Maternal propionate supplementation ameliorates glucose and lipid metabolic disturbance in hypoxia-induced fetal growth restriction.

Intrauterine growth restriction (IUGR), one of the major complications of pregnancy, is characterized by low birth weight and results in higher risks for long-term problems including developing metabolic and cardiovascular diseases. Short-chain fatty acids (SCFAs), especially propionate, have been reported to correct glucose and lipid disorders in metabolic diseases. We hypothesized that maternal propionate supplementation could prevent glucose and lipid metabolic disturbance in hypoxia-induced IUGR. Here, in our study, maternal hypoxia was induced from gestational day (GD) 11 to GD 17.5 to establish an IUGR mouse model. Maternal propionate treatment reversed reduced birth weight in male IUGR offspring. Hepatic transcriptomics demonstrated that SP treatment significantly lowered glucose and lipid metabolism-related genes (Scd1, G6pc, Pck1 and Fasl) in IUGR offspring. KOG enrichment analysis showed that propionate-induced down-regulated differential expressed genes (DEGs) mainly belonged to lipid transport and metabolism. KEGG enrichment results showed that the down-regulated DEGs were mostly enriched in PPAR and FoxO signaling pathways. We also found that maternal oral administration of SP decreased serum lipid content, attenuated hepatic insulin resistance and liver lipid accumulation, reduced hepatic key gene expressions of gluconeogenesis and lipogenesis, increased energy expenditure and improved liver function in 11-week-old male IUGR offspring. These results indicate that maternal propionate supplementation increases birth weight and corrects hepatic glucose and lipid metabolic disturbance and energy expenditure in male mice born with IUGR, which may provide a basis for using propionate to treat IUGR disease.

Functional coix seed protein hydrolysates as a novel agent with potential hepatoprotective effect.

The aim of this study is to explore the hepatoprotective potential of coix seed protein hydrolysates (CPP) against alcohol-induced liver injury, and investigate the underlying mechanisms. The hepatoprotective activity of CPP at 0, 10, 30, 50 mg per kg BW was demonstrated in vivo by using ICR male mice fed with 40% v/v alcohol (5 ml per kg body weight) daily to induce alcoholic liver injury. CPP could significantly improve the alcohol metabolism in liver as evidenced by the enhanced activity of aspartate aminotransferase (AST) and alanine aminotransferase (ALT). The overexpression of serum tumor necrosis factor-α (TNF-α) and interleukin-ß (IL-ß) by alcohol induced injury was altered by CPP administration. The lipid peroxidation was also retarded by CPP by suppressing malondialdehyde (MDA) level and increasing the activity of liver superoxide dismutase (SOD). The findings from the present study suggested that CPP produced significant hepatoprotection and showed potential to be used as a dietary supplement or the ingredient of functional food.