The effects of insulin levels, both high and low, on the body, has been extensively researched. However, emerging research aiming to understand the link between type 2 diabetes and memory impairment disorders such as Alzheimer indicates that insulin may affect the brain more than previously thought.
Insulin. Image Credit: Sherry Yates Young / Shutterstock
What is Insulin?
Insulin is a hormone which is secreted by the β cells of the pancreatic islets of Langerhans and plays a role in the maintenance of blood glucose levels. This is achieved by managing protein, lipid, and carbohydrate metabolism, aiding the uptake of cellular glucose, and cell division and growth.
Insulin regulates the metabolism and is the key that unlocks the cell's glucose channel - Vector Image Credit: Designua / Shutterstock
Does Insulin Affect the Brain?
Neuroscientists at the University at Albany have begun to research the association between type 2 diabetes and neurological disorders characterized by memory impairment such as Alzheimer’s disease. Their research aimed to gather evidence on whether insulin affects the brain and impairs aspects of its functionality, such as memory.
This particular study built on previous studies and investigated brain metabolism during a series of cognitive tasks that focused on identifying the precise mechanisms by which the hormone affects the brain. It was found that GluT4, an insulin-regulated glucose transporter, was a target in the brain for insulin. This research is another integral step in over a decade’s worth of research which also includes original findings that indicate that insulin is required by the hippocampus in order to consolidate memories.
The hippocampus is considered to be the hub for memory consolidation in the brain and is located just under the cortex. Furthermore, it plays an integral role in not only the formation of new memories but also the movement of information between long-term and short-term memory.
Research has found that memory impairment is present not only in Alzheimer’s disease, but in a range of other health issues including type 2 diabetes. The neuroscientists at University at Albany found that memory impairments can occur if the brain is unable to receive glucose where and when needed. Specifically, they believed that GluT4 may, in fact, be linked to several diseases.
How Important is this Research?
This research adds to a growing body of literature which has found links between insulin and blood glucose and the brain. It has subsequently paved the way for a further series of studies which aims to identify the different mechanisms by which insulin regulates memory. At the moment, it seems that this regulation varies across mechanisms and stages of memory. Further work is being carried out such as those that examine the relationship between insulin and beta-amyloid - a protein that is highly concentrated in the brain of those with Alzheimer's and can create deficits in brain metabolism.
The researchers are also looking at the implications of other factors such as the impact of hypoglycemia, different types of diets (such as high-fat diets), and zinc as a regulator of hippocampal memory.
The researchers also noted that a major risk factor for developing Alzheimer’s is type 2 diabetes. By increasing our understanding of why this occurs, and by which mechanisms, it would aid the development in the next steps in methods to prevent or treat Alzheimer’s disease.
- Fogwe, L .A & Mesfin F. B. (2019). Neuroanatomy, Hippocampus. StatPearls. https://www.ncbi.nlm.nih.gov/books/NBK482171/
- Wilcox, G. (2005). Insulin and Insulin Resistance. The Clinical Biochemist Reviews. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1204764/
- Pearson-Leary J., Jahagirdar V., Sage. J., et al. (2018). Insulin modulates hippocampally-mediated spatial working memory via glucose transporter-4. Behavioural Brain Research. DOI: 10.1016/j.bbr.2017.09.033
- Pearson-Leary, J., Jahagirdar, V., Sage, J., et al. (2019). Insulin modulated hippocampally-mediated spatial working memory via glucose transported-4. Behavioural Brain Research. DOI: 10.1016/j.bbr.2017.09.033