No abstract

Five days of treatment by DEX and a dose of 0.75 mg/kg/d induced a marked catabolic state.

Aged rats are more sensitive to injury, possibly through an impairment of nitrogen and glutamine (Gln) metabolisms mediated by glucocorticoids. We studied the metabolic kinetic response of adult and old rats during glucocorticoid treatment. The male Sprague-Dawley rats were 24 or 3 mo old. Both adult and old rats were divided into 7 groups. Groups labeled G3, G5, and G7 received, by intraperitoneal injection, 1.50 mg/kg of dexamethasone (Dex) for 3, 5, and 7 days, respectively. Groups labeled G3PF, G5PF, and G7PF were pair fed to the G3, G5, or G7 groups and were injected with an isovolumic solution of NaCl. One control group comprised healthy rats fed ad libitum. The response to aggression induced specifically by Dex (i.e., allowing for variations in pair-fed controls) appeared later in the aged rats (decrease in nitrogen balance from day 1 in adults but only from day 4 in old rats). The adult rats rapidly adapted to Dex treatment, whereas the catabolic state worsened until the end of treatment in the old rats. Gln homeostasis was not maintained in the aged rats; despite an early increase in muscular Gln synthetase activity, the Gln pool was depleted. These results suggest a kinetic impairment of both nitrogen and muscle Gln metabolisms in response to Dex with aging.

The procyanidolic oligomers coming from Vitis vinifera L. (two fractions) and Cupressus sempervirens L. (three fractions), and the monomers, (+)-catechin, (-)-epicatechin were tested for their effects on angiotensin I converting enzyme (ACE) activity. The oligomers are the most active (dose '5U of 0.08 mg/mI for the fraction A of Vitis, the most active substance). Monomers have little activity. In vivo, the vasopressive response to Ang I is inhibited by approximately 20% to 40 % in the rabbit after administration of procyanidolic oligo

An impairment of muscle glutamine metabolism in response to dexamethasone (DEX) occurs with aging. To better characterize this alteration, we have investigated muscle glutamine release with regard to muscle glutamine production (net protein breakdown, de novo glutamine synthesis) in adult and old glucocorticoid-treated rats. Male Sprague-Dawley rats (3 or 24 mo old) were divided into seven groups: three groups received 1.5 mg/kg of DEX once a day by intraperitoneal injection for 3, 5, or 7 days; three groups were pair fed to the three treated groups, respectively; and one control group of healthy rats was fed ad libitum. Muscle glutamine synthetase activity increased earlier in old rats (day 3) than in adult rats (day 7), whereas an increase in muscle glutamine release occurred later in old rats (day 5) than in adult DEX-treated rats (day 3). Consequently, muscle glutamine concentration decreased later in old rats (day 5) than in adults (day 3). Finally, net muscle protein breakdown increased only in old DEX-treated rats (day 7). In conclusion, the impairment of muscle glutamine metabolism is due to a combination of an increase in glutamine production and a delayed increase in glutamine release.