origins of Health and Disease

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