Human obesity is a global epidemic, which causes a rapidly increased frequency of diabetes and cardiovascular disease. One reason for obesity is the ready availability of refined food products with high caloric density, an evolutionarily new event, which makes over-consumption of food inevitable. Fat is a food product with high caloric density. The mechanism for regulation of fat intake has therefore been studied to a great extent. Such studies have shown that, as long as fat stays in the intestine, satiety is promoted. This occurs through the fat-released peptide hormones, the best known being CCK (cholecystokinin), which is released by fatty acids. Hence, retarded fat digestion with prolonged time for delivery of fatty acids promotes satiety. Pancreatic lipase, together with its protein cofactor, co-lipase, is the main enzymatic system responsible for intestinal fat digestion. We found that biological membranes, isolated from plants, animals or bacteria, inhibit the lipase/co-lipase-catalysed hydrolysis of triacylglycerols even in the presence of bile salt. We propose that the inhibition is due to binding of lipase/co-lipase to the membranes and adsorption of the membranes to the aqueous/triacylglycerol interface, thereby hindering lipase/co-lipase from acting on its lipid substrate. We also found that chloroplast membranes (thylakoids), when added to refined food, suppressed food intake in rats, lowered blood lipids and raised the satiety hormones, CCK and enterostatin. Consequently, the mechanism for satiety seems to be retardation of fat digestion allowing the fat products to stay longer in the intestine.
Thylakoid membranes (TMs) are uniquely suited for photosynthesis owing to their distinctive structure and composition. Substantial efforts have been directed towards use of isolated photosynthetic reaction centers (PRCs) for solar energy harvesting, however, few studies investigate the communication between whole TMs and electrode surfaces, due to their complex structure. Here we report on a promising approach to generate photosynthesis-derived bioelectricity upon illumination of TMs wired with an osmium-redox-polymer modified graphite electrode, and generate a photocurrent density of 42.4 μA cm(-2).
Thylakoids are membranes isolated from plant chloroplasts which have previously been shown to inhibit pancreatic lipase/colipase catalysed hydrolysis of fat in vitro and induce short-term satiety in vivo. The purpose of the present study was to examine if dietary supplementation of thylakoids could affect food intake and body weight during long-term feeding in mice. Female apolipoprotein E-deficient mice were fed a high-fat diet containing 41% of fat by energy with and without thylakoids for 100 days. Mice fed the thylakoid-enriched diet had suppressed food intake, body weight gain and body fat compared with the high-fat fed control mice. Reduced serum glucose, serum triglyceride and serum free fatty acid levels were found in the thylakoid-treated animals. The satiety hormone cholecystokinin was elevated, suggesting this hormone mediates satiety. Leptin levels were reduced, reflecting a decreased fat mass. There was no sign of desensitization in the animals treated with thylakoids. The results suggest that thylakoids are useful to suppress appetite and body weight gain when supplemented to a high-fat food during long-term feeding.
Photosynthesis is a sustainable process for the conversion of light energy into chemical energy. Thylakoids in energy‐transducing photosynthetic membranes are unique in biological membranes because of their distinguished structure and composition. The quantum trapping efficiency of thylakoid membranes is appealing in photobioelectrochemical research. In this study, thylakoid membranes extracted from spinach are shown to communicate with a gold‐nanoparticle‐modified solid gold electrode (AuNP–Au) through a series of quinone derivatives. Among these, para‐benzoquinone (PBQ) is found to be the best soluble electron‐transfer mediator, generating the highest photocurrent of approximately 130 μA cm−2 from water oxidation under illumination. In addition, the photocurrent density is investigated as a function of applied potential, the effect of light intensity, quinone concentration, and amount of thylakoid membrane. Finally, the source of photocurrent is confirmed by using 3‐(3,4‐dichlorophenyl)‐1,1‐dimethylurea (known by its trade name, Diuron), an inhibitor of photosystem II, which decreases the total photocurrent by 50 %.
A method for preparation of thylakoids from plant leaves on a large scale is described. The method involves: 1) disruption of the cells with a blender followed by filtration to remove large cell debris and non disrupted cells. 2) precipitation of the thylakoids by adjusting the pH to the isoelectric point, pH 4.7. 3) a washing step by dilution of the precipitate in water followed by precipitation at the same pH. 4) concentration of the precipitate by freeze- thawing or freeze -drying to get the final product. The product is characterized, with respect to protein composition, by SDS-PAGE and mass-spectroscopy, the content of carotenoids, particularly the xanthophylls violaxanthin, antheraxanthin, and zeaxanthin. The thylakoid preparation has about the same capacity to inhibit pancreatic lipase/colipase activity as thylakoids prepared by standard laboratory methods using sucrose in the medium and centrifugation. In a study with mice, it was found that, when the thylakoids were added to the food over 32 days, they significantly reduced the body weight gain and the percentage body fat. The large scale method described here allows studies on the effect of thylakoids in appetite regulation on experimental animals in a longer lasting time and also on humans.
Thylakoid membranes, derived from chloroplasts, have previously been shown to retard fat digestion and lower blood glucose levels after oral intake. The purpose of the present study was to investigate the effect of thylakoid membranes on the passage of methyl-glucose, dextran and ovalbumin over rat intestine in vitro using Ussing chambers. The results show that thylakoids retard the passage of each of the test molecules in a dose-dependent way. The thylakoids appear to be attached on the mucosal surface and a mechanism is suggested that the thylakoids delay the passage of the test molecules by sterical hindrance. The present results indicate that thylakoid membranes may be useful both to control intestinal absorption of glucose and to enhance the barrier function of the intestine.
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