Maternal Overnutrition in Beef Cattle: Effects on Fetal Programming, Metabolic Health, and Postnatal Outcomes

Abstract

Maternal overnutrition and targeted supplements during pregnancy strongly affect fetal development in beef cattle, influencing gene expression, tissue development, and productivity after birth. As modern feeding practices often result in cows receiving energy and protein above requirements, understanding the balance between adequate nutrition and overconditioning is critical for sustainable beef production. This review synthesizes findings from recent studies on maternal overnutrition and supplementation, focusing on macronutrients (energy, protein, methionine) and key micronutrients (e.g., selenium, zinc). It evaluates the timing and impact of supplementation during different gestational stages, with emphasis on fetal muscle and adipose tissue development, immune function, and metabolic programming. The role of epigenetic mechanisms, such as DNA methylation and non-coding RNAs, is also discussed in relation to maternal dietary inputs. Mid-gestation supplementation promotes muscle growth by activating muscle-specific genes, whereas late-gestation diets enhance marbling and carcass traits. However, maternal overnutrition may impair mitochondrial efficiency, encourage fat deposition over muscle, and promote collagen synthesis, reducing meat tenderness. Recent evidence highlights sex-specific fetal programming differences, the significant impact of maternal diets on offspring gut microbiomes, and breed-specific nutritional responses, and multi-OMICs integration reveals metabolic reprogramming mechanisms. Targeted trace mineral and methionine supplementation enhance antioxidant capacity, immune function, and reproductive performance. Precision feeding strategies aligned with gestational requirements improve feed efficiency and minimize overfeeding risks. Early interventions, including protein and vitamin supplementation, optimize placental function and fetal development, supporting stronger postnatal growth, immunity, and fertility. Balancing nutritional adequacy without excessive feeding supports animal welfare, profitability, and sustainability in beef cattle systems.

Keywords: adipogenesis; beef cattle production; fetal programming; maternal nutrition; muscle development.

Figure 1

Critical windows of fetal development and the impact of maternal nutrition during pregnancy. This timeline illustrates key stages of embryonic and fetal development, highlighting periods of primary and secondary myogenesis, adipogenesis, and muscle fiber hypertrophy. MO and supplementation at different stages affect muscle and fat development. Early protein supplementation enhances muscle fiber formation, while MO in late gestation promotes intramuscular fat deposition and marbling. Controlled supplementation ensures optimal growth, balancing muscle development and fat accumulation.

Figure 2

Maternal nutrition reprograms key fetal pathways. Gold (myogenesis), orange (adipogenesis), green (fibrogenesis), and blue (energy metabolism) arrows indicate major developmental axes. Upward (↑) and downward (↓) arrows show increased or decreased activity under protein/micronutrient supplementation or MO, respectively. Icons denote the maternal plane (cow), muscle fiber development (muscle icon), fat deposition (fat droplet), collagen deposition (collagen icon), and mitochondrial/energy pathways (mitochondrion). Abbreviations: MYF5 (myogenic factor 5), MyoD (myoblast determination protein 1), KRT8/18 (keratins 8 and 18), PPARG (peroxisome proliferator-activated receptor γ), FABP4 (fatty acid binding protein 4), ZFP423 (zinc finger protein 423), COL1A2/COL3A1 (collagen types I α2/III α1), THBS1 (thrombospondin 1), RUNX1 (runt-related transcription factor 1), MMP2 (matrix metalloproteinase 2), IGF1 (insulin-like growth factor 1), FOXO1 (forkhead box O1), PPARGC1A (PPAR γ coactivator 1 α), CPT2 (carnitine palmitoyltransferase 2).

Figure 3

Maternal nutrition during pregnancy differentially programs myogenesis and adipogenesis. The blue central box denotes the maternal dietary plane. The orange pathway (left) traces myogenesis: protein, energy, and micronutrient supplementation increase muscle-fiber number, growth flexibility, and antioxidant capacity; epigenetic activation via DNA methylation and lncRNA networks further upregulates myogenic genes. The yellow pathway (right) traces adipogenesis: MO or targeted micronutrients upregulate adipocyte differentiation and fat deposition through miRNA regulation and lncRNA-mediated gene control; a balanced micronutrient supply can instead improve marbling while limiting excess fat. Arrow thickness indicates the direction of regulation: upward arrows = stimulation; downward arrows = repression. Abbreviations: MO, MO; lncRNA, long non-coding RNA; miRNA, microRNA.

Figure 4

Postnatal outcomes linked to specific maternal nutrition strategies. The central blue ellipse denotes the overarching theme of Postnatal Outcomes of Maternal Nutrition. The five colored ovals highlight major performance domains: green = Growth Performance; yellow = Immune Function and Health; dark grey = Reproductive Development; orange = Carcass and Meat Quality; and brown = Metabolic Health and Efficiency. Under each domain, the grey rectangles list representative gestational interventions (e.g., protein-plus-energy, trace-mineral or micronutrient supplementation, balanced diets), and the white rectangles below summarize the principal offspring responses. Upward arrows indicate the direction of improvement. Key reported benefits include higher birth and weaning weights, stronger neonatal immunity, earlier puberty and improved fertility, superior marbling and tenderness (higher USDA grading), and enhanced energy partitioning with better mitochondrial efficiency. Abbreviation: USDA, United States Department of Agriculture.