Having chronically elevated blood sugar and HbA1c is one thing, but even if they’re normal, there is a hormone called insulin that controls the blood sugar levels. If insulin becomes resistant after repeated bouts of blood sugar spikes, that itself can contribute to high blood sugar levels. However, having high levels of insulin, a sign that shows it’s resistant, can also lead to other symptoms including the brain. This chronically high levels of insulin is what we call ‘hyperinsulinemia.’
Hyperinsulinemia can contribute to a cascade of events over time contributing to metabolic syndrome, with one common one being weight gain and increased adipose mass (Erion & Corkey, 2017). As homeostasis plays a role in keeping basal levels of insulin in the body, there is an enzyme that regulates the level of insulin called Insulin-degrading Enzyme.
Insulin-degrading enzyme (IDE) is a zinc metallopeptidase that degrades specific peptides, including insulin and amyloid beta-peptide (Song, Rodgers & Hersh, 2018). There is a growing number of studies reporting the secretion of IDE playing an important role in degrading insulin and amyloid beta-peptide (Song, Rodgers & Hersh, 2018) and thus implicated in Alzheimer’s Disease. This implication leads to future research regarding potential allosteric activation of IDE against beta-amyloid as a new strategy in Alzheimer’s Disease treatment (Kurochkin, Guarnera & Berezovsky, 2018).
If there’s too much insulin, then your body needs to use up the IDE stores, and thus won’t have as much to contribute to the balancing act of amyloid plaque. This can set the balance off and contribute to the development of beta-amyoid plaque.
