Hüseyin Kamil

Taha Toros Arşivi, Dosya No: 123-Hidiv Ailesiİstanbul Kalkınma Ajansı (TR10/14/YEN/0033) İstanbul Development Agency (TR10/14/YEN/0033

D-Tagatose increases butyrate production by the colonic microbiota in healthy men and women

D-Tagatose is partly absorbed in the stomach and small intestine. Most of it is fermented by the large intestinal microbiota. The effect of D-tagatose on the composition of the microbiota and production of short chain fatty acids (SCFAs) was studied in vivo and in vitro. Gastrointestinal (GI) complaints were also studied. The in vivo study was performed according to a randomized, placebo-controlled, double-blind, five-way cross-over design in healthy subjects (12 men and 18 women). All subjects consumed 30 g raspberry jam containing 7.5 or 12.5 g D-tagatose, 7.8 g fructo-oligosaccharides (positive reference), 7.6 g D-tagatose plus 7.5 g fructo-oligosaccharides, or 15.1 g sucrose (negative reference) at breakfast for 2 weeks in different orders. At the end of each treatment period lipids and safety parameters in blood and GI complaints were evaluated by questionnaires, and faecal microbiota and SCFAs were measured. Furthermore, test-tube incubations of faecal slurries with D-tagatose, fructo-oligosaccharides and sucrose were performed. An in vitro model simulating the large intestine was used to assess the mechanistic effect of D-tagatose on microbiota composition and SCFA production. The high-tagatose treatment resulted in increased numbers of faecal lactobacilli in men, but not in women. Also in vitro, lactobacilli increased. Both the test-tube incubations of fresh faeces from the in vivo study with D-tagatose and the study in the in vitro model showed increased butyrate production after all treatments with D-tagatose. High-tagatose, but not low-tagatose, resulted in a slightly increased defecation frequency and stools of thinner consistency. Only a few GI complaints were reported. The data indicate that daily consumption of 7.5 or 12.5 g D-tagatose may lead to increased production of butyrate and to an increase of lactobacilli, without serious GI complaints. In view of the health-promoting effects of butyrate and lactobacilli, D-tagatose may be considered a prebiotic substrate. © 2005 Taylor & Francis Group Ltd

Effects of sugar intake on body weight: a review

Weight reduction programmes are mainly focused on reducing intake of fat and sugar. In this review we have evaluated whether the replacement of dietary (added) sugar by low-energy sweeteners or complex carbohydrates contributes to weight reduction. In two experimental studies, no short-term differences in weight loss were observed after use of aspartame as compared to sugar in obese subjects following a controlled energy-restricted diet. However, consumption of aspartame was associated with improved weight maintenance after a year. In two short-term studies in which energy intake was not restricted, substitution of sucrose by artificial sweeteners, investigated mostly in beverages, resulted in lower energy intake and lower body weight. Similarly, two short-term studies, comparing the effect of sucrose and starch on weight loss in obese subjects did not find differences when the total energy intake was equal and reduced. An ad libitum diet with complex carbohydrates resulted in lower energy intake compared to high-sugar diets. In two out of three studies, this was reflected in lower body weight in subjects consuming the complex carbohydrate diet. In conclusion, a limited number of relatively short-term studies suggest that replacing (added) sugar by lowenergy sweeteners or by complex carbohydrates in an ad libitum diet might result in lower energy intake and reduced body weight. In the long term, this might be beneficial for weight maintenance. However, the number of studies is small and overall conclusions, in particular for the long term, cannot be drawn

Dietary trans alpha-linolenic acid from deodorised rapeseed oil and plasma lipids and lipoproteins in healthy men: the TransLinE Study.

: Br J Nutr 2001 Mar;85(3):387-92 Related Articles, Books, LinkOut Comment in: Br J Nutr. 2001 Mar;85(3):249-50. Dietary trans alpha-linolenic acid from deodorised rapeseed oil and plasma lipids and lipoproteins in healthy men: the TransLinE Study. Vermunt SH, Beaufrere B, Riemersma RA, Sebedio JL, Chardigny JM, Mensink RP, TransLinE Investigators a. Maastricht University, Department of Human Biology, Maastricht, The Netherlands. TRANS: isomers of alpha-linolenic acid, which are formed by deodorization of refined vegetable oils, can be found in significant amounts in edible oils. Effects of trans alpha-linolenic acid on plasma lipoproteins are unknown. We therefore investigated the effects of trans alpha-linolenic acid on plasma lipids and lipoproteins in healthy European men. Eighty-eight healthy men from three European countries (France, Scotland, UK and the Netherlands) first consumed for 6 weeks a diet with experimental oils 'free' of trans fatty acids (run-in period). For the next 6 weeks, they were randomly allocated to a diet with experimental oils 'high' or 'low' in trans alpha-linolenic acid. Daily total trans alpha-linolenic acid intake in the high trans group was 1410 (range 583-2642) mg. Experimental oils were provided as such, or incorporated into margarines, cheeses, muffins and biscuits. The high trans alpha-linolenic acid diet significantly increased the plasma LDL-:HDL-cholesterol ratio by 8.1 % (95 % CI 1.4, 15.3; and the total cholesterol:HDL-cholesterol ratio by 5.1 % (95 % CI 0.4, 9.9; compared with the low-trans diet. This was largely explained by an increase in LDL-cholesterol on the high-trans diet, while no change was observed in the low-trans group (mean treatment effect of 4.7 % (95 % CI -0.8, 10.5; No effects were found on total cholesterol and HDL-cholesterol, triacylglycerols, apolipoprotein B and A-1, and lipoprotein(a) concentrations. In conclusion, trans alpha-linolenic acid may increase plasma LDL-:HDL-cholesterol and total cholesterol:HDL-cholesterol ratios. Whether diet-induced changes in these ratios truly affects the risk for CHD remains to be established

