Effect of Some Antidepressants on Glycaemia and Insulin Levels of Normoglycaemic and Alloxan-induced Hyperglycaemic Mice

Erenmemişoğlu, Aydın; Özdoğan, Ümit Kazim; Saraymen, Recep; Tutuş, Ahmet

doi:10.1211/0022357991772899

Cited by 57 publications

(35 citation statements)

References 10 publications

(17 reference statements)

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“…The administration of sertraline reduces glycemia in fasting diabetic mice (14) and decreases fasting and glucose overload glycemia in diabetic and non-diabetic rats (12). However, in the present study, insulinemia was increased by sertraline treatment only after glucose overload.…”

contrasting

confidence: 75%

Plasma insulin levels are increased by sertraline in rats under oral glucose overload

Gomez

Huber

Lhullier

et al. 2001

Braz J Med Biol Res

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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 increases and sertraline 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. Adult male Wistar rats were fasted and treated with saline or 30 mg/kg sertraline 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 + fasting group: 31.10 ± 2.48, overload group: 34.1 ± 3.40, and overload + sertraline group: 43.73 ± 5.14 µU/ml. Insulinemia was significantly increased in the overload + sertraline group. There were no differences between the other groups. No difference in glucose/insulin ratios could be detected between groups. The overload + sertraline 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 increases glucose-stimulated insulin secretion without any change in peripheral insulin sensitivity.

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contrasting

confidence: 75%

Plasma insulin levels are increased by sertraline in rats under oral glucose overload

Gomez

Huber

Lhullier

et al. 2001

Braz J Med Biol Res

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“…First, because the circulating 5-HT concentrations rose, it is possible that 5-HT had a direct effect to reduce glucose uptake by muscle, the predominant insulin-responsive peripheral tissue involved in glucose disposal in the dog. This explanation seems unlikely, however, because peripheral administration of the 5-HT precursor 5-hydroxytryptophan or various selective serotonin reuptake inhibitors to monoamine oxidase inhibitor-treated mice has a hypoglycemic rather than a hyperglycemic effect (24 -27), an action apparently independent of changes in insulin concentrations (25)(26)(27). Moreover, 5-HT Fig.…”

mentioning

confidence: 99%

Portal Serotonin Infusion and Glucose Disposal in Conscious Dogs

Moore

Geho²,

Lautz

et al. 2004

Diabetes

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P oor control of postprandial glycemia in type 2 diabetes is associated with elevated rates of all-cause mortality (1), making postprandial hyperglycemia an attractive pharmaceutical target. Individuals who have type 2 diabetes and receive monoamine oxidase inhibitors demonstrate more frequent episodes of hypoglycemia (2), and those who take selective serotonin reuptake inhibitors have improved glucose tolerance (3) compared with similar individuals who do not take these drugs. Moreover, intraperitoneal administration of serotonin (5-hydroxytryptamine [5-HT]) or its precursor 5-hydroxytryptophan has a hypoglycemic effect in mice (4). 5-HT accumulated in both the liver and the brain of the mice, leaving a question of which tissue was responsible for the hypoglycemia. However, in subsequent studies, the mice were also treated with carbidopa, an inhibitor of peripheral but not central aromatic amino acid decarboxylase. Neither hypoglycemia nor hepatic accumulation of 5-HT was observed in carbidopa-treated mice, although brain levels of 5-HT were even higher than in the absence of carbidopa. Thus, it seemed that hypoglycemia was related to the elevation of hepatic 5-HT (5). We hypothesized that 5-HT can reduce postprandial glycemia by enhancing NHGU and examined this hypothesis in conscious dogs in which the pancreatic hormones and hepatic glucose load (HGL) could be fixed. RESEARCH DESIGN AND METHODSAnimals and surgical procedures. Studies were carried out on 16 conscious 42-h-fasted mongrel dogs of either sex with a mean weight of 24 Ϯ 1 kg. Diet and housing were as previously described (6), and the protocol was approved by the Vanderbilt University Medical Center Animal Care Committee.Approximately 16 days before study, each dog underwent a laparotomy for placement of ultrasonic flow probes around the portal vein and the hepatic artery, as well as for insertion of silicone rubber catheters for sampling in a hepatic vein, the portal vein, and a femoral artery and for infusion into a splenic and a jejunal vein as described in detail elsewhere (6,7). Criteria for study were as previously described (6,7).On the morning of the study, catheters and flow probe leads were exteriorized from their subcutaneous pockets (6,7). The splenic and jejunal catheters were used for intraportal infusion of insulin (Eli Lilly & Co., Indianapolis, IN), glucagon (GlucaGen; Bedford Laboratories, Bedford, OH), and 5-HT (5-HT creatinine sulfate complex; Sigma, St. Louis, MO). Angiocaths (Deseret Medical, Sandy, UT) were inserted into three peripheral veins. Experimental design. Each experiment consisted of a 90-min equilibration period (Ϫ120 to Ϫ30 min), a 30-min basal period (Ϫ30 to 0 min), and a 270-min experimental period (0 to 270 min) divided into four subperiods (P1, 0 -90 min; P2, 90 -150 min; P3, 150 -210 min, and P4, 210 -270 min). At Ϫ120 min, a primed, continuous infusion of [3-3 H]glucose and a continuous infusion of indocyanine green dye (5 g ⅐ kg Ϫ1 ⅐ min Ϫ1 ) were begun in all dogs, with the exception of two that did not re...

