JOEL CLAUDIO HEIMANN
Projetos de Pesquisa
Unidades Organizacionais
Departamento de Clínica Médica, Faculdade de Medicina - Docente
LIM/16 - Laboratório de Fisiopatologia Renal, Hospital das Clínicas, Faculdade de Medicina - Líder
LIM/16 - Laboratório de Fisiopatologia Renal, Hospital das Clínicas, Faculdade de Medicina - Líder
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- Igf1 DNA methylation, epigenetics, and low-salt diet in fetal programming(2019) SIQUEIRA, F. R. De; FURUKAWA, L. N. S.; HEIMANN, J. C.All cells of an organism share the same DNA sequence from the time they are stem cells up to the time they are fully differentiated, distinct greatly in relation to the profile of expressed genes. Changes in gene expression which do not involve changes in DNA sequence of the nucleotides are currently known as an epigenetic phenomenon. Epigenetic changes play a fundamental role in the human gene expression and in the mechanism of association between events that occur early in life and alterations in adult life. Thus, in response to an adverse environment in which pregnant women are exposed during the perinatal or neonatal period, epigenetic modifications may lead to alterations in growth and metabolism in later life. Modification of histones (proteins found in eukaryotic cell nucleus) and DNA methylation (a process by which methyl groups are added to DNA) are the major epigenetic mechanisms involved in the regulation of gene expression. Maternal insults, mainly inadequate nutrition that may occur during sensitive or critical periods of fetal development (periods of rapid cell division), can program changes in the structure and functionality of cells, tissues, and/or organ systems. These changes may result in premature consequences in the offspring such as low birth weight and/or chronic diseases (hypertension, insulin resistance, obesity, etc.) in adulthood. A low-salt diet during pregnancy has been associated with low birth weight and chronic diseases in adult offspring, at least in the experimental setting. The expression of genes as insulin-like growth factors is regulated in a tissue-specific manner and can be altered by nutritional and endocrine conditions in utero. It is known that the major mediator of fetal growth is insulin-like growth factor type 1 (IGF-1) and insulin. The low birth weight may be due to low serum IGF-1 and/or by Igf1 epigenetic changes in fetus in response to low-salt intake during pregnancy. This observation might underlie the altered offspring phenotypes in this model since growth and insulin sensitivity are modulated by hepatic IGF-1. A low birth weight is related to low Igf1 gene expression and high Igf1 DNA methylation levels induced by low-salt intake during pregnancy. The variation in the IGF-1 serum levels may be due to changes in Igf1 gene promoter methylation. This concept is supported by increased methylation that is often associated with reduced gene expression. The methylation of genes changed as the offspring aged, indicating that epigenetic changes can occur and can be reversed during postnatal life. Further studies are needed to confirm or not if the observed results are reproducible in humans in order to recommend low dietary salt consumption during pregnancy. © Springer Nature Switzerland AG 2019. All rights reserved.
bookPart 0 Citação(ões) na Scopus Impact of low-salt diet(2019) SIQUEIRA, F. R. De; OLIVEIRA, K. C. De; HEIMANN, J. C.; FURUKAWA, L. N. S.Studies in experimental animals and in groups of humans and epidemiological studies have shown that the sodium chloride or salt (sodium, Na, NaCl) plays an important role mainly in the regulation of blood pressure and represents an important environmental factor involved in the genesis of cardiovascular diseases. Therefore, salt intake in the population has been a constant concern. Variable blood pressure responses to different content in sodium intake are found in experimental hypertension models and in humans, and the reasons for such heterogeneity are not fully elucidated. The reduction of dietary sodium intake is recommended by public health as one of the non-medicated treatments for hypertension and consequently reducing the risk of cardiovascular diseases. However, some studies have demonstrated side effects of salt dietary restriction, reporting changes in glucose metabolism (hyperinsulinemia and insulin resistance), and these alterations are gender and time specific in experimental and population studies. © Springer Nature Switzerland AG 2019.- Myocardial hypertrophy induced by high salt consumption is prevented by angiotensin II AT2 receptor agonist(2019) DOPONA, E. P. B.; ROCHA, V. F.; FURUKAWA, L. N. S.; OLIVEIRA, I. B.; HEIMANN, J. C.Background and aims: Although many studies have reported the effects of AT1 receptor on dietary salt overload, the role of AT2 receptor in this model is far from completely elucidated. The present study aimed to better understand the role of AT2 receptor in cardiac structure alterations in response to chronic high salt intake in rats. Methods and results: Male Wistar rats were fed a normal or high salt diet from weaning until 18 weeks of age. Both groups were subdivided into two groups. Starting at 7 weeks of age, rats were treated with or without compound 21 (0.3 mg/kg/day, n = 16), an AT2 receptor agonist. Metabolics and structural parameters were measured. BP, transverse cardiomyocyte and intersticial fibrose was higher in animals fed with high salt diet compared with normal salt fed animals. Conclusion: Compound 21 prevented the development of cardiac hypertrophy and fibrosis, reduced the increase in blood pressure and prevented the lower weight gain in animals fed a high salt diet.
