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Nutrition


Metabolic and Transcriptomic Responses of Weaned Pigs Induced by Different Dietary Amylose and Amylopectin Ratio
Published: Tuesday, November 30, 2010
Author: He Jun et al.

by He Jun, Chen Daiwen, Yu Bing

Starch is one of the major dietary energy sources for mammals. However, the nutritional value of starch largely depends on its amylose and amylopectin ratio. In this study, the overall metabolic and transcriptomic responses of weaned pigs fed with different dietary starches were assessed. Sixteen weaned pigs were randomly allotted to two experimental diets containing either of pure cassava starch (CS) or maize starch (MS) as the sole energy source (the amylose-amylopectin ratio were 0.25 and 0.43, respectively). Results indicated that the body weight gain was not affected by different dietary starches. However, a moderate fatty liver was observed in CS-fed group. Long-term ingestion of CS not only increased the total liver fat content, but significantly elevated the liver triglyceride and cholesterol content (P<0.05). In addition, the serum insulin and cholesterol concentrations were both elevated in CS-fed group (P<0.05). Microarray analysis led to the identification of 648 genes differentially expressed in liver (P<0.05), and a lot of them were involved in lipid and carbohydrate metabolism. Additionally, pathway analysis indicated that both the insulin and PPAR signaling pathways were acutely affected by dietary amylose-amylopectin ratio. Long-term ingestion of CS activated the transcription of lipogenic genes such as hmgr and fasn, but decreased the expression of lipolytic genes such as aox1, ppara and fbp. The microarray results correlated well with the measurements of several key enzymes involved in hepatic lipid metabolism. Our results suggested that both the metabolic and transcriptomic responses of weaned pigs were tightly regulated by dietary starch composition, and a high amylose ratio starch (i.e MS) may be more healthful for mammals as the long-term energy source by down-regulation of hepatic lipogenesis and steroidogenesis.
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