Estrogen augments serotonergic activity in postmenopausal women.

To investigate the influence of estrogen replacement on serotonergic activity in postmenopausal women, the serotonin agonist meta-chlorophenylpiperazine (m-CPP) (0.5 mg/kg) was given orally to 18 normal postmenopausal women, 11 of whom were also tested following 30 days' treatment with estrogen transdermal patches (estraderm 0.1 mg).

Insulin stimulates glucose transport in isolated human adipose cells through a translocation of intracellular glucose transporters to the plasma membrane: a preliminary report.

Insulin's effect on glucose transport activity and the subcellular distribution of glucose transporters have been examined in isolated human abdominal adipose cells, by measuring 3-O-methylglucose transport and specific D-glucose-inhibitable cytochalasin B binding to plasma membranes and low-density microsomes, respectively. Insulin appears to stimulate glucose transport in isolated human adipose cell through the translocation of glucose transporters from a large intracellular pool to the plasma membrane as initially postulated for rat adipose and muscle cells.

Stability of lactate dehydrogenase at different storage temperatures.

The effect of storing human serum, cord blood serum or heparinized plasma at 25 degrees C, 4 degrees C & -20 degrees C on the activity and isoenzyme distribution of lactate dehydrogenase (LD) was studied. Cellulose acetate and agarose electrophoresis, as well as an immunochemical inhibition technique, were used for isoenzyme quantification. In contrast to previous reports, cryo-instability was found only in specimens stored at 4 degrees C.

Mechanism of insulin's stimulatory action on glucose transport in the isolated rat adipose cell.

The mechanism by which insulin stimulates glucose transport in the rat adipose cell has been shown to be a rapid, reversible, and energy-dependent process. Stimulation is achieved by the translocation of glucose transporters from an intracellular pool to the plasma membrane where their insertion is ultimately responsible for the increase in transport activity. The reversal of this process also occurs rapidly at 37 degrees C, with the transporters reappearing in the intracellular pool.

Insulin-induced translocation of intracellular glucose transporters in the isolated rat adipose cell.

Three techniques have now been used to demonstrate that insulin stimulates glucose transport in isolated rat adipose cells through the translocation of glucose transporters from a large intracellular pool to the plasma membrane. By using a specific D-glucose-inhibitable cytochalasin B-binding assay, most of the basal cell's transporters are found associated with a low-density microsomal membrane fraction. However, although Golgi marker enzyme activities are also enriched in this fraction, their distributions over all fractions do not parallel that of the transporters.