Prenatal origins of productivity and quality of beef

Abstract

RuminantsBoard-invited review Prenatal origins of productivity and quality of beef ABSTRACT -The productive traits of beef cattle are orchestrated by their genetics, postnatal environmental conditions, and also by the intrauterine background. Both under-or overnutrition, as specific dietary components, are able to promote persistent effects on the offspring. This occurs because dietary factors act not only affecting the availability of substrates for fetal anabolism and oxidative metabolism, but also as signals that regulate several events toward fetal development. Therefore, this study aimed to summarize the gestational nutrition effects on the offspring performance and meat quality in a long term. Overall, studies have shown that many of these alterations are under the control of epigenetic mechanisms, as DNA methylation, histones modification, and non-coding RNA. The current knowledge has indicated that the fetal programming responses are dependent on the window of fetal development in which the dietary treatment is applied, the intensity of maternal nutritional stimuli, and the treatment application length. Collectively, studies demonstrated that muscle cell hyperplasia is impaired when maternal requirements were not achieved in the second third of gestation, which limits the formation of a greater number of muscle fibers and the offspring growth potential in a long term. Changes in muscle fibers metabolism and in collagen content were also reported as consequence of a dietary perturbation during pregnancy. In contrast, a maternal overnutrition during the late pregnancy has been associated with beneficial responses on meat quality. In summary, ensuring an adequate maternal environment during the fetal development is crucial to enhance the productive responses in beef cattle operations.

Protein Supplementation during Mid-Gestation Alters the Amino Acid Patterns, Hepatic Metabolism, and Maternal Skeletal Muscle Turnover of Pregnant Zebu Beef Cows

“…This occurs because the use of some substrates from maternal energy reserves (such as long-chain fatty acids, non-esterified acids, and ketoacids) is limited by the placenta [ 8 ]. In this sense, amino acids from maternal skeletal muscle tissue may be partitioned to improve fetal access to amino acids and glucose [ 9 ]. The glucose required by gestational tissues is, in turn, supported by the increased hepatic uptake of endogenous substrates [ 10 , 11 ].…”