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Published on: April 26, 2019
Maternal high-fat intake predisposes nonalcoholic fatty liver disease in C57BL/6 offspring
Bianca M Gregorio1, Vanessa Souza-Mello, Jorge J Carvalho
1Institute of Biology, Laboratory of Morphometry and Cardiovascular Morphology, State University of Rio de Janeiro, Biomedical Center, Rio de Janeiro, Brazil.
Insights
Maternal high-fat diet during pregnancy or lactation programs offspring for nonalcoholic fatty liver disease. This dietary exposure in critical periods leads to hepatic steatosis and insulin resistance in adult mice.
Area of Science:
- Reproductive biology
- Metabolic disorders
- Hepatology
Background:
- Maternal nutrition significantly impacts offspring development and long-term health.
- High-fat diets are increasingly prevalent and linked to metabolic dysfunction.
Purpose of the Study:
- To investigate if maternal high-fat diet (HF) during critical gestational and/or lactational periods predisposes offspring to nonalcoholic fatty liver disease (NAFLD).
Main Methods:
- Male C57BL/6 mice offspring were exposed to maternal HF diet during gestation (G), lactation (L), or both (GL).
- A group (GL/HF) continued HF diet postweaning.
- Analyses included body mass, plasma parameters, and liver structure.
Main Results:
- Offspring exposed to maternal HF diet exhibited insulin resistance and altered glucose transporter-2 expression.
- Hepatic steatosis was observed in offspring from G, L, GL, and GL/HF groups, most severely in GL/HF.
- Increased sterol regulatory element-binding protein-1c expression was noted in G, GL, and GL/HF offspring.
Conclusions:
- Maternal exposure to high-fat chow during critical developmental windows programs the liver for adverse remodeling.
- This "programming" effect increases susceptibility to NAFLD in adult offspring.
Objective:
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.
Study Design:
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.
Results:
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.
Conclusion:
Programming by HF chow predisposes hepatic adverse remodeling in the liver of adult offspring.

