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Review
. 2023 Aug 31;15(1):179.
doi: 10.1186/s13098-023-01149-z.

Antidepressants and type 2 diabetes: highways to knowns and unknowns

Nahi Sabih Alruwaili  1 , Hayder M Al-Kuraishy  2 , Ali I Al-Gareeb  2 , Ali K Albuhadily  2 , Amany E Ragab  3 , Ahmad Awad Alenazi  4 , Athanasios Alexiou  5   6 , Marios Papadakis  7 , Gaber El-Saber Batiha  8
Affiliations
Review

Antidepressants and type 2 diabetes: highways to knowns and unknowns

Nahi Sabih Alruwaili et al. Diabetol Metab Syndr. .

Abstract

Type 2 diabetes (T2D) is a metabolic disease caused by the development of insulin resistance (IR), relative insulin deficiency, and hyperglycemia. Hyperglycemia-induced neurochemical dysregulation activates the progression of depression in T2D patients. Therefore, management of depression by antidepressant agents improves glucose homeostasis and insulin sensitivity. However, prolong use of antidepressant drugs may increase the risk for the development of T2D. However, there is strong controversy concerning the use of antidepressant drugs in T2D. Therefore, this review try to elucidate the potential effects of antidepressant drugs in T2D regarding their detrimental and beneficial effects.

Keywords: Antidepressants; Depression; Type 2 diabetes.

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Conflict of interest statement

The authors declare no competing interests.

Figures

Fig. 1
Fig. 1
The link between depression and T2D: Biological burden such as central insulin resistance, and psychological burden such as disability in diabetes increase risk of depression. Inflammation and increase the activity of hypothalamic-pituitary-adrenal (HPA) axis in depression increase risk for diabetes
Fig. 2
Fig. 2
 A) Pathophysiology of depression: Tryptophan (Trp) is converted to 5-hyroxytryptamine (5HT). Over-expression of pre-synaptic 5HT1A which inhibit the release of 5HT from presynaptic neurons or down-regulation of 5HT1A heteroreceptors which mediate action of 5HT at postsynaptic neurons, leading to the reduction of glutamate (Glu) and upregulation of N-methyl-D-aspartate (NMDA) receptors and upregulation of amino-methyl propionic acid (AMPA) receptors. These changes reduce expression of brain-derived neutrophic factor (BDNF) and impairment of neuronal plasticity. B) How insulin modulates the effect of 5-HT at the molecular level: insulin by binding to insulin receptors results in increase in the synthesis of BDNF and neuronal plasticity as mediated through protein kinase B and its action on m-TOR (mechanistic target of rapamycin) and glycogen synthase kinase 3
Fig. 3
Fig. 3
Mechanism of action of antidepressant
Fig. 4
Fig. 4
Detrimental and beneficial effects of the use of antidepressants in T2D.
See this image and copyright information in PMC

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