Depression and type 2 diabetes: A causal relationship and mechanistic pathway

Author:

Khawagi Wael Y.1,Al‐kuraishy Hayder M.2,Hussein Nawar R.3,Al‐Gareeb Ali I.2,Atef Esraa4,Elhussieny Omnya5,Alexiou Athanasios6789ORCID,Papadakis Marios10,Jabir Majid S.11ORCID,Alshehri Abdullah A.1,Saad Hebatallah M.12ORCID,Batiha Gaber El‐Saber13

Affiliation:

1. Department of Clinical Pharmacy, College of Pharmacy Taif University Taif Saudi Arabia

2. Department of Clinical Pharmacology and Medicine, College of Medicine Mustansiriyah University Baghdad Iraq

3. College of Pharmacy, Pharmacology Department Al‐Farahidi University Baghdad Iraq

4. Respiratory Therapy Department Mohammed Al‐Mana College for Medical Sciences Dammam Saudi Arabia

5. Department of Histology and Cytology, Faculty of Veterinary Medicine Matrouh University Marsa Matruh Egypt

6. University Centre for Research & Development, Chandigarh University Chandigarh‐Ludhiana Highway Mohali India

7. Department of Research and Development Funogen Athens Greece

8. Department of Research and Development AFNP Med Wien Austria

9. Department of Science and Engineering Novel Global Community Educational Foundation Hebersham New South Wales Australia

10. Department of Surgery II, University Hospital Witten‐Herdecke University of Witten‐Herdecke Wuppertal Germany

11. Applied Science Department University of Technology Baghdad Iraq

12. Department of Pathology, Faculty of Veterinary Medicine Matrouh University Marsa Matruh Egypt

13. Department of Pharmacology and Therapeutics, Faculty of Veterinary Medicine Damanhour University Damanhour Egypt

Abstract

AbstractDepression is a mood disorder that may increase risk for the development of insulin resistance (IR) and type 2 diabetes (T2D), and vice versa. However, the mechanistic pathway linking depression and T2D is not fully elucidated. The aim of this narrative review, therefore, was to discuss the possible link between depression and T2D. The coexistence of T2D and depression is twice as great compared to the occurrence of either condition independently. Hyperglycaemia and dyslipidaemia promote the incidence of depression by enhancing inflammation and reducing brain serotonin (5‐hydroxytryptamine [5HT]). Dysregulation of insulin signalling in T2D impairs brain 5HT signalling, leading to the development of depression. Furthermore, depression is associated with the development of hyperglycaemia and poor glycaemic control. Psychological stress and depression promote the development of T2D. In conclusion, T2D could be a potential risk factor for the development of depression through the induction of inflammatory reactions and oxidative stress that affect brain neurotransmission. In addition, chronic stress in depression may induce the development of T2D through dysregulation of the hypothalamic–pituitary–adrenal axis and increase circulating cortisol levels, which triggers IR and T2D.

Publisher

Wiley

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