The Later Effects of DHA in Diet on Regulating Transcription of Lipid Genes of Broiler

The effect of docosahexaenoic acid （DHA） on lipid metabolism in broiler were studied in order to provide test results for polyunsaturated fatty acids （PUFA） regulating fatty deposition. 1-wk-old Arbor Acres （AA） broiler were fed with DHA microalgae and slaughtered after 2 wk. The tissues were stored for isolating total RNA. RT-PCR was used to analyze the expression changes of genes. DHA microalgae significantly increased average body gain and feed conversion rates, reduced the levels of total cholesterol （TC）, total glycerin （TG）, and low-density lipoprotein cholesterol （LDL-C） in serum and increased the content of high-density lipoprotein cholesterol. 1 wk later, the effects were still remained. In liver tissue, DHA microalgae increased the expression of PPARα and carnitine palmitoyltransferase-1 （CPT-1）. 1 wk later, it was observed that DHA up-regulated the expression of fatty acid synthase （FAS）, acetyl CoA carboxylase （ACC）, lipoprotein lipase （LPL） and carnitine palmitoyltransferase-1 （CPT-1）. 2 wk later, it still increased the expressions of FAS and CPT-1, but a converse result was observed for ACC and LPL. In adipose tissue, DHA microalgae suppressed the expression of PPARα and LPL, up-regulated the expression of ACC, FAS, and CPT-1. After withdrawal, the expression of genes in test group was significantly lower than that in control group （P0.01）. In the muscle of chest, DHA microalgae significantly inhibited the gene expression （P0.01）. 1 wk later, the expressions of FAS, LPL and CPT-1 in test group were significantly higher than that in control group （P0.05）. 2 wk later, it was shown that DHA significantly inhibited fat synthesis and decomposition. In the leg, there was not any PPARα expression being detected, probably because of the less expression in muscle tissues or the regulation of PPARα had no relation to the case. DHA microalgae promote fat synthesis in the liver and inhibit in adipose and muscle tissues. It still has effects after 1 wk of withdrawal.

Effect of an Ilex asprella root decoction on the related genes of lipid metabolism from chronic stress and hyperlipidemic fatty liver in rats

Background The gradually increasing changes in a human hyperlipidemic diet along with chronic stress might play an important role in the increased numbers of fatty liver. This study investigated the effects of Ilex asprella root decoction on related genes of lipid metabolism in chronic stress in hyperlipidemic fatty liver in rats. Methods Forty-eight male Wistar rats were randomly divided into four groups： normal control group, model control group, simvastatin group, and Ilex asprella root group. To establish chronic stress and hyperlipidemic fatty liver models in rats, the levels of serum lipids, glucose, liver index, insulin （INS）, insulin resistant （IR） index, adiponectin, superoxide dismutase （SOD）, glutathione peroxidase （GSH-pX）, glutathione （GSH）, liver X receptor （LXR）, and sterol responsive element binding protein （$REBP）-lc in rats were measured. Results When compared to the normal control group, the levels of serum lipids, glucose, liver index, INS, IR index, and GSH in the model control group significantly increased （P 〈0.01）. The protein levels of LXRa and SREBP-lc increased （P 〈0.05）, and the serum adiponectin and the SOD and GSH-pX decreased significantly （P 〈0.01）. When compared to the model control group, the levels of serum lipids, glucose, liver index, INS, IR index, SOD, and GSH-pX in the simvastatin group and Ilex asprella root group increased in varying degrees （P 〈0.01 or 0.05）; the serum adiponectin and GSH decreased （P 〈0.05）, while the protein levels of LXRa and SREBP-lc decreased in varying degrees （P 〈0.01 or 0.05）. When compared to the simvastatin group, the IR index and protein levels of LXRa in the Ilex asprella root group decreased （P 〈0.05）, and the serum adiponectin and SOD increased （P 〈0.05）. Conclusion The Ilex asprella root decoction has some protective effects on regulating the related genes of lipid metabolism caused by chronic stress and hyperlipidemic fatty liver in rats.