Insulin resistance, glucose regulation, obesity and mood: A review of the literature.

Research output: Contribution to conference (non-published works)Abstract

Abstract

Background/Aims: Insulin is one of the most potent anabolic agents involved in the macronutrients synthesis and storage. It plays a pivotal role in the development of obesity while within the central nervous system acts as a growth factor in synaptogenesis and nerve growth. Therefore the lack of insulin or presence of insulin resistance (IR) could potentially lead to cognitive decline and impaired learning. This review focuses on animal and human studies that assess the relationship between the IR and regulation of cognitive function and mood.
Methods: Literature searches were conducted on electronic databases examining the association between insulin resistance, glucose regulation, obesity, cognitive function and mood.
Results: In animal models, the central focus is on effects to the hypothalamic-pituitary-adrenal axis (HPA-axis), an area identified as the most likely area to influence mood and stress. Damage to the insulin receptors in this region was found to be associated with the increase in food intake and occurrence of adiposity. In humans, these areas play a central role in motivation and decision making. Furthermore, IR and major depressive illness share several pathologies, including disorders of the HPA-axis, the autonomic nervous system, platelets and endothelial function.
Conclusions: There is increasing evidence suggesting a close association between the obesity and mood disorders such as depression, anxiety, panic and bipolar disorders. However, there is no clear evidence of individual aspects that can be ascribed as pathological drivers of the problem.
Original languageEnglish
Pages1-23
Number of pages23
DOIs
Publication statusPublished - 2015
EventAnnual Scientific Meeting of the Nutrition-Society-of-Australia -
Duration: 1 Jan 2011 → …

Conference

ConferenceAnnual Scientific Meeting of the Nutrition-Society-of-Australia
Period1/01/11 → …

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