SOY LECITHIN POWDER 99% OIL FREE
Dietary lecithin protects against cholestatic liver disease in cholic acid-fed Abcb4- deficient mice
1: Pediatr Res. 2007 Feb;61(2):185-90
Dietary lecithin protects against cholestatic liver disease in cholic acid-fed Abcb4- deficient mice.
Unite de recherche en gastroenterologie-nutrition, Research Centre, CHU Sainte-Justine, Montreal, Quebec H3T 1C5, Canada.
Mutations in multidrug resistance 3 gene (MDR3 or ABCB4) underlie progressive familial intrahepatic cholestasis type 3 (PFIC3), a severe pediatric liver disease progressing to cirrhosis. Abcb4-/- mice exhibit slowly developing hepatic lesions that can be accelerated by feeding a cholic acid (CA)-supplemented diet. We investigated the beneficial effects of a soybean lecithin (L)-supplemented diet in this model of liver disease. Abcb4-/- mice and wild-type (WT) controls were divided in four groups by the diet they were fed: control (C) diet, L-supplemented diet, CA-supplemented diet, and L- and CA-supplemented (L+CA) diet. After 2 wk on these regimens, liver enzymes and bilirubin were measured in serum with bile flow, total bile acids, and cholesterol (CHOL) and phospholipid (PL) concentrations in bile. Ductular hyperplasia, portal fibroblastic cell proliferation, myofibroblast activation, and hepatic fibrosis were quantified on liver sections. Abcb4-/- mice fed the C diet exhibited mild liver damage. CA produced very high elevations of serum liver enzymes and bilirubin with significant bile duct proliferation, peribiliary fibroblast activation, and fibrosis. The L-supplemented diet dramatically mitigated the hepatic damage in CA-supplemented diet animals. We conclude that L is protective against liver disease in Abcb4-/- mice and suggest that it could offer potential benefit in PFIC3.
PMID: 17237720 [PubMed - in process
The role of dietary choline in the beneficial effects of lecithin on the secretion of biliary lipids in rats
1: Biochim Biophys Acta. 1998 Aug 28;1393(2-3):223-34.
The role of dietary choline in the beneficial effects of lecithin on the secretion of biliary lipids in rats.
Department of Nutrition, Universite de Montreal, Que., Canada.
Earlier studies showed that dietary soybean lecithin increases biliary lipid secretion, which mainly comes from the contribution of high density lipoprotein (HDL) and hepatic microsomal pools of phosphatidylcholine and cholesterol. In addition, a lecithin diet enhances bile secretion and prevents bile acid-induced cholestasis. This study evaluated the contribution of choline, a component of lecithin, to the observed effect of lecithin on biliary secretory function. Rats were fed either a control diet (CD), a choline diet (ChD) or a lecithin-enriched diet (LD) for 2 weeks. Results showed that like LD, ChD induced an increase in bile flow and bile acid secretion rate when compared with the control diet. However, unlike LD, ChD did not significantly increase biliary phospholipids and cholesterol output. An increase of hydrophilic bile acids (i.e. ursodeoxycholic and muricholic acids) in bile of rats fed choline could explain why the biliary phospholipid and cholesterol secretion was not increased. During taurocholic acid infusion, both experimental diets increased bile flow and the bile acid secretion rate maximum (BASRm). The cholestasis usually observed after the BASRm is reached was inhibited by ChD and LD. Both diets induced a decrease in plasma cholesterol (total and HDL), however, only LD induced statistically significant changes. Analysis of total cholesterol and phospholipid content of microsomes and canalicular membranes indicated no statistically significant difference between control and experimental groups either under basal conditions or after bile acid infusion. Similarly, the phospholipid classes and fatty acid composition of biliary phosphatidylcholine were not altered by feeding ChD and LD. We conclude that choline contributes to the beneficial effect of a lecithin diet on bile secretion. It is postulated that this effect may be attributed to modulation of HDL and an enhancement of the cholesterol and phospholipid pools destined for biliary secretion.
PMID: 9748591 [PubMed - indexed for MEDLINE]
Alterations in lipoprotein defense against oxidative stress in metabolic syndrome
1: Curr Atheroscler Rep. 2006 Nov;8(6):501-9.
Alterations in lipoprotein defense against oxidative stress in metabolic syndrome.
