Changes in milk performance and hepatic metabolism in mid-lactating dairy goats after being fed a high concentrate diet for 10 weeks.

Feeding a high concentrate (HC) diet is a widely used strategy for supporting high milk yields, yet it may cause certain metabolic disorders. This study aimed to investigate the changes in milk production and hepatic metabolism in goats fed different proportions of concentrate in the diet for 10 weeks. In total, 12 mid-lactating goats were randomly assigned to an HC diet (65% concentrate of dry matter, n=6) or a low concentrate (LC) diet (35% concentrate of dry matter, n=6). Compared with LC, HC goats produced greater amounts of volatile fatty acids and produced more milk and milk lactose, fat and protein (P<0.01). HC goats showed a greater concentration of ATP, NAD, plasma non-esterified fatty acids and hepatic triglycerides than LC goats (P<0.05). Real-time PCR results showed that messenger RNA (mRNA) expression of gluconeogenic genes, namely, glucose-6-phosphatase, pyruvate carboxylase and phosphoenolpyruvate carboxykinase were significantly up-regulated and accompanied greater gluconeogenic enzyme activities in the liver of HC goats. Moreover, the expression of hepatic lipogenic genes including sterol regulatory element-binding protein 1c, fatty acid synthase and diacylglycerol acyltransferase mRNA was also up-regulated by the HC diet (P<0.05). HC goats had greater hepatic phosphorylation of AMP-activated protein kinase than LC (P<0.05). Furthermore, histone-3-lysine-27-acetylation contributed to this elevation of gluconeogenic gene expression. These results indicate that lactating goats fed an HC diet for 10 weeks produced more milk, which was associated with up-regulated gene expression and enzyme activities involved in hepatic gluconeogenesis and lipogenesis.

Tissue inhibitor of metalloproteinase-2 G-418C polymorphism is associated with an increased risk of gastric cancer in a Chinese population.

AIMS: To examine the effect of the TIMP-2 G-418C polymorphism on gastric cancer risk. METHODS: We conducted a hospital-based, case-control study using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method in 412 individuals (206 gastric cancer patients and 206 age, sex matched cancer-free controls). RESULTS: The genotype and allele frequencies were significantly different (P = 0.007 and 0.005, respectively) between cases and controls. Further analysis showed that the variant TIMP-2 genotypes (CC+GC) had a 51% increased risk of gastric cancer compared with GG [adjusted odds ratio (OR) 1.51, 95% confidence interval (CI) 1.00-2.26, P = 0.049]. The elevated gastric cancer risk was especially evident in younger individuals (age < 58 years old) (adjusted OR 2.21, 95% CI 1.18-4.16) and smokers (adjusted OR 2.61, 95% CI 1.01-6.72). However, no significant association was observed between the variant genotypes and clinicopathological features of gastric cancer. CONCLUSIONS: These findings suggest that the TIMP-2 G-418C polymorphism is a genetic predisposing factor for gastric cancer.