Effects of different antipsychotics and the antidepressant mirtazapine on glucose transporter mRNA levels in human blood cells

Heiser, Philip; Singh, Siddharth; Krieg, Jürgen-Christian; Vedder, Helmut

doi:10.1016/j.jpsychires.2005.04.016

Cited by 20 publications

(8 citation statements)

References 22 publications

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“…For example, it was reported that olanzapine but not risperidone increased basal insulin release when applied at 1 μM to isolated pancreatic islets and insulin-secreting INS-1 cells. It was also reported that olanzapine increased glucose transporter 5 mRNA level in human leukemic cell line U937 at 200 μg/ml (640 μM) (Heiser et al, 2006). These findings may explain the increased appetite and weight gain observed in olanzapine-treated patients (Heiser et al, 2006;Melkersson, 2004;Melkersson and Jansson, 2005).…”

Section: Discussionmentioning

confidence: 81%

“…It was also reported that olanzapine increased glucose transporter 5 mRNA level in human leukemic cell line U937 at 200 μg/ml (640 μM) (Heiser et al, 2006). These findings may explain the increased appetite and weight gain observed in olanzapine-treated patients (Heiser et al, 2006;Melkersson, 2004;Melkersson and Jansson, 2005). It was previously reported that glycogen synthesis and insulin signaling in L6 rat skeletal muscle cells were impaired after treatment with 100 μM olanzapine, which may explain the induction of insulin resistance observed in olanzapinetreated patients (Engl et al, 2005).…”

Section: Discussionmentioning

confidence: 81%

“…A number of recent studies have documented the effects of olanzapine and related drugs on insulin secretion from isolated pancreatic islets or insulin-secreting cells (Johnson et al, 2005;Melkersson, 2004;Melkersson and Jansson, 2005) as well as the effect of insulin on peripheral target tissues (Engl et al, 2005;Heiser et al, 2006;Robinson et al, 2006). For example, it was reported that olanzapine but not risperidone increased basal insulin release when applied at 1 μM to isolated pancreatic islets and insulin-secreting INS-1 cells.…”

Section: Discussionmentioning

confidence: 99%

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The Antipsychotic Olanzapine Induces Apoptosis in Insulin-secreting Pancreatic β Cells by Blocking PERK-mediated Translational Attenuation

Ozasa

Okada

Nadanaka

et al. 2013

Cell Struct. Funct.

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ABSTRACT. Patients with schizophrenia receive medication to alleviate various symptoms, but some efficacious second generation antipsychotics, particularly olanzapine, can cause obesity, dyslipidemia, and diabetes mellitus. It has been generally considered that olanzapine contributes to the development of diabetes by inducing obesity and subsequent insulin resistance. In this study, we examined the effect of olanzapine and risperidone, another second generation antipsychotic, on a hamster pancreatic β cell line, and found that both evoked mild endoplasmic reticulum (ER) stress, as evidenced by mild activation of the ER stress sensor molecule PERK. Surprisingly, only olanzapine induced marked apoptosis. Phosphorylation of the α subunit of eukaryotic initiation factor 2, an event immediately downstream of PERK activation, was not observed in cells treated with olanzapine, protein synthesis continued despite PERK activation, and ER stress was thereby sustained. Secretion of insulin was markedly inhibited, and both proinsulin and insulin accumulated inside olanzapine-treated cells. Inhibition of protein synthesis and knockdown of insulin mRNA, which result in less unfolded protein burden, both attenuated subsequent olanzapine-induced apoptosis. Given clinical observations that some patients taking olanzapine exhibit hyperlipidemia and hyperglycemia without gaining weight, our observations suggest that damage to pancreatic β cells may contribute to the undesirable metabolic consequences of olanzapine treatment in some cases.

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Section: Discussionmentioning

confidence: 81%

Section: Discussionmentioning

confidence: 81%

Section: Discussionmentioning

confidence: 99%

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The Antipsychotic Olanzapine Induces Apoptosis in Insulin-secreting Pancreatic β Cells by Blocking PERK-mediated Translational Attenuation

Ozasa

Okada

Nadanaka

et al. 2013

Cell Struct. Funct.

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“…In accordance with a recent study, 24 we found no activating effects of risperidone. Several mechanistic differences of these antipsychotics have been reported in other systems, mostly animal studies, 47–50 but none of these reports concerned the possible mechanisms of antipsychotics that can affect haemostasis.…”

Section: Discussionmentioning

confidence: 99%

IN VITRO EFFECTS OF ANTIPSYCHOTICS ON HUMAN PLATELET ADHESION AND AGGREGATION AND PLASMA COAGULATION

Axelsson

Hägg²,

Eriksson

et al. 2007

Clin Exp Pharma Physio

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1. Several studies suggest an association between venous thromboembolism and the use of antipsychotic drugs, especially clozapine, but the biological mechanisms are unknown. It has been suggested that antipsychotic drugs enhance aggregation of platelets and thereby increase the risk of venous thrombosis. The purpose of the present study was to examine the effects of clozapine and its main metabolite, N-desmethyl clozapine, as well as olanzapine, risperidone and haloperidol, on platelet adhesion and aggregation and on plasma coagulation in vitro. 2. Blood was collected from healthy subjects free of medication. Platelet adhesion to different protein surfaces and aggregation were measured in microplates. The coagulation methods of activated partial thromboplastin time (APTT) and prothrombin time were performed in platelet-poor plasma. 3. Clozapine was the only compound that increased platelet adhesion and aggregation and shortened APTT. The effect appeared at therapeutic concentrations and was significant but weak. 4. This weak effect of clozapine on haemostasis may explain, in part, the association of this compound and venous thromboembolism.

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“…Corresponding Author, E-mail: ccrofts@aut.ac.nz. 1 Medications known to down regulate GLUT4 include: clozapine 72 ; ritonavir 73 ; statins 74 ; and corticosteroids. 75 Plasma insulin is increased by exogenous insulin, insulin secretagogues, or insulin mimetics, prescribed to manage hyperglycemia.…”

mentioning

confidence: 99%

Hyperinsulinemia: Best management practice

et al. 2016

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Chronic hyperinsulinemia associated with insulin resistance is directly and indirectly associated with many metabolic disorders that contribute to significant morbidity and mortality. Because hyperinsulinemia is not widely recognised as an independent health risk, there are few studies that assess management strategies. Medication management may not address the multiple issues associated with hyperinsulinemia. Lifestyle management includes physical activity, especially high intensity interval training, and dietary management. Reducing carbohydrate quantity and increasing nutrient density are discussed with carbohydrate-restricted and Mediterranean diets conferring additional benefits to a low-fat diet. Physical activity and dietary management provide the foundation for hyperinsulinemia management and may work synergistically. Of these principles, a combination of resistance and high intensity interval training, and carbohydrate restriction provide the two most effective frontline management strategies for managing hyperinsulinemia.

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Effects of different antipsychotics and the antidepressant mirtazapine on glucose transporter mRNA levels in human blood cells

Cited by 20 publications

References 22 publications

The Antipsychotic Olanzapine Induces Apoptosis in Insulin-secreting Pancreatic β Cells by Blocking PERK-mediated Translational Attenuation

The Antipsychotic Olanzapine Induces Apoptosis in Insulin-secreting Pancreatic β Cells by Blocking PERK-mediated Translational Attenuation

IN VITRO EFFECTS OF ANTIPSYCHOTICS ON HUMAN PLATELET ADHESION AND AGGREGATION AND PLASMA COAGULATION

Hyperinsulinemia: Best management practice

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