PD389 - INTRAUTERINE FOOD RESTRICTION IS ASSOCIATED WITH A PRO-APOPTOTIC HEPATIC GENE EXPRESSION PROFILE IN ADULT LOW-BIRTH-WEIGHT RATS
PD389
INTRAUTERINE FOOD RESTRICTION IS ASSOCIATED WITH A PRO-APOPTOTIC HEPATIC GENE EXPRESSION PROFILE IN ADULT LOW-BIRTH-WEIGHT RATS
S. Andreotti1, R. R. Ferreira2, G. A. Azevedo2, L. R. Giaquinto2,3, R. G. Landgraf4, M. A. Landgraf3,*
1Physiology, Universidade de São Paulo, 2Medicine, Universidade Federal de São Paulo, São Paulo, 3Universidade Paulista, Santos, 4Pharmaceutical Sciences, Universidade Federal de São Paulo, Diadema, Brazil
Rationale: Intrauterine undernutrition is known to induce long-lasting metabolic alterations in the offspring. This study investigated whether low birth weight, resulting from maternal food restriction, is associated with changes in the hepatic expression of apoptosis-related genes in adult rats.
Methods: Twelve-week-old male Wistar rats were allocated into two groups: normal birth weight (NBW), born to dams fed ad libitum, and low birth weight (LBW), born to dams subjected to 50% food restriction throughout gestation. Liver weight was recorded, and tissue samples from a hepatic lobe were collected. The expression levels of Caspase-3, Caspase-8, Caspase-9, and BAX were quantified by real-time PCR, normalized to B2M, and analyzed using the 2−ΔΔCt2−ΔΔCt method (CEUA UNIFESP 9816040716).
Results: At 12 weeks of age, LBW rats exhibited body weights comparable to NBW animals; however, liver weight was significantly reduced in the LBW group. Compared to NBW rats, LBW animals showed significantly increased hepatic expression of Caspase-3 (1.664; p=0.0027), Caspase-8 (1.382; p=0.0027), and BAX (1.420; p=0.0056). Caspase-9 expression was modestly elevated in the LBW group (1.153), although this difference did not reach statistical significance.
Conclusion: Low birth weight induced by intrauterine nutritional restriction is associated with increased hepatic expression of apoptosis-related genes in adult offspring. These findings suggest a pro-apoptotic molecular profile in the liver and support the hypothesis that fetal undernutrition may increase hepatic vulnerability later in life.
Disclosure of Interest: None declared