MiR-129 plays a crucial role in regulating various cellular processes, including adipogenesis; however, its downstream molecular mechanisms remain unclear. In this study, we demonstrated that miR-129 promotes yak adipogenesis in vitro via the PI3K/AKT pathway. Overexpression and interference of miR-129 in yak intramuscular preadipocytes (YIMAs) enhanced and inhibited cell differentiation, respectively, with corresponding changes in cell proliferation. Further investigation revealed that miR-129 enhances AKT and p-AKT activity in the AKT pathway without affecting cell apoptosis, and a specific inhibitor (LY294002) was used to confirm that miR-129 regulates YIMAs proliferation and differentiation through the PI3K/AKT pathway. Our findings suggest that miR-129 promotes yak adipogenesis by enhancing PI3K/AKT pathway activity. This study provides the foundation to precisely elucidate the molecular mechanism of miR-129 in YIMAs adipogenesis and develop advanced miRNA-based strategies to improve meat nutrition and obesity-related ailments in beef production.

The yak (Bos grunniens) has exceptional hypoxia resilience, making it an ideal model for studying high-altitude adaptation. Here, we investigated the effects of oxygen concentration on yak cardiac fibroblast proliferation and the underlying molecular regulatory pathways using RNA sequencing (RNA-seq) and metabolic analyses. Decreased oxygen levels significantly inhibited cardiac fibroblast proliferation and activity. Intriguingly, while the mitochondrial DNA (mtDNA) content remained stable, we observed coordinated upregulation of mtDNA-encoded oxidative phosphorylation components. Live-cell metabolic assessment further demonstrated that hypoxia led to mitochondrial respiratory inhibition and enhanced glycolysis. RNA-seq analysis identified key hypoxia adaptation genes, including glycolysis regulators (e.g., HK2, TPI1), and hypoxia-inducible factor 1-alpha (HIF-1α), with Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses highlighting their involvement in metabolic regulation. The protein–protein interaction network identified three consensus hub genes across five topological algorithms (CCNA2, PLK1, and TP53) that may be involved in hypoxia adaptation. These findings highlight the importance of metabolic reprogramming underlying yak adaptation to hypoxia, providing valuable molecular insights into the mechanisms underlying high-altitude survival.

The goal of this study was to determine the metabolism of multiparous female yaks during the late perinatal period and identify its effects on reproductive recovery in order to explain the low reproduction rate of yaks. Eight multiparous female yaks were randomly selected as the sample, and serum was collected from the yaks every 7 days from the day of delivery until 28 days after the delivery (five time points). The presence of serum metabolic profiles and reproductive hormones was identified using ELISA. The key metabolites were identified using liquid chromatography–mass spectrometry, and a dynamic metabolic network representation was created using bioinformatics analysis. A total of 117 different metabolites were identified by calculating the fold change of the metabolite expression at each time point. The dynamic metabolic network was created to represent the activities of the key metabolites, metabolic indexes and reproductive hormones. The initial efficiency of the glucose metabolism in the late perinatal period was found to be low, but it increased during the final period. The initial efficiencies of the lipid and amino acid metabolisms were high but decreased during the final period. We inferred that there was a postpartum negative energy balance in female yaks and that the synthesis and secretion of estrogen were blocked due to an excessive fatty acid mobilization. As a result, the reproductive hormone synthesis and secretion were maintained at a low level in the late perinatal period, and this was the main reason for the delayed recovery of the reproductive function postpartum. However, the specific mechanism needs to be further verified.