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Restricting food intake to a level below that consumed voluntarily (85%, 70% and 50% of the ad libitum energy intake for 3 or 30 days) and re-feeding ad libitum for 48 h results in an increase of malic enzyme (ME) gene expression in rat white adipose tissue. The increase of ME gene expression was much more pronounced in rats main­tained on restricted diet for 30 days than for 3 days. The changes in ME gene expres­sion resembled the changes in the content of SREBP-1 in white adipose tissue. A sim­ilar increase of serum insulin concentration was observed in all groups at different degrees of caloric restriction and refed ad libitum for 48 h. Caloric restriction and refeeding caused on increase of ME activity also in brown adipose tissue (BAT) and liver. However, in liver a significant increase of ME activity was found only in rats maintained on the restricted diet for 30 days. No significant changes after caloric re­striction and refeeding were found in heart, skeletal muscle, kidney cortex, and brain. These data indicate that the increase of ME gene expression after caloric re- striction/refeeding occurs only in lipogenic tissues. Thus, one can conclude that calo­ric restriction/refeeding increases the enzymatic capacity for fatty acid biosynthesis.
The high level of cadmium in the abdominal muscle of the brown shrimp Crangon crangon is due to the serious pollution of the water in the Gulf of Gdańsk. The inhibition of malic enzyme (ME) activity by cadmium, and in consequence the reduced formation of NADPH, could interfere with cellular mechanisms for detoxifying the organism and reducing oxidative stress. The reduced glutathione (GSH) concentration in the abdominal muscle of C. crangon was calculated to be 5.8 mM. The objective of this study was to evaluate the part played by GSH in the effect of cadmium on the activity of NADP-dependent malic enzyme from abdominal muscles of brown shrimps. This enzyme is activated by certain divalent cations (Mg, Mn). The results demonstrate that cadmium inhibits ME activity from shrimp muscle, and that GSH and albumin can reduce this cadmium-inhibited NADP-dependent malic enzyme activity.
Weight cycling is one of the widely used weight reduction strategies; however, the adverse effects of this method include regaining significant amounts of weight. The molecular mechanisms underlying weight gain following cycles of dietary deprivation and refeeding are still poorly understood. One of the possibilities is that repeated loss and gain of weight may promote fat deposition in adipose tissue. To test this hypothesis we investigated serum leptin levels and lipogenic enzyme activities in white adipose tissue (WAT) of male Wistar rats during 12 days of ad libitum feeding following multiple cycles of alternating food deprivation and refeeding. Rats subjected to eight cycles of food deprivation and refeeding (MFR group) showed significantly decreased circulating leptin levels when compared with control rats (nearly 50% decrease in leptin levels, P < 0.01). Throughout 12 days of ad libitum feeding, serum leptin levels increased modestly but remained significantly (24%, P < 0.05) lower than control levels. Fatty acid synthase (FAS) and malic enzyme (ME) activities (chosen as representatives of enzymes directly involved in fatty acid synthesis) were found to be considerably higher in WAT of MFR rats refed for 3 days in comparison to control rats, and remained elevated even after 12 days of refeeding. These observations suggest that the elevation of lipogenic enzyme activities induced by multiple cycles of dietary deprivation followed by refeeding persists for several days, markedly increasing the lipogenic capacity of adipose tissue, which, accompanied by a decrease in circulating leptin levels, may promote weight gain.
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