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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

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

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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]
Total Authors: 10
[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
Total Affiliations: 2
Document type: Journal article
Source: NUTRIENTS; v. 11, n. 9 SEP 2019.
Web of Science Citations: 0

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)

FAPESP's process: 13/07607-8 - OCRC - Obesity and Comorbidities Research Center
Grantee:Licio Augusto Velloso
Support type: Research Grants - Research, Innovation and Dissemination Centers - RIDC
FAPESP's process: 14/08913-8 - Mechanisms involved in the late-onset pancreatic beta cell disfunction induced by maternal glucocorticoid excess at the end of pregnancy
Grantee:Silvana Auxiliadora Bordin da Silva
Support type: Regular Research Grants
FAPESP's process: 15/25597-5 - Hepatic microRNA expression profile in Goto-Kakizaki rats and wistar rats subjected to metabolic programming by prenatal exposure to glucocorticoid excess
Grantee:Tanyara Baliani Payolla
Support type: Scholarships in Brazil - Doctorate