CELL BIOLOGY SYMPOSIUM: METABOLIC RESPONSES TO STRESS: FROM ANIMAL TO CELL: Poor maternal nutrition during gestation: effects on offspring whole-body and tissue-specific metabolism in livestock species1,2

Abstract

Poor maternal nutrition, both restricted-feeding and overfeeding, during gestation can negatively affect offspring growth, body composition, and metabolism. The effects are observed as early as the prenatal period and often persist through postnatal growth and adulthood. There is evidence of multigenerational effects demonstrating the long-term negative impacts on livestock production. We and others have demonstrated that poor maternal nutrition impairs muscle growth, increases adipose tissue, and negatively affects liver function. In addition to altered growth, changes in key metabolic factors, increased glucose concentrations, insulin insensitivity, and hyperleptinemia are observed during the postnatal period. Furthermore, there is recent evidence of altered metabolism in specific tissues (e.g., muscle, adipose, and liver) and stem cells. The systemic and local changes in metabolism demonstrate the importance of determining the mechanism(s) by which maternal diet programs offspring growth and metabolism in an effort to develop novel management practices to improve the efficiency of growth and health in these offspring.

Prenatal High‐Sucrose Diet Induced Vascular Dysfunction in Thoracic Artery of Fetal Offspring

“…[ 25–29 ] Recently, many researchers pointed that prenatal malnutrition was closely linked with development of multiple organs via different mechanisms in offspring. [ 30–33 ] In the present study, we first validated that prenatal high‐sucrose diet increased maternal weight before delivery, but it had no effect on the fetal number. Consistent with a population‐based cohort study with 40 years of follow‐up investigated that prenatal hyperglycemia increased rates of early onset cardiovascular diseases from childhood to early adulthood, [ 34 ] our previous data confirmed that prenatal high sucrose impaired the micro‐vascular function of adult and aged offspring.…”

Association of Prenatal Famine Exposure With Inflammatory Markers and Its Impact on Adulthood Liver Function Across Consecutive Generations

“…Hence, when a pregnant mother was undernourished, her body fat mobilization could be facilitated to increase energy supply for fetal growth, thereby resulting in severe lipid metabolism disorder. Several animal studies supported this point and found that intrauterine malnutrition has a likelihood of eliciting oxidative stress (OS) through inducing lipid metabolism disorder to inhibit fetal hepatic development (26,27). Mounting evidence suggested that OS and inflammation were the important pathogenetic factors in many forms of liver diseases, regardless of etiology.…”

“…The findings of the current study were in agreement with the two previous studies ( 14 , 15 ), which showed that the impact of prenatal and postnatal famine exposure on the risk of NAFLD was more pronounced in women rather than in men. In addition, there were animal models revealing the impact of gestational nutritional conditions on the liver ( 26 , 27 ). It is noteworthy that the mortality selection hypothesis is viewed as a reasonable explanation for the difference of famine exposure on the sex-specific effect.…”

DNA Methylation of Genes Participating in Hepatic Metabolisms and Function in Fetal Calf Liver Is Altered by Maternal Undernutrition during Gestation

“…In the early life stages of mammals, the nutrient levels of proteins, amino acids (AAs), carbohydrates, fatty acids (FAs), vitamins, and minerals are crucial for development, growth, and subsequent health maintenance [ 1 ]. The deficiency of these nutrients in maternal nutrition during gestation has a severe impact on the fetus, leading to fetal growth restriction (FGR) [ 1 , 2 ]. The malnourished fetal environment does not satisfy the demand for energy and resources to accumulate proteins for skeletal muscle growth in fetal calves [ 3 ].…”