Alcohol consumption stimulates early stemps in reverse cholesterol transport

Alcohol consumption is associated with increased HDL cholesterol levels, which may indicate stimulated reverse cholesterol transport. The mechanism is, however, not known. The aim of this study was to evaluate the effects of alcohol consumption on the first two steps of the reverse cholesterol pathway: cellular cholesterol efflux and plasma cholesterol esterification. Eleven healthy middle-aged men consumed four glasses (40 g of alcohol) of red wine, beer, spirits (Dutch gin), or carbonated mineral water (control) daily with evening dinner, for 3 weeks, according to a 4 X 4 Latin square design. After 3 weeks of alcohol consumption the plasma ex vivo cholesterol efflux capacity, measured with Fu5AH cells, was raised by 6.2% (P <0.0001) and did not differ between the alcoholic beverages. Plasma cholesterol esterification was increased by 10.8% after alcohol (P = 0.008). Changes were statistically significant after beer and spirits, but not after red wine consumption (P = 0.16). HDL lipids changed after alcohol consumption; HDL total cholesterol, HDL cholesteryl ester, HDL free cholesterol, HDL phospholipids and plasma apolipoprotein A-I all increased (P <0.01). In conclusion, alcohol consumption stimulates cellular cholesterol efflux and its esterification in plasma. These effects were mostly independent of the kind of alcoholic beverage

Alcohol consumption stimulates early steps in reverse cholesterol transport

Alcohol consumption is associated with increased HDL cholesterol levels, which may indicate stimulated reverse cholesterol transport. The mechanism is, however, not known. The aim of this study was to evaluate the effects of alcohol consumption on the first two steps of the reverse cholesterol pathway: cellular cholesterol efflux and plasma cholesterol esterification. Eleven healthy middle-aged men consumed four glasses (40 g of alcohol) of red wine, beer, spirits (Dutch gin), or carbonated mineral water (control) daily with evening dinner, for 3 weeks, according to a 4 x 4 Latin square design. After 3 weeks of alcohol consumption the plasma ex vivo cholesterol efflux capacity, measured with Fu5AH cells, was raised by 6.2% (P < 0.0001) and did not differ between the alcoholic beverages. Plasma cholesterol esterification was increased by 10.8% after alcohol (P = 0.008). Changes were statistically significant after beer and spirits, but not after red wine consumption (P = 0.16). HDL lipids changed after alcohol consumption; HDL total cholesterol, HDL cholesteryl ester, HDL free cholesterol, HDL phospholipids and plasma apolipoprotein A-I all increased (P < 0.01). In conclusion, alcohol consumption stimulates cellular cholesterol efflux and its esterification in plasma. These effects were mostly independent of the kind of alcoholic beverage. Chemicals/CAS: Apolipoprotein A-I; Cholesterol Esters; Cholesterol, 57-88-5; Ethanol, 64-17-5; HDL cholesteryl ester; HDL-triglyceride; Lipoproteins, HDL; Phospholipids; Triglyceride

Alcohol consumption stimulates early stemps in reverse cholesterol transport

Alcohol consumption is associated with increased HDL cholesterol levels, which may indicate stimulated reverse cholesterol transport. The mechanism is, however, not known. The aim of this study was to evaluate the effects of alcohol consumption on the first two steps of the reverse cholesterol pathway: cellular cholesterol efflux and plasma cholesterol esterification. Eleven healthy middle-aged men consumed four glasses (40 g of alcohol) of red wine, beer, spirits (Dutch gin), or carbonated mineral water (control) daily with evening dinner, for 3 weeks, according to a 4 X 4 Latin square design. After 3 weeks of alcohol consumption the plasma ex vivo cholesterol efflux capacity, measured with Fu5AH cells, was raised by 6.2% (P <0.0001) and did not differ between the alcoholic beverages. Plasma cholesterol esterification was increased by 10.8% after alcohol (P = 0.008). Changes were statistically significant after beer and spirits, but not after red wine consumption (P = 0.16). HDL lipids changed after alcohol consumption; HDL total cholesterol, HDL cholesteryl ester, HDL free cholesterol, HDL phospholipids and plasma apolipoprotein A-I all increased (P <0.01). In conclusion, alcohol consumption stimulates cellular cholesterol efflux and its esterification in plasma. These effects were mostly independent of the kind of alcoholic beverage

The effect of dietary trans alpha-linolenic acid on plasma lipids and platelet fatty acid composition: the transline study

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