conferenceObject Lysine Specific Demethylase-1 Deficiency Accelerates the Development of Hypertension and Renal Damage During Long Term Sodium Intake(2019) KATAYAMA, Isis Akemi; CULLINANE, Danielle L.; WILLIAMS, Gordon H.; HEIMANN, Joel Claudio; POJOGA, Luminita H.conferenceObject Male Mice Heterozygous LSD1 Knockout Gene Prevented the Effect of High Sodium Intake on Renal Fibrosis and AT1 Conformational Status(2019) NASCIMENTO, Mariana Moura; KATAYAMA, Isis Akemi; POJOGA, Luminita H.; HEIMANN, Joel Claudio- Effect of maternal periodontitis on GLUT4 and inflammatory pathway in adult offspring(2019) MATTERA, Maria Sara de Lima Coutinho; CHIBA, Fernando Yamamoto; LOPES, Flavia Lombardi; TSOSURA, Thais Veronica Saori; PERES, Maria Angelica; BRITO, Victor Gustavo Balera; OLIVEIRA, Sandra Helena Penha de; PEREIRA, Renato Felipe; MARANI, Fernando; SANTOS, Rodrigo Martins dos; BELARDI, Bianca Elvira; TESSARIN, Gestter Willian Lattari; BENITES, Mariana Lopes; ERVOLINO, Edilson; HEIMANN, Joel Claudio; SUMIDA, Doris HissakoBackground Maternal periodontal disease leads to low birth weight (LBW), insulin resistance (IR), increased TNF-alpha levels, and alterations in insulin signaling in adult offspring. TNF-alpha has been associated with the stimulation of IKK beta/NF-kappa B, resulting in the decreased expression of GLUT4. Another mechanism that may be involved in decreasing GLUT4 expression is DNA methylation. This study aimed to evaluate in the adult offspring of rats with periodontal disease: IR, inflammatory pathways, DNA methylation, and expression of GLUT4. Methods Female Wistar rats were distributed into control and experimental periodontal disease groups. Seven days after induction of periodontal disease, both groups were mated with healthy male rats. After weaning, male offspring were distributed into control offspring (CN-o) and periodontal disease offspring (PED-o) groups. Body weights were measured from 0-75 days of age. At day 75, the following were measured in the offspring: IR (HOMA-IR index); TNF-alpha and NF-kappa Bp65 content in the gastrocnemius muscle (GM) by western blotting; IKK alpha/beta, JNK, ERK 1/2, NF-kappa Bp65, and NF-kappa Bp50 phosphorylation status in the GM by western blotting; DNA methylation by restriction digest and real-time PCR(qAMP); and expression of GLUT4 mRNA in the GM by real-time PCR. Results LBW, IR, increases in TNF-alpha, IKK alpha/beta, ERK 1/2, NF-kappa Bp65, and NF-kappa Bp50 decreased expression of GLUT4 mRNA were observed in the PED-o rats. No differences were identified in JNK phosphorylation status and DNA methylation in the evaluated regions of the GLUT4-encoding gene Slc2a4. Conclusion Maternal periodontal disease causes LBW, IR, activation of inflammatory pathways, and decreased GLUT4 expression in the GM of adult offspring.