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

Author(s)

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]

Affiliation

^[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

• Document type: Journal article
• Source: NUTRIENTS; v. 11, n. 9 SEP 2019.
• Web of Science Citations: 0

Abstract

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 Opportunities: 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 Opportunities: 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 Opportunities: Scholarships in Brazil - Doctorate