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In Utero Dexamethasone Exposure Exacerbates Hepatic Steatosis in Rats That Consume Fructose During Adulthood

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Autor(es):
Payolla, Tanyara B. [1] ; Teixeira, Caio J. [2] ; Sato, Fabio T. [1] ; Murata, Gilson M. [1] ; Zonta, Gizela A. [1] ; Sodre, Frhancielly S. [1] ; Campos, Carolina V. [1] ; Mesquita, Filiphe N. [2] ; Anhe, Gabriel F. [2] ; Bordin, Silvana [1]
Número total de Autores: 10
Afiliação do(s) autor(es):
[1] Univ Sao Paulo, Inst Biomed Sci, Dept Physiol & Biophys, BR-05508000 Sao Paulo - Brazil
[2] Univ Estadual Campinas, Fac Med Sci, Dept Pharmacol, BR-13083887 Sao Paulo - Brazil
Número total de Afiliações: 2
Tipo de documento: Artigo Científico
Fonte: NUTRIENTS; v. 11, n. 9 SEP 2019.
Citações Web of Science: 0
Resumo

Distinct environmental insults might interact with fructose consumption and contribute to the development of metabolic disorders. To address whether in utero glucocorticoid exposure and fructose intake modulate metabolic responses, adult female Wistar rats were exposed to dexamethasone (DEX) during pregnancy, and the offspring were administered fructose at a later time. Briefly, dams received DEX during the third period of pregnancy, while control dams remained untreated. Offspring born to control and DEX-treated mothers were defined as CTL-off and DEX-off, respectively, while untreated animals were designated CTL-off-CTL and DEX-off-CTL. CLT-off and DEX-off treated with 10% fructose in the drinking water for 8 weeks are referred to as CTL-off-FRU and DEX-off-FRU. We found that fructose promoted glucose intolerance and whole-body gluconeogenesis in both CTL-off-FRU and DEX-off-FRU animals. On the other hand, hepatic lipid accumulation was significantly stimulated in DEX-off-FRU rats when compared to the CTL-off-FRU group. The DEX-off-FRU group also displayed impaired very-low-density lipoprotein (VLDL) production and reduced hepatic expression of apoB, mttp, and sec22b. DEX-off-FRU has lower hepatic levels of autophagy markers. Taken together, our results support the unprecedented notion that in utero glucocorticoid exposure exacerbates hepatic steatosis caused by fructose consumption later in life. (AU)

Processo FAPESP: 13/07607-8 - CMPO - Centro Multidisciplinar de Pesquisa em Obesidade e Doenças Associadas
Beneficiário:Licio Augusto Velloso
Linha de fomento: Auxílio à Pesquisa - Centros de Pesquisa, Inovação e Difusão - CEPIDs
Processo FAPESP: 14/08913-8 - Avaliação dos mecanismos envolvidos no comprometimento funcional tardio das ilhotas pancreáticas de ratas expostas ao excesso de glicocorticóides no final da gestação
Beneficiário:Silvana Auxiliadora Bordin da Silva
Linha de fomento: Auxílio à Pesquisa - Regular
Processo FAPESP: 15/25597-5 - Perfis de expressão hepática de miRNA em ratos Goto-Kakizaki e ratos submetidos à reprogramação fenotípica por excesso de glicocorticóides
Beneficiário:Tanyara Baliani Payolla
Linha de fomento: Bolsas no Brasil - Doutorado