Abstract
BackgroundShort-term OE (oleoyl-estrone) treatment causes significant decreases in rat weight mainly due to adipose tissue loss. The aim of this work was to determine if OE treatment affects the expression of genes that regulate lipid metabolism in white adipose tissue.ResultsGene expression in adipose tissue from female treated rats (48 hours) was analysed by hybridization to cDNA arrays and levels of specific mRNAs were determined by real-time PCR. Treatment with OE decreased the expression of 232 genes and up-regulated 75 other genes in mesenteric white adipose tissue. The use of real-time PCR validate that, in mesenteric white adipose tissue, mRNA levels for Lipoprotein Lipase (LPL) were decreased by 52%, those of Fatty Acid Synthase (FAS) by 95%, those of Hormone Sensible Lipase (HSL) by 32%, those of Acetyl CoA Carboxylase (ACC) by 92%, those of Carnitine Palmitoyltransferase 1b (CPT1b) by 45%, and those of Fatty Acid Transport Protein 1 (FATP1) and Adipocyte Fatty Acid Binding Protein (FABP4) by 52% and 49%, respectively. Conversely, Tumour Necrosis Factor (TNFα) values showed overexpression (198%).ConclusionShort-term treatment with OE affects adipose tissue capacity to extract fatty acids from lipoproteins and to deal with fatty acid transport and metabolism.
Highlights
Short-term OE treatment causes significant decreases in rat weight mainly due to adipose tissue loss
Since OE is synthesized from estrone by adipose cells [3] and released into the bloodstream, where its concentrations correlates with body fat mass [4,5], OE has been postulated as a lipostatic signal regulating body fat mass
The expression profile of the 1168 genes included in the specific Atlas Rat Array 1.2 (Clontech) was analyzed in the mesenteric white adipose tissue from control animals and treated with oleoyl-estrone
Summary
Short-term OE (oleoyl-estrone) treatment causes significant decreases in rat weight mainly due to adipose tissue loss. The short-term effects of OE treatment in rats, involve the decrease in food intake, a decrease in body weight and an impressive decrease of cholesterol levels, mainly due to the sharp decrease of HDL-cholesterol that results in an increased cholesterol turnover rate [6]. This pattern has been reproduced in obese humans [7]. The involvement of receptors different from classic estrogen receptors has been proposed [9], it seems that the mechanism involves pathways other than those activated by forced food restriction, as pair-fed models [11]
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