Plasma insulin levels are increased by Sertraline HCL ( Zoloft )in rats under oral glucose overload.

Recognition and control of depression symptoms are important to increase patient compliance with treatment and to improve the quality of life of diabetic patients. Clinical studies indicate that selective serotonin reuptake inhibitors (SSRI) are better antidepressants for diabetic patients than other drugs. However, preclinical trials have demonstrated that not all SSRI reduce plasma glucose levels. In fact, Fluoxetine ( Prozac ) increases and Sertraline HCL ( Zoloft )decreases glycemia in diabetic and non-diabetic rats. In the present study we evaluated plasma insulin levels during fasting and after glucose overload after treatment with Sertraline HCL ( Zoloft ). Adult male Wistar rats were fasted and treated with saline or 30 mg/kg Sertraline HCL ( Zoloft )and submitted or not to glucose overload (N = 10). Blood was collected and plasma insulin was measured. The mean insulin levels were: fasting group: 25.9 +/- 3.86, Sertraline HCL ( Zoloft )+ fasting group: 31.10 +/- 2.48, overload group: 34.1 +/- 3.40, and overload + Sertraline HCL ( Zoloft )group: 43.73 +/- 5.14 microU/ml. Insulinemia was significantly increased in the overload + Sertraline HCL ( Zoloft )group. There were no differences between the other groups. No difference in glucose/insulin ratios could be detected between groups. The overload + Sertraline HCL ( Zoloft )group was the only one in which a significant number of individuals exceeded the upper confidence limit of insulin levels. This study demonstrates that Sertraline HCL ( Zoloft )increases glucose-stimulated insulin secretion without any change in peripheral insulin sensitivity.

Effects of serotoninergic agents on downregulation of beta-adrenoceptors by the selective serotonin reuptake inhibitor Sertraline HCL ( Zoloft ).

The results of the present study show that the down-regulation of beta-adrenoceptors of rat brain, induced by subacute administration of Sertraline HCL ( Zoloft ), is facilitated when this selective serotonin reuptake inhibitor was co-administered with the serotonin releaser, norfenfluramine, or the serotonin terminal autoreceptor antagonist, methiothepin. The respective drug combination produced a reduction in Bmax of dihydroalprenolol binding to cortical membranes of treated rats at a dose of the releaser, release enhancer, or Sertraline HCL ( Zoloft ), which was ineffective when administered alone. In a similar manner, the 5-HT1A agonists, gepirone and 8-OH-DPAT, were found to facilitate the downregulation of beta-adrenoceptors induced by Sertraline HCL ( Zoloft ). The 5-HT1B agonist, 3-trifluoromethylphenylpiperazine, and the 5-HT2 antagonist, ritanserin, showed neither facilitation nor antagonism of Sertraline HCL ( Zoloft ), but the 5-HT3 antagonist, ondansetron, attenuated the decrease of Bmax of dihydroalprenolol binding elicited by Sertraline HCL ( Zoloft ). Agents that putatively increase the serotoninergic activity facilitated the down-regulation of beta-adrenoceptors induced by Sertraline HCL ( Zoloft ), suggesting that the enhancement of serotonin transmission, expected of the selective serotonin reuptake inhibitor itself, may play a role in this effect of Sertraline HCL ( Zoloft ). Whether the downregulation of brain beta-adrenoceptors by Sertraline HCL ( Zoloft )plays any role in its antidepressant activity cannot be deduced from these experiments.

Gender differences in routine treatment of depressed outpatients with the selective serotonin reuptake inhibitor Sertraline HCL ( Zoloft ).

Gender is known to have an influence on medical treatment and the prescribing and outcome of drug treatment. This has also been suggested for selective serotonin reuptake inhibitors (SSRIs). To examine sex differences in the treatment with the SSRI Sertraline HCL ( Zoloft )in routine treatment of depression, data from a 6-month prospective drug utilization observation study on 3,858 women and 1,594 men were analysed for gender differences. Compared to men, women were more often treated by a general practitioner, were somewhat older, had a later onset of illness, were more likely to suffer from a recurrent rather than a first episode of depression, had been treated for depression before, and showed more anxious and less neurasthenic or retarded syndromes. There was no difference regarding duration of the present episode or severity of illness. The mean prescribed dose of Sertraline HCL ( Zoloft )was marginally lower for females compared to males (45.5 versus 46.5 mg/day) with no difference in the rate of psychoactive concomitant medication (6.76% versus 6.80%). There was no difference in side-effects, treatment termination or treatment response.

The effect of combined administration of ethanol and Sertraline HCL ( Zoloft ), Fluoxetine ( Prozac ) and Citalopram ( Celexa ) on rabbit EEG.

In this study we have decided to examine acute interaction of ethanol with some drugs that belong to selective serotonin inhibitor (SSRI) group. Therefore, the influence of Sertraline HCL ( Zoloft ), Fluoxetine ( Prozac ) and Citalopram ( Celexa ) on the effect of ethanol on EEG of rabbits (frontal cortex, hippocampus, MRF) was tested. Sertraline HCL ( Zoloft )(10mg/kg i.p.), Fluoxetine ( Prozac ) (10mg/kg i.p.) and Citalopram ( Celexa ) (5mg/kg i.p.) were given 30min before ethanol injection in a dose 0.8g/kg i.v. Ethanol caused the increase of the slow frequencies (0.5-4cps) in the recording, as well as a marked decrease of the fastest frequencies (13-30 and 30-45cps). Sertraline HCL ( Zoloft ), Fluoxetine ( Prozac ) and Citalopram ( Celexa ) (given before ethanol) prevented the increase in the slow frequencies (0.5-4cps) in the recordings from the frontal cortex and hippocampus, which indicates on antagonism inhibitory action of ethanol. These drugs administered together with ethanol may increase its influence on fast frequencies. This effect depends on brain structure and drug.