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Rotavirus (RV) mainly infects intestinal epithelial cells, which leads to diarrhea in newborn piglets with dysfunction in the intestinal mucosal mechanical barrier. Sodium butyrate (SB) is one of the metabolites excreted by gut microbes. However, the protective effect of SB on RV infection induced intestinal mucosal mechanical barrier injury and its potential mechanism has not been well elucidated. In the present study, IPEC-J2 cells with RV infection was a model of intestinal mucosal mechanical barrier injury. Our results demonstrated that the appropriate concentration of SB can effectively alleviate TJ structural damage and up-regulating the expression of TJ-related genes. Furthermore, the appropriate concentration of SB can effectively reverse the increase of intracellular reactive oxygen species (ROS) and malondialdehyde (MDA) level induced by RV infection. Meanwhile, the levels of antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-px) and antioxidant proteins NAD(P)H dehydrogenase quinone 1 (NQO1) and heme oxygenase-1 (HO-1) were increased through SB treatment. In addition, we found that SB increased cellular antioxidant capacity by activating the adenosine monophosphate-activated protein kinase (AMPK)-nuclear factor erythroid 2-related factor (Nrf2) signaling pathway and the cytoprotective effect of SB is limited by GPR109A siRNA. Thus, our findings revealed that SB reduces oxidative stress caused by RV infection and restores the intestinal mucosal mechanical barrier function by activating the AMPK-Nrf2 signal pathway mediated by the receptor GPR109A.

As a type of non-coding RNA, microRNAs are widely involved in the biological processes of animals. In the present study, the expression of miR-152 in glycolytic muscle fibers (Longissimus thoracis, LT) was lower than that of oxidative muscle fibers (Psoas major, PM). Using dual luciferase assay, miR-152 was shown to target muscle pyruvate kinase (PKM) to perform biological functions. Moreover, overexpression of miR-152 in primary porcine cells inhibited PKM gene expression and reduced lactic acid production in cells, whereas inhibition of miR-152 expression promoted PKM gene expression and increased lactic acid production. Correlation analysis showed that the expression of miR-152 was significantly positively correlated with the ultimate pH of LT after slaughter, while the expression of the PKM gene was significantly negatively correlated with the final pH of LT. In vivo and in vitro experiments discussed herein suggest that miR-152 may affect muscle pH by targeting the expression of the PKM gene. Our findings enrich the understanding of the genetic regulatory network that influences pork quality.

Obesity due to excessive lipid accumulation is closely associated with metabolic diseases such as type 2 diabetes, insulin resistance and inflammation. Therefore, a detailed understanding of the molecular mechanisms that underlie adipogenesis is crucial to develop treatments for diseases related to obesity. Here, we found that the microRNA-204-5p (miR-204-5p) was expressed at low levels in fat tissues from obese mice fed long-term with a high-fat diet (HFD). Overexpression or inhibition of miR-204-5p in vitro in 3T3-L1 preadipocytes significantly inhibited or promoted 3T3-L1 proliferation, respectively, an effect mediated by regulating cell proliferation factors. miR-204-5p also induced preadipocyte apoptosis by directly targeting the 3' UTR region of Bcl-2, reducing the constitutive suppression of Bcl-2 on p53-dependent apoptosis. Interestingly, overexpression of miR-204-5p during adipocyte differentiation significantly increased the number of oil red O+ cells, triglyceride accumulation and the expression of markers associated with adipocyte differentiation. In contrast, inhibition of miR-204-5p had the opposite effect on 3T3-L1 adipocyte differentiation. Luciferase activity assays and qRT-PCR showed that miR-204-5p regulates adipocyte differentiation by negatively regulating KLF3, a negative regulator of lipogenesis. Taken together, our findings showed that miR-204-5p inhibits proliferation and induces apoptosis of preadipocytes by regulating Bcl-2, but also promotes adipocyte differentiation by targeting KLF3.

MicroRNAs (miRNAs) are small, non-coding RNAs that affect the post-transcriptional regulation of a variety of biological pathways. A previous study found out that miR-200b was important in the metabolism of obesity, but the mechanism of miR-200b regulateing adipogenesis is not fully understood.. In the present study, we observed that miR200b expression decreased both in obese mice and during the process of 3T3-L1 adipogenic differentiation. Overexpression of miR-200b promoted adipocyte proliferation by regulating the expression of cell cycle-regulated factors.Furthermore, overexpression of miR-200b reduced lipid accumulation and triglyceride content in adipocytes, and accompanied by a marked decrease in the expression of adipocyte-specific genes involved in fatty acid synthesis. Luciferase activity assays confirmed that miR-200b regulated adipocyte differentiation by directly targeting KLF4, and miR-200b suppressed the expression of KLF4 in both mRNA level and protein level. Moreover, the expression levels of downstream genes of KLF4, such as C/EBPβ, C/EBPα, KLF5 and PPARγ, were decreased in 3T3-L1 cells by miR-200b overexpression. Taken together, these results indicate that miR-200b may be involved in adipogenesis and could be a target for therapeutic intervention in obesity and metabolic syndrome.

In skeletal muscle, the composition of the fiber types has a profound impact on athletic performance, such as endurance or strength output. The proportions of muscle fiber types have also been associated with certain diseases, including dyskinesia, obesity and insulin resistance. Genistein, a natural estrogen, has been demonstrated to regulate fatty acid oxidation and insulin sensitivity in skeletal muscle. However, it is unknown whether genistein can regulate skeletal muscle fiber types. Furthermore, the mechanism of its effect on skeletal muscle energy metabolism is not entirely clear. In this study, in vivo and in vitro experiments were used to explore the effect of genistein on the muscle fiber-type transitions and muscle metabolism. The results indicated that genistein not only promotes skeletal muscle development but increases the expression of slow muscle fibers in mice as well. It was also demonstrated that genistein altered the ratios of fiber type and promoted mitochondrial biogenesis in C2C12 myoblasts. Interestingly, the expression of miR-222 was decreased by genistein, and it was demonstrated that this microRNA targets the PGC1α gene. In C2C12 myoblasts, miR-222 appears to regulate fiber type conversion and mitochondrial biogenesis. However, this function was significantly reduced following genistein treatment. These results suggest that miR-222 may be involved in the regulation of genistein on skeletal muscle fiber and muscle metabolism, and genistein may be used to improve muscle health.