The carcass and meat quality traits of pig breeds living at three different altitudes (Yorkshire pigs, YP: 500m; Qingyu Pigs, QYP: 1500m; Tibetan pigs, TP: 2500m) were compared. It was observed that there are obvious differences in pig breeds with respect to performance parameters. Specifically, YP had the best carcass traits, showing high slaughter rates and leanest meat. Conversely, QYP had the highest back fat thickness and intramuscular fat (IMF) content. For the high-altitude breed TP, the animals exhibited low L* and high a* values. The genotypes contributing to the observed phenotypes were supported by a PCR analysis. The glycolytic genes expression (HK, PFK, PK) were highest in YP, whereas expression of genes related to adipogenesis (C/EBPα, FABP4, SCD1) were highest in QYP. As expected, genes associated with angiogenesis and hypoxia (HIF1a, VEGFA) were expressed at the highest levels in TP. The composition and proportion of amino and fatty acids in pig muscles at the three altitudes examined also varied substantially. Among the breeds, TP had the highest proportion of umami amino acids, whereas QYP had the highest proportion of sweet amino acids. However, TP also exhibited the highest proportion of essential fatty acids and the lowest proportion of n6:n3. This study explains the high-altitude adaptive evolution and the formation of meat quality differences in different altitude pigs from various angles and provides a reference for local pork food processing and genetic improvement of local pigs.

Adipogenesis is a complex biological process and the main cause of obesity. Recently, microRNAs (miRNAs), a class of small endogenous non-coding RNAs, have been proven to play an important role in adipogenesis by the post-transcriptional regulation of target genes. In this current study, we observed an increment of miR-152 expression during the process of 3T3-L1 cell audiogenic differentiation. A functional analysis indicated that the overexpression of miR-152 inhibited pre-adipocyte proliferation and suppressed the expression of some cell cycle-related genes. Moreover, the overexpression of miR-152 promoted lipid accumulation in 3T3-L1 preadipocytes accompanied by increase of the expression of some pro-audiogenic genes. Additionally, a dual-luciferase reporter assay demonstrated lipoprotein lipase (LPL) was a direct target gene of miR-152 during preadipocyte differentiation. Further analysis showed that miR-152 was positively correlated with adipogenesis and intramuscular fat formation in vivo. Taken together, our findings suggest that miR-152 could suppress 3T3-L1 preadipocyte proliferation, whereas it could promote 3T3-L1 preadipocyte differentiation by negatively regulating LPL. The findings indicate that miR-152 might have a therapeutic significance for obesity and obesity-related metabolic syndrome.