Supplemental effect of different levels of taurine in Modena on boar semen quality during liquid preservation at 17°C.

Peroxidation damage induces sublethal injury to boar sperm during the storage process. Taurine has already been demonstrated to protect cells effectively from oxidant-induced injury. This study was aimed to evaluate the effect of different concentrations of taurine (0.5, 1, 5 and 10 mmol/L) in Modena diluent on boar sperm quality during liquid storage at 17°C. Ejaculates from sexually mature Duroc pigs were collected, pooled and preserved in the Modena containing different concentrations of taurine. Sperm motility, plasma membrane integrity, acrosome integrity, total antioxidative capacity (T-AOC) activity and malondialdehyde content (MDA) were examined every 24 h. Modena diluent containing taurine suppressed the reduction in sperm qualities during the process of liquid preservation compared with those of the control group. After 5 days of liquid preservation, the addition of taurine at 5 mmol/L had the optimal effect on survival time as well as maintenance of motility, plasma membrane integrity, acrosomal integrity, T-AOC activity and MDA content. These results may suggest the possibility that the proper addition of taurine to the semen extender improves the swine production system using artificial insemination by the suppressing of sperm damage and subsequent dysfunction during liquid preservation.

The effects of different levels of superoxide dismutase in Modena on boar semen quality during liquid preservation at 17°C.

This study was conducted to investigate the influence of superoxide dismutase (SOD) on the quality of boar semen during liquid preservation at 17°C. Semen samples from 10 Duroc boars were collected and pooled, divided into five equal parts and diluted with Modena containing different concentrations (0, 100, 200, 300 and 400 U/mL) of SOD. During the process of liquid preservation at 17°C, sperm motility, acrosome integrity, membrane integrity, total antioxidant capacity (T-AOC) activity, malondialdehyde (MDA) content and hydrogen peroxide (H2 O2 ) content were measured and analyzed every 24 h. Meanwhile, effective survival time of boar semen during preservation was evaluated and analyzed. The results indicated that different concentrations of SOD in Modena showed different protective effects on boar sperm quality. Modena supplemented with SOD decreased the effects on reactive oxygen species on boar sperm quality during liquid preservation compared with that of the control group. The added 200 U/mL SOD group showed higher sperm motility, membrane integrity, acrosome integrity, effective survival time and T-AOC activity. Meanwhile, the added 200 U/mL SOD group showed lower MDA content and H2 O2 content. In conclusion, addition of SOD to Modena improved the boar sperm quality by reducing oxidative stress during liquid preservation at 17°C and the optimum concentration was 200 U/mL.

Mulberry 1-Deoxynojirimycin Inhibits Adipogenesis by Repression of the ERK/PPARγ Signaling Pathway in Porcine Intramuscular Adipocytes.

Intramuscular fat (IMF), which is modulated by adipogenensis of intramuscular adipocytes, plays a key role in pork quality associated with marbling, juiceness, and flavor. However, the regulatory mechanism of 1-deoxynojirimycin (DNJ) on adipogenesis is still unknown. Here, we found that both DNJ (2.0, 3.0, 4.0, 5.0, and 6.0 µM) and rosiglitazone (RSG; 0.1, 0.2, 0.3, 0.4, and 0.5 mM) had no effect on cell viability. Moreover, 4 µM DNJ significantly inhibited adipogenesis, whereas 0.4 mM RSG increased lipogenesis of porcine intramuscular adipocytes. Interestingly, DNJ sharply inhibited phosphorylation of extracellular regulated protein kinases 1/2 (ERK1/2), but did not change phosphorylation of AKT (protein kinase B) in intramuscular adipocytes. We further found that the inhibitory adipogenesis of DNJ was attenuated by RSG via up-regulation of PPARγ. On the basis of the above findings, we suggest that DNJ inhibited adipogenesis through the ERK/PPARγ signaling pathway in porcine intramuscular adipocytes.

Suppression of mTORC1 activation in acid-α-glucosidase-deficient cells and mice is ameliorated by leucine supplementation.

Pompe disease is due to a deficiency in acid-α-glucosidase (GAA) and results in debilitating skeletal muscle wasting, characterized by the accumulation of glycogen and autophagic vesicles. Given the role of lysosomes as a platform for mTORC1 activation, we examined mTORC1 activity in models of Pompe disease. GAA-knockdown C2C12 myoblasts and GAA-deficient human skin fibroblasts of infantile Pompe patients were found to have decreased mTORC1 activation. Treatment with the cell-permeable leucine analog L-leucyl-L-leucine methyl ester restored mTORC1 activation. In vivo, Pompe mice also displayed reduced basal and leucine-stimulated mTORC1 activation in skeletal muscle, whereas treatment with a combination of insulin and leucine normalized mTORC1 activation. Chronic leucine feeding restored basal and leucine-stimulated mTORC1 activation, while partially protecting Pompe mice from developing kyphosis and the decline in muscle mass. Leucine-treated Pompe mice showed increased spontaneous activity and running capacity, with reduced muscle protein breakdown and glycogen accumulation. Together, these data demonstrate that GAA deficiency results in reduced mTORC1 activation that is partly responsible for the skeletal muscle wasting phenotype. Moreover, mTORC1 stimulation by dietary leucine supplementation prevented some of the detrimental skeletal muscle dysfunction that occurs in the Pompe disease mouse model.

[Effect of emodin on proliferation and differentiation of rat preadipocytes].

OBJECTIVE: To study the effect of emodin (EMO) on the proliferation and differentiation of rat preadipocytes. METHOD: Separating and culturing rat preadipocytes, grouping the wells that preadipocytes were growing according to certain concentration such as 0, 5, 10, 20, 40, 80, 160 micromol x L(-1) randomly, MTT spectrophotometry and flow cytometry (FCM) were adopted to determine the effect of EMO on proliferation of rat preadipocytes. The accumulation of TG (triglyceride) in adipocytes was assayed by oil red O staining, and the morphological changes of the adipocytes were determined by morphology observation. RESULT: EMO in the range of 20-160 micromol x L(-1) could inhibit the proliferation and differentiation of preadipocytes in a dose and time dependent manner, and induce apoptosis of preadipocytes in a certain degree. CONCLUSION: EMO should have a potential to serve as a fat-reducing drug.