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Beta cell content

Thakkar SK, Maziya-Dixon B, Dixon AG and Failla ML. 2007. Beta-carotene micellarization during in vitro digestion and uptake by Caco-2 cells is directly proportional to beta-carotene content in different genotypes of cassava. J Nutr 137 2229-2233. [Pg.220]

Commercially significant zeolites include the synthetic zeolites type A (LTA), X (FAU), Y (FAU), L (LTL), mordenite (MOR), ZSM-5 (MFI), beta ( BEA/BEC), MCM-22 (MTW), zeolites E (EDI) andW (MER) and the natural zeolites mordenite (MOR), chabazite (CHA), erionite (ERl) and clinoptiloUte (HEU). Details of the structures of some of these are given in this section. Tables in each section lists the type material (the common name for the material for which the three letter code was established), the chemical formula representative of the unit cell contents for the type material, the space group and lattice parameters, the pore structure and known mineral and synthetic forms. [Pg.35]

Insulin is released into the blood from the beta cells in the pancreas in response to the rise in blood sugar following a meal. The amount released is to some degree related to the amount of body fat the larger the adipose tissue content of the body, the greater the insulin release (Heini et al. 1998). [Pg.10]

Chronic exposure to free fatty acid reduces pancreatic beta cell insulin content by increasing basal insulin secretion that is not compensated for by a corresponding increase in proinsulin biosynthesis translation. [Pg.15]

Wells, L.J., Lazarow, A. Organ cultures of pancreases of fetuses from diabetic rats Effects of high-glucose media upon the granulation of the beta cells and upon the insulin content of the media. Diabetes 16, 846-851 (1967)... [Pg.535]

In view of the rapid rate at which alloxan is destroyed within the body (24) (half-life of about 1 min.) it seems doubtful w hether an increased rate of destruction of alloxan within the liver or kidney (occurring as a consequence of an increased GSH content) would materially affect the amount of alloxan reaching the beta cell. Inasmuch as thiouracil treatment increased the GSH content of the liver and kidney without changing the blood GSH level (34), it seems probable that the increased resistance to alloxan which follows thiouracil treatment is due to a parallel increase in the concentration of GSH within the beta cell. [Pg.236]

On the basis of theoretical considerations, it had been su ested that the beta cell may have a low GSH content (44). The synthesis of insulin by the beta cell appears to be dependent upon a continuous supply of sulfur-amino acids, for when rabbits are placed on a cystine-methionine-deficient diet the insulin content of the pancreas is decreased (32). Insulin, in contrast to most other proteins, contains 12 % cystine (45). Since cysteine or its oxidized derivative, cystine, is a constituent of both GSH and of insulin, there may well be competition for this amino acid within the beta cell. Thus the GSH concentration within the beta cell may be low as a consequence of insulin synthesis (44). Furthermore, the oxidation-reduction potential in the beta cell may favor the oxidation of GSH to its oxidized form (GSSG) (44). Both of these factors would increase the susceptibility of the beta cells to alloxan, for it is the reduced form of GSH which reacts with alloxan (26). [Pg.236]

Since alloxan, in doses greater than that required to produce diabetes, likewise destroys the liver, kidney (13, 15, 55), and adrenal cortical (56) cells as well as the beta cells, it would be difficult to attribute the diabetogenic mechanism of alloxan to an inactivation of a specialized enzyme system which is present only in the beta cells. If alloxan inactivates an essential sulfhydryl enzyme or coenzyme which is widely distributed, then selective beta-cell destruction could be due to a low GSH content, to a more rapid uptake of alloxan, or to a less rapid rate of destruction of alloxan within the beta cells. Larger doses of alloxan would produce widespread necrosis. [Pg.237]

If diabetogenic compounds similar to alloxan or dehydroascorbic acid contribute to the progressive destruction of the beta cells in Uie partially depancreatized animal, then one would expect that the GSH which is present within these cells would likewise protect them. It was therefore important to determine whether the factors which influence the GSH content of the blood and tissues could likewise influence the rate of onset and progression of diabetes in the partially depancreatized animals. [Pg.240]

The aluminum content of the as-synthesized zeolites also influences their X-ray powder diffraction pattern. The height of the main peak in the patterns decreases with decreasing Si/Al ratio in the zeolite, but their width increases simultaneously so that the area remains practically constant for all samples. On the other hand, the dhki distance corresponding to the diffraction peak at 43 of 20 correlated linearly with the aluminum content of the zeolite (Figure 4). However, the lack of knowledge of the crystal structure of Beta zeolite makes it impossible to correlate the Al content and unit cell parameters. [Pg.54]

Molvig, J., Pociot, F., Worsaae, H., Wogensen, L.D., Baek, L., Christensen, P., Mandrup-Poulsen, T., Andersen, K., Madsen, P., and Dyerberg, J., Nerup, J. 1991. Dietary supplementation with omega-3-polyunsaturated fatty acids decreases mononuclear cell proliferation and interleukin-1 beta content but not monokine secretion in healthy and insulin-dependent diabetic individuals. Scand. J. Immunol. 34, 399-A10. [Pg.136]


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See also in sourсe #XX -- [ Pg.269 ]




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