Service d'Endocrinologie-Metabolisme, Pavillon Benjamin Delessert, Hopital de la Pitie, 83 Boulevard de l'Hopital, 75651 Paris Cedex 13, France. boris.hansel@odessaglobe.com
Metabolic syndrome (MetS) is a high-risk condition for premature atherosclerotic vascular disease. Patients with MetS display a lipoprotein profile in which dense low-density lipoproteins (LDL), which are more susceptible to oxidation, predominate. Oxidation of lipoproteins can be attenuated in vivo by enzymatic and nonenzymatic antioxidant defenses, but high-density lipoproteins (HDL) play a key role in the protection of LDL from oxidation. Such activity depends on the presence of apolipoproteins (apoA-I, apoA-II, apoA-IV, apoE) and enzymes (paraoxonase 1, platelet activating factor-acetylhydrolase, lecithin:cholesterol acyltransferase, glutathione peroxidase). The impairment of HDL antioxidative activity in MetS is partly related to an enrichment of small HDL in triglycerides and their depletion in cholesteryl esters, to the replacement of apoA-I by serum amyloid A, and to glycation and oxidation of apoA-I. Therapeutic normalization of the quantity and the quality of HDL particles may constitute a novel approach to attenuate atherosclerosis and cardiovascular risk in MetS.
PMID: 17045077 [PubMed - indexed for MEDLINE]
Reduced lecithin: retinol acyltransferase expression correlates with increased pathologic tumor stage in bladder cancer.
: Clin Cancer Res. 2004 May 15;10(10):3429-37.
Reduced lecithin: retinol acyltransferase expression correlates with increased pathologic tumor stage in bladder cancer.
Department of Urology, New York Presbyterian Hospital-Weill-Cornell Medical Center, New York, New York 10021, USA.
PURPOSE: Retinoids, which include vitamin A (retinol; ROL) and its derivatives, have been investigated in the treatment of bladder cancer. We have shown that expression of the enzyme lecithin:ROL acyltransferase (LRAT), which converts ROL to retinyl esters, is reduced in several human cancers. Here we evaluated expression of LRAT protein and mRNA in normal and malignant bladder tissue specimens from human patients. We also examined the effect of retinoids on LRAT expression in bladder cancer cell lines. EXPERIMENTAL DESIGN: We evaluated 49 bladder cancer specimens for LRAT protein expression using immunohistochemistry with affinity-purified antibodies to human LRAT. LRAT mRNA expression was assessed using reverse transcription-PCR in bladder specimens from an additional 16 patients. We examined the effect of retinoic acid and ROL on LRAT mRNA expression in five human bladder cancer cell lines. RESULTS: LRAT protein was detected throughout the nonneoplastic bladder epithelium in all of the specimens. In bladder tumors, LRAT protein expression was reduced compared with the nonneoplastic epithelium or was completely absent in 7 of 32 (21.9%) superficial tumors versus 16 of 17 (94.1%) invasive tumors (P < 0.001). All of the non-neoplastic bladder specimens tested (11 of 11) showed LRAT mRNA expression, compared with 5 of 8 (62%) superficial tumors and 0 of 5 (0%) invasive tumors (P = 0.001). Three of five human bladder cancer cell lines expressed LRAT mRNA independent of retinoid exposure, whereas in two cell lines LRAT mRNA expression was induced by retinoid treatment. CONCLUSIONS: We report a significant reduction in LRAT expression in bladder cancer. Moreover, we demonstrate an inverse correlation of LRAT mRNA and protein expression with increasing tumor stage. These data suggest that loss of LRAT expression is associated with invasive bladder cancer.
PMID: 15161698 [PubMed - indexed for MEDLINE]
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Effects of ingesting soy or egg lecithins on serum choline, brain choline and brain acetylcholine
: J Nutr. 1981 Jan;111(1):166-70.
Effects of ingesting soy or egg lecithins on serum choline, brain choline and brain acetylcholine.
Rats were fed lecithins, derived from eggs or soybeans, to determine whether the fatty acid composition of the phosphatidylcholine altered choline availability. Rats were fed either a single meal containing 5 g phosphatidylcholine or a lecithin-containing diet for 3 weeks, including approximately 5 g phosphatidylcholine per day. Each form of dietary lecithin elevated blood choline, brain choline and brain acetylcholine significantly (P < 0.05). There was no difference in response to egg- or soy-derived lecithin.
PMID: 7192727 [PubMed - indexed for MEDLINE]
Lecithin consumption increases acetylcholine concentrations in rat brain and adrenal gland
1: Science. 1978 Oct 13;202(4364):223-5.
Lecithin consumption increases acetylcholine concentrations in rat brain and adrenal gland.
Consumption of a single meal containing lecithin, the major source of choline occurring naturally in the diet, increased the concentrations of choline and acetylcholine in rat brain and adrenal gland. Hence, the concentration of acetylcholine in the tissues may normally be under direct, short-term nutritional control.
PMID: 694529 [PubMed - indexed for MEDLINE]