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“…Treatment with antidepressants can directly interfere with blood glucose levels or may interact with hypoglycemic agents. In a recent preclinical study it was demonstrated that prolonged treatment with nortriptyline increases blood glucose in diabetic and nondiabetic mice, while fluoxetine and sertraline decrease it (19). Therefore, treatment with antidepressants for diabetic individuals must consider the variability in blood glucose level control at different times and a comparison of the available antidepressant agents is recommended.…”

Section: Introductionmentioning

confidence: 99%

Acute effect of different antidepressants on glycemia in diabetic and non-diabetic rats

Gomez

Huber

Tombini

et al. 2001

Braz J Med Biol Res

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Diabetic patients have a 20% higher risk of depression than the general population. Treatment with antidepressant drugs can directly interfere with blood glucose levels or may interact with hypoglycemic agents. The treatment of depression in diabetic patients must take into account variations of glycemic levels at different times and a comparison of the available antidepressant agents is important. In the present study we evaluated the interference of antidepressants with blood glucose levels of diabetic and non-diabetic rats. In a first experiment, male adult Wistar rats were fasted for 12 h. Imipramine (5 mg/kg), moclobemide (30 mg/kg), clonazepam (0.25 mg/kg), fluoxetine (20 mg/kg) sertraline (30 mg/kg) or vehicle was administered. After 30 min, fasting glycemia was measured. An oral glucose overload of 1 ml of a 50% glucose solution was given to rats and blood glucose was determined after 30, 60 and 90 min. Imipramine and clonazepam did not change fasting or overload glycemia. Fluoxetine and moclobemide increased blood glucose at different times after the glucose overload. Sertraline neutralized the increase of glycemia induced by oral glucose overload. In the second experiment, non-diabetic and streptozotocininduced diabetic rats were fasted, and the same procedures were followed for estimation of glucose tolerance 30 min after glucose overload. Again, sertraline neutralized the increase in glycemia after glucose overload both in diabetic and non-diabetic rats. These data raise the question of whether sertraline is the best choice for prolonged use for diabetic individuals, because of its antihyperglycemic effects. Clonazepam would be useful in cases with potential risk of hypoglycemia.

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Effect of Some Antidepressants on Glycaemia and Insulin Levels of Normoglycaemic and Alloxan-induced Hyperglycaemic Mice

Cited by 57 publications

References 10 publications

Plasma insulin levels are increased by sertraline in rats under oral glucose overload

Plasma insulin levels are increased by sertraline in rats under oral glucose overload

Portal Serotonin Infusion and Glucose Disposal in Conscious Dogs

Acute effect of different antidepressants on glycemia in diabetic and non-diabetic rats

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