Maternal high-fat intake predisposes nonalcoholic fatty liver disease in C57BL/6 offspring

• Published in: American journal of obstetrics and gynecology Vol. 203; no. 5; pp. 495.e1 - 495.e8
• Main Authors: Gregorio, Bianca M., Souza-Mello, Vanessa, Carvalho, Jorge J., Mandarim-de-Lacerda, Carlos A., Aguila, Marcia B.
• Format: Journal Article
• Language: English
• Published: United States Mosby, Inc 01.11.2010
• Subjects: Alanine Transaminase - metabolism; Alkaline Phosphatase - metabolism; Analysis of Variance; Animals; Blood Glucose; Blotting, Western; Body Weight; Dietary Fats - metabolism; Disease Susceptibility - metabolism; Enzyme-Linked Immunosorbent Assay; fatty liver; Fatty Liver - etiology; Fatty Liver - metabolism; Female; fetal programming; Glucose Tolerance Test; Insulin - blood; Insulin Resistance; Liver - metabolism; liver steatosis; liver ultrastructure; Male; maternal high-fat diet; Maternal Nutritional Physiological Phenomena - physiology; Mice; Obstetrics and Gynecology; Pregnancy; Prenatal Exposure Delayed Effects - metabolism; Radioimmunoassay; Tumor Necrosis Factor-alpha - metabolism; liver steatosis; liver ultrastructure; fatty liver; fetal programming; maternal high-fat diet
• ISSN: 0002-9378; 1097-6868; 1097-6868
• DOI: 10.1016/j.ajog.2010.06.042

This work aimed to verify the hypothesis that maternal intake of high-fat diet in critical periods of pregnancy and/or suckling period predisposes nonalcoholic fatty liver disease in adult C57BL/6 mice offspring. Male pups were divided into 5 groups: (1) SC, from standard chow–fed dams; (2) G, from high-fat chow (HF)–fed dams during the gestation (G) period; (3) L, from HF-fed dams during the lactation (L) period; (4) GL, from HF-fed dams during the gestation and lactation (GL) periods; and (5) GL/HF, from HF-fed dams during GL, maintaining an HF diet from postweaning to adulthood. We analyzed body mass, plasma blood, and liver structure. The G offspring showed insulin resistance and lower glucose transporter-2 expression. Hepatic steatosis was present in the G, L, GL, and mainly in GL/HF offspring. Sterol regulatory element-binding protein-1c expression was higher in G, GL, and GL/HF offspring. Programming by HF chow predisposes hepatic adverse remodeling in the liver of adult offspring.