The Effect Of DHA On Mice Lipogenesis And Lipolysis Genes Transcription Expression

Dietary intake of lipids amounts to 25%–45% of total energy in human body. Most of the dietary fatty acids are derived from meats, oils and dairy products, giving rise to a large intake of saturated as well as monounsaturated fatty acids. represent the most established risk factor in our diets for obesity, diabetes, cardiovascular disease (CVD), and so on, whereas PUFAs probably are the most important lipids that would provide beneficial effects if the dietary intake is increased. Docosahexaenoic acid (DHA) is one kind of n-3 PUFAs, palys important roles in maintaining biomembrane interity, treating hyperlipemia, keeping away from CVD and so on. Adipose plays a critical role in energy balance as essential tissue in energy metabolism. If lipid matbolism disorder happens, there will be many pathological changes in human body. As transcription factors, Peroxisome proliferator-activated receptor (PPARγ) and Sterol regulatory element binding protein-1c (SREBP-1c) are known to regulate expression of many enzymes. Fatty acid synthetase (FAS) is a key enzyme in lipogenesis. Hormone-sensitive lipase (HSL) was ever seemed as the only enzyme in lipolysis, however, triglyceride hydrolyase (TGH) has been found as another enzyme in recent years. In this study, these factors and enzymes are detected on transcription level in mice adipose tissue, liver and adipocyte, which were treated by different concentration of DHA. We also analysised the correlation between adipocyte proliferation and differentiation and SREBP-1c, FAS and HSL gene expression, and tried to explore the effects of DHA on lipogenesis and lipolysis genes. The main results were summarized as following:1. Mice were treated with DHA in short time, PPARγ, FAS, HSL and TGH gene expression were increased in adipose tissue, but SREBP-1c gene expression was decreased. However, in liver PPARγ, SREBP-1c, FAS and HSL gene expression were downregulated by DHA, it had no change on TGH gene expression. It is illustrated that DHA could promote liplyosis in adipose and inhibit lipogenesis in liver. And also perhaps DHA could inhibit liver liplyosis by reducing HSL gene expression.2. Mice were treated with DHA in intragastric administration for 3 weeks, ADG of mice was decreased significant in dose-independence. In adipose PPARγ, HSL and TGH gene expression were upregulated by DHA, but had no difference in SREBP-1c gene expression. In liver PPARγ, SREBP-1c and FAS gene expression were down regulated, but HSL gene expression was increased, and TGH gene expression had no difference compared with the control. It is illustrated that mice were treated by DHA for long time, liplyosis in adipose tissue was prometed, and lipogenesis in liver was depressed. And the ADG was decrease because of decreasing in fat accumulation.3. Mice adipocytes were treated by DHA for 24 h, proliferation of adipocytes had no difference, but the proliferation was inhibited in 48 h. DHA could increase PPARγgene expression which was marker gene in adipocyte differentiation. SREBP-1c, FAS and HSL gene expression was also increased. We also do the correlation between proliferation and differentiation of adipocyte and these genes. Results showed that proliferation of adipocyte had negative correation with SREBP-1c gene expression, no correation with FAS gene expression, and positive correation with HSL gene expression. Differentiation of adipocyte had positive correation with SREBP-1c and FAS gene expression and no correation with HSL gene expression. It is illustrated that DHA could inhibit proliferation and promote differentiation of mice adipocyte.