The association between antidepressant use and hypoglycaemia in diabetic patients: a nested case–control study

Derijks, Hieronymus J.; Heerdink, Eibert R.; Koning, Fred H. De; Janknegt, Robert; Klungel, Olaf H.; Egberts, A.C.G.

doi:10.1002/pds.1562

Cited by 37 publications

(43 citation statements)

References 42 publications

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“…, 1997;Rubin et al, 2008;Brown et al, 2008;Derijks et al, 2008;Andersohn et al, 2009;Kivimäki et al, 2010;Khoza et al, 2011).…”

Section: Antidepressants Are Cytotoxic To Min6unclassified

“…However, clinical studies indicate that the tricyclic antidepressant (TCA) and serotonin selective reuptake inhibitor (SSRI) classes of AD are particularly associated with increased risks of hyperglycaemia and type 2 diabetes mellitus (T2D) (Lustman et al, 1997;Rubin et al, 2008;Brown et al, 2008;Derijks et al, 2008;Andersohn et al, 2009;Kivimäki et al, 2010;Khoza et al, 2011). Although weight gain is a common side effect of AD usage (Uguz et al, 2015) and a risk factor for T2D (Andersohn et al, 2009;Kivimäki et al, 2010;), when weight is controlled for, ADs still increase T2D risk (Rubin et al, 2008;Pan et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

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Editor’s Highlight: Therapeutic Concentrations of Antidepressants Inhibit Pancreatic Beta-Cell Function via Mitochondrial Complex Inhibition

Elmorsy

Al‐Ghafari

Helaly

et al. 2017

Toxicological Sciences

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Diabetes mellitus risk is increased by prolonged usage of antidepressants (ADs). Although various mechanisms are suggested for their diabetogenic potential, whether a direct effect of ADs on pancreatic β-cells is involved is unclear. We examined this idea for three ADs:paroxetine, clomipramine and, with particular emphasis, fluoxetine, on insulin secretion, mitochondrial function, cellular bioenergetics, K ATP channel activity and caspase activity in murine and human cell-line models of pancreatic β-cells. Metabolic assays showed that these ADs decreased the redox, oxidative respiration and energetic potential of β-cells in a time and concentration dependent manner at concentrations (100 nM) well within their plasma therapeutic window. These effects were related to inhibition of mitochondrial complex I and III activity.Consistent with impaired mitochondrial function, lactate output was increased and insulin secretion decreased. Neither fluoxetine, antimycin nor rotenone could reactivate K ATP channel activity blocked by glucose unlike the mitochondrial uncoupler, FCCP. Chronic, but not acute, AD increased oxidative stress and activated caspases, 3, 8 and 9. To conclude, paroxetine, clomipramine and fluoxetine were all found to be cytotoxic at therapeutic concentrations on pancreatic beta-cells; an action suggested to arise by inhibition of mitochondrial bioenergetics, oxidative stress and induction of apoptosis. These actions may help explain the diabetogenic potential of these ADs in humans.

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“…, 1997;Rubin et al, 2008;Brown et al, 2008;Derijks et al, 2008;Andersohn et al, 2009;Kivimäki et al, 2010;Khoza et al, 2011).…”

Section: Antidepressants Are Cytotoxic To Min6unclassified

Section: Introductionmentioning

confidence: 99%

Editor’s Highlight: Therapeutic Concentrations of Antidepressants Inhibit Pancreatic Beta-Cell Function via Mitochondrial Complex Inhibition

Elmorsy

Al‐Ghafari

Helaly

et al. 2017

Toxicological Sciences

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“…Such changes in emotion are usually associated with a decreased self-reported energy level and self-efficacy that can degrade cognitive performance. Of particular importance is that in depression, selective serotonin reuptake inhibitors are associated with a progressively increased risk of severe hypoglycemia (58). Other types of antidepressants may be more appropriate for diabetic individuals with high risk of severe hypoglycemia.…”

Section: Anxiety and Depressionmentioning

confidence: 99%

Glycemic Control and Hypoglycemia

et al. 2008

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“…In contrast to the studies linking antidepressants use and increased risk for diabetes, recent studies report that use of antidepressants may increase the risk for hypoglycemia [8,9]. A recent analysis of spontaneous reports in the World Health Organization (WHO) Adverse Drug Reaction Database showed that use of antidepressants increases the risk for both hyperglycemia and hypoglycemia [9].…”

Section: Introductionmentioning

confidence: 98%

Glucose dysregulation associated with antidepressant agents: an analysis of 17 published case reports

Khoza

Barner

2011

Int J Clin Pharm

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It is not clear from published case reports whether changes in glucose regulation, following antidepressant therapy initiation are due to antidepressants or changes in mood and lifestyle. Nonetheless, healthcare providers should be aware of the potential changes in glucose regulation especially in the first month of antidepressant therapy, and use appropriate clinical and laboratory monitoring to prevent serious adverse events in patients at risk.

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The association between antidepressant use and hypoglycaemia in diabetic patients: a nested case–control study

Abstract: It is important for diabetic patients using antidepressants for more than 3 years to pay attention for symptoms of hypoglycaemia and strict blood glucose self-monitoring.

Cited by 37 publications

References 42 publications

Editor’s Highlight: Therapeutic Concentrations of Antidepressants Inhibit Pancreatic Beta-Cell Function via Mitochondrial Complex Inhibition

Editor’s Highlight: Therapeutic Concentrations of Antidepressants Inhibit Pancreatic Beta-Cell Function via Mitochondrial Complex Inhibition

Glycemic Control and Hypoglycemia

Glucose dysregulation associated with antidepressant agents: an analysis of 17 published case reports

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