"We evaluated a representative splicing factor, SFRS10, downregulated in both obese human liver and muscle and in high-fat-fed mice, and determined metabolic impact of reduced expression. SFRS10-specific siRNA induces lipogenesis and lipid accumulation in hepatocytes. Moreover, Sfrs10 heterozygous mice have increased hepatic lipogenic gene expression, VLDL secretion, and plasma triglycerides. We demonstrate that LPIN1, a key regulator of lipid metabolism, is a splicing target of SFRS10; reduced SFRS10 favors the lipogenic ß isoform of LPIN1. Importantly, LPIN1ß-specific siRNA abolished lipogenic effects of decreased SFRS10 expression," wrote J. Pihlajamaki and colleagues, Joslin Diabetes Center.
The researchers concluded: "Together, our results indicate that reduced expression of SFRS10, as observed in tissues from obese humans, alters LPIN1 splicing, induces lipogenesis, and therefore contributes to metabolic phenotypes associated with obesity."
Pihlajamaki and colleagues published their study in Cell Metabolism (Expression of the splicing factor gene SFRS10 is reduced in human obesity and contributes to enhanced lipogenesis. Cell Metabolism, 2011;14(2):208-18).
For additional information, contact J. Pihlajamaki, Research Division, Joslin Diabetes Center, Harvard Medical School, Boston, MA 02215, United States.
Keywords: City:Boston, State:Massachusetts, Country:United States, Region:North and Central America, Genetics, Bariatrics, Overnutrition, Diet and Nutrition, Nutrition Disorders.
This article was prepared by Health & Medicine Week editors from staff and other reports. Copyright 2012, Health & Medicine Week via NewsRx.com.
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