The impact of excessive gestational weight gain on fetal hepatic lipid metabolism and the regulatory mechanism / 中华实用儿科临床杂志

Objective:A rat model of excessive gestational weight gain (EGWG) was constructed to investigate the impact of EGWG on fetal hepatic lipid metabolism and the relevant regulatory mechanism.Methods:Healthy Sprague-Dawley rats were caged together and tested for pregnancy.Rats with the sperm observed under microscope were considered pregnant for 0.5 days.Pregnant rats were divided into the normal diet (ND) group and high-fat diet (HFD) group by the random number table method, with 8 rats in each group.The body weight during pregnancy of the pregnant rats was recorded.Cesarean section was performed at day 21.5 of gestation and the birth weight of the fetal rats was recorded.Hepatic lipid deposition of the pregnant and fetal rats was examined by hematoxylin-eosin (HE) staining and oil red O staining.Triglyceride (TG) and cholesterol (TC) levels in livers and serum of the pregnant and fetal rats were detected by glycerol phosphate oxidase-peroxidase(GPO-PAP) method.The mRNA and protein expression levels of key genes FASN and SREBP1c in hepatic lipid metabolism of fetal rats were measured by real-time polyme-rase chain reaction (RT-PCR) and Western blot.Differences between the two groups were compared by independent sample t test. Results:There was no difference in pre-pregnancy body weight between the HFD group and the ND group, but the differences in the weight and the weight gain during pregnancy gradually enlarged between the two groups.At day 21.5 of gestation, the weight of the pregnant rats[(467.75±22.05) g vs.(430.88±18.80) g, t=-3.600, P=0.003], the weight gain of the pregnant rats during pregnancy[(181.50±9.68) g vs.(148.50±10.86) g, t=-6.415, P<0.001] and the birth weight of the fetal rats[(5.51±0.17) g vs.(4.85±0.35) g, t=-4.779, P<0.001] of the HFD group were significantly higher than those of the ND group.Both HE staining and oil red O staining presented increased hepatic lipid deposition in the pregnant and fetal rats of the HFD group.The hepatic and serum TG and TC levels of the pregnant and fetal rats of the HFD group were significantly higher than those of the ND group (all P<0.05). RT-PCR and Western blot showed that the mRNA and protein levels of key genes FASN and SREBP1c in hepatic lipid metabolism of fetal rats of the HFD group were significantly higher than those of the ND group (all P<0.05). Conclusions:An EGWG model can be successfully constructed by a 21-day HFD during pregnancy.EGWG can lead to hepatic lipid deposition in the fetal rats.The mechanism may be related to the expression changes of key genes FASN and SREBP1c in hepatic lipid metabolism of fetal rats.

New insight into inter-organ crosstalk contributing to the pathogenesis of non-alcoholic fatty liver disease (NAFLD)

Non-alcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver dysfunction and a significant global health problem with substantial rise in prevalence over the last decades. It is becoming increasingly clear that NALFD is not only predominantly a hepatic manifestation of metabolic syndrome, but also involves extra-hepatic organs and regulatory pathways. Therapeutic options are limited for the treatment of NAFLD. Accordingly, a better understanding of the pathogenesis of NAFLD is critical for gaining new insight into the regulatory network of NAFLD and for identifying new targets for the prevention and treatment of NAFLD. In this review, we emphasize on the current understanding of the inter-organ crosstalk between the liver and peripheral organs that contributing to the pathogenesis of NAFLD.

Progress in the programming effect of early nutrition on hepatic lipid metabolism / 国际儿科学杂志

The early life of nutrition is closely related to obesity and metabolic syndrome in adult.Lipid metabolic dysfunction is one of the important mechanisms in the development of adult diseases.Liver plays a key role in lipid metabolism.Hepatic lipid metabolism mainly includes fatty acid uptake,synthesis,esterification,oxidation and export.Exposed to a optimal nutrition environment in early life might lead to some adaptive effects in the liver and its organization structure,cell numbers and metabolic function.These adaptive responses might play a persistent effect in each way of hepatic lipid metabolism.Clarifying the programming effect of early nutrition on hepatic lipid metabolism and the relative molecular mechanism might provide related theoretical basis and practical molecular target for the prevention of adult diseases during childhood.