Salecan is a recently identified water-soluble viscous extracellular b-1,3-D-glucan polysaccharide from an Agrobacterium species. It is a high-molecular-mass polymer (about 2 £ 10 6 Da) and composed of a linear chain of glucosyl residues linked through a repeat unit of seven b-(1,3) and two a-(1,3) glucosidic bonds. In the present study, we examined the effects of dietary Salecan fed at 2 and 5 % in a high-fat diet (64 % energy) in C57BL/6J mice. After 6 weeks, mice fed 2 and 5 % Salecan had significantly lower body weight, fat mass and percentage of body fat mass compared with those fed a high-fat cellulose (control) diet. Both the Salecan groups significantly and dose-dependently improved glucose tolerance, with a 9 and 26 % reduction of glucose AUC, respectively. Liver and adipose tissue weights were also significantly decreased by the Salecan treatment. Supplementation with 5 % Salecan led to lower serum TAG, total cholesterol (TC) and HDL-cholesterol (52, 18 and 19 %, respectively) and lower hepatic TAG by 56 % and TC by 22 % compared with the high-fat cellulose control group. Dietary Salecan intake caused an obvious elevation of fat in the faeces. Supplementation with Salecan disturbed bile acid-promoted emulsification and reduced the size of emulsion droplets in vitro. These results indicate that Salecan decreases fat absorption, improves glucose tolerance and has biologically important, dose-related effects on reducing high-fat diet-induced obesity.Key words: Salecan: b-Glucans: High-fat diet: Obesity: Glucose tolerance Obesity represents one of the most serious global health issues. Environmental and genetic factors play an important role in the increase in obesity that is affecting the whole of mankind on a large scale. Among these, diet-induced obesity has become one of the most critical medical problems in the world (1) . Obesity is defined medically as a state of increased body weight, more specifically adipose tissue, of sufficient magnitude to produce adverse health consequences (2,3) . The excessive fat accumulation in adipose tissue, liver and other organs strongly predisposes obese individuals to the development of metabolic changes that increase overall morbidity risk. Obesity is associated with insulin resistance (4) , a state of low-grade chronic inflammation (5) and the metabolic syndrome. The metabolic syndrome is related to higher circulating levels of inflammatory markers, many of which enhance tumour growth (6) . Clearly, prevention and management of obesity are relevant to health promotion.The predominant obesity-causing factor is energy imbalance. While pharmaceutical treatments for obesity have been extensively researched, only a few drugs have been approved for long-term use in significantly obese patients by the Food and Drug Administration. However, they have adverse effects including gastrointestinal discomfort, flatulence and diarrhoea (7) . In addition to prescription drugs, nutritional supplements for weight loss are popular in the over-the-counter market. Although suc...
This article is available online at http://www.jlr.org version to active-form retinoic acid, which interacts with the nuclear receptors of the RXR and RAR families, functioning as hormone-activated factors in the regulation of the expression of multiple genes ( 1, 2 ). Also, vitamin A mediates vision cycles through its metabolite, 11-cis retinaldehyde, which is the active chromophore in rhodopsin ( 3, 4 ). Most of the retinoids in the body are accounted for by the retinyl esters stored in the liver ( 5, 6 ). The formation and hydrolysis of retinyl esters are key reactions for maintaining a constant concentration of free retinol in circulation. It has been demonstrated that lecithin:retinol acyltransferase and acylCoA:retinol acyltransferase contribute to the storage of retinoids by the conversion of circulatory free retinol to retinyl esters ( 7,8 ). The enzymes catalyzing the reverse reaction, designated retinyl ester hydrolase (REH), promote the liberation of retinol from stored retinyl esters in the liver into general circulation. Mice fed a vitamin A-defi cient diet for 6 weeks decreased the hepatic retinyl esters ( 9 ), and in vitamin A-defi cient rats, the liver uptake of retinol from blood was obviously impaired ( 10 ). However, the identity, function, and regulation of hepatic enzymes potentially involved in catalyzing the hydrolysis of retinyl esters remain unclear ( 11,12 ).The bile salt-activated carboxylester lipase, an enzyme found in the pancreas and liver cells of several mammalian species, was thought to be the main hepatic REH ( 13 ). Mice defi cient in carboxylester lipase exhibit normal levels of intestinal and hepatic uptake of retinyl esters and maintain REH activity in the liver and pancreas, suggesting that in the mouse liver and pancreas, there is an REH distinct from carboxylester lipase ( 14 ).
Environmental light is involved in the regulation of photochemical reaction in mouse retina. It remains unclear whether light-mediated increase in all-trans retinoic acid (ATRA) synthesis in retina will result in altering the circulatory levels of ATRA and regulating downstream gene expression and physiological function. Here we showed circulatory levels of ATRA decreased in mice under constant darkness and elevated by light exposure. Fat gene pancreatic lipase-related protein 2 (mPlrp2) and its partner procolipase (mClps), but not hepatic lipase (mHl), activated in livers for responding to lack of light illuminating. Light-triggered alterations in circulatory ATRA levels regulated ecto-5'-nucleotidase gene expression by retinoic acid receptor retinoic acid receptor-alpha and modulated 5'-AMP levels in blood and were associated with mPlrp2 and mClps expression in the livers. Mice deficient in adenosine receptors displayed mPlrp2 and mClps expression in livers under 12-h light, 12-h dark cycles. Caffeine blocked adenosine receptors and induced hepatic mPlrp2 and mClps expression in wild-type mice. Mice activated in hepatic mPlrp2 and mClps expression lowered hepatic and serum lipid levels and markedly elevated circulatory levels of all-trans retinol. Our results suggest environmental light influence hepatic lipid homeostasis by light-modulated retinoic acid signaling associated with mPlrp2 and mClps gene expression in livers.
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