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PLoS One
2013 Jan 01;811:e79446. doi: 10.1371/journal.pone.0079446.
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Diets containing sea cucumber (Isostichopus badionotus) meals are hypocholesterolemic in young rats.
Olivera-Castillo L, Davalos A, Grant G, Valadez-Gonzalez N, Montero J, Barrera-Perez HA, Chim-Chi Y, Olvera-Novoa MA, Ceja-Moreno V, Acereto-Escoffie P, Rubio-Piña J, Rodriguez-Canul R.
Abstract
Sea cucumber is widely consumed as a putative functional food. It contains many biologically-active substances, but only limited research on its properties in vivo has been done. The effects of different meals containing Isostichopus badionotus, a sea cucumber from southeast Mexico, on growth performance and body lipid profile in young rats were analyzed. Sea cucumber body wall was either lyophilized, cooked (100 °C, 1 h in water) and lyophilized, or oven-dried (70 °C for 12 h). It was then ground and incorporated into cholesterol-containing diets. I. badionotus meals supported growth and improved lipid profile in rats. In particular, serum cholesterol, low density lipoproteins, triglycerides concentration and atherogenic index values were greatly reduced by some I. badionotus containing diets. Liver total lipids, triglycerides and cholesterol were also reduced. Cooking or heat-treatment of the meals lowered but did not abolish their hypolipidemic potency. Gene expression analysis of several key genes involved in cholesterol and lipid metabolism in liver showed that diets containing I. badionotus repressed the induction of key genes associated with dyslipidemia exerted by cholesterol supplementation. Consumption of I. badionotus from the Yucatan Peninsula is beneficial for dyslipidemia, although biological effect is clearly dependent on preparation method.
Figure 1. Body weight in rats during dietary supplementation period.Growth during a 16-day period in rats (63 ± 4 g initial weight) fed equivalent daily amounts of a lactalbumin control diet with no added cholesterol (CNC); a lactalbumin control diet with 2% added cholesterol (CC); a diet containing 50% protein from cooked sea cucumber meal (CS50); one containing 50% protein from oven-cooked sea cucumber (OS50); or one containing 50% protein from lyophilized washed sea cucumber meal (LWS50). Values are means ± SD, N = 5.
Figure 3. Effect of sea cucumber supplementation on expression of genes involved in lipid metabolism, a schematic representation.Rats were fed a lactalbumin control diet with no added cholesterol (CNC); a lactalbumin control diet with 2% added cholesterol (CC); a diet containing 50% protein from cooked sea cucumber meal (CS50); one containing 50% protein from oven-cooked sea cucumber (OS50); or one containing 50% protein from lyophilized washed sea cucumber meal (LWS50) for 16 days. Livers were collected to analyze mRNA expression. Gene expression was determined by RT-PCR analysis. Data were normalized to actin mRNA and fold-change are shown as the mean (n=5) ± SEM. Different letters within individual bar graphs indicate statistical difference (p<0.05). Schematically, increased cellular cholesterol levels leads to decreased cholesterol biosynthesis through the 3-Hydroxy-3-methylglutaryl CoA reductase (HMGCR) pathway and increased cholesterol efflux through the ATP-binding cassette transporter A1 and G1(ABCA1, ABCG1). In hepatocytes cholesterol elimination through the bile is mediated by Cholesterol 7 alpha-hydroxylase (CYP7A1). Excess of free cholesterol can be converted to their oxidized-derivatives the oxysterols, which are the natural ligands of the nuclear receptor Liver X receptor (LXR). LXR regulate the expression of ABCA1, ABCG1 and other enzymes involved in lipogenesis. High density lipoproteins (HDL) can be directly and selectively taken up by the liver via SCARB1. In hepatocytes, excess of lipids can be secreted via apolipoprotein-B (APOB)-containing lipoproteins (very low density lipoprotein [VLDL]). Triglycerides are synthesized from citrate through different enzymes including Acetyl-CoA carboxylase (ACC1) and fatty acid synthase (FASN) through the de novo fatty acid synthesis pathway. The carnitine acyltransferase (CROT) and carnitine palmitoyltransferase (CPT 1A) provide crucial steps in the transport of long fatty acids from the peroxisomes and to the mitochondria, respectively, regulating fatty acid oxidation. The peroxisome proliferator-activated receptors (PPARs) and their cofactors (PPARGC1A and PPARGC1B) can regulate different aspects of lipid and glucose metabolism. The sterol regulatory element binding proteins (SREBPs) can regulate cholesterol homeostasis (SREBP2) and fatty acid biosynthesis (SREBP1c).The carbohydrate-responsive element-binding protein (ChREBP) can regulate glycolysis and de novo fatty acid synthesis in the liver.
Figure 4. Effect of sea cucumber supplementation on expression of genes involved in lipid metabolism, a schematic representation.Rats were fed a lactalbumin control diet with no added cholesterol (CNC); a lactalbumin control diet with 2% added cholesterol (CC); a diet containing 50% protein from cooked sea cucumber meal (CS50); one containing 50% protein from oven-cooked sea cucumber (OS50); or one containing 50% protein from lyophilized washed sea cucumber meal (LWS50) for 16 days. Livers were collected to analyze mRNA expression. Gene expression was determined by RT-PCR analysis. Data were normalized to actin mRNA and fold-change are shown as the mean (n=5) ± SEM. Different letters within individual bar graphs indicate statistical difference (p<0.05). Schematically, increased cellular cholesterol levels leads to decreased cholesterol biosynthesis through the 3-Hydroxy-3-methylglutaryl CoA reductase (HMGCR) pathway and increased cholesterol efflux through the ATP-binding cassette transporter A1 and G1(ABCA1, ABCG1). In hepatocytes cholesterol elimination through the bile is mediated by Cholesterol 7 alpha-hydroxylase (CYP7A1). Excess of free cholesterol can be converted to their oxidized-derivatives the oxysterols, which are the natural ligands of the nuclear receptor Liver X receptor (LXR). LXR regulate the expression of ABCA1, ABCG1 and other enzymes involved in lipogenesis. High density lipoproteins (HDL) can be directly and selectively taken up by the liver via SCARB1. In hepatocytes, excess of lipids can be secreted via apolipoprotein-B (APOB)-containing lipoproteins (very low density lipoprotein [VLDL]). Triglycerides are synthesized from citrate through different enzymes including Acetyl-CoA carboxylase (ACC1) and fatty acid synthase (FASN) through the de novo fatty acid synthesis pathway. The carnitine acyltransferase (CROT) and carnitine palmitoyltransferase (CPT 1A) provide crucial steps in the transport of long fatty acids from the peroxisomes and to the mitochondria, respectively, regulating fatty acid oxidation. The peroxisome proliferator-activated receptors (PPARs) and their cofactors (PPARGC1A and PPARGC1B) can regulate different aspects of lipid and glucose metabolism. The sterol regulatory element binding proteins (SREBPs) can regulate cholesterol homeostasis (SREBP2) and fatty acid biosynthesis (SREBP1c).The carbohydrate-responsive element-binding protein (ChREBP) can regulate glycolysis and de novo fatty acid synthesis in the liver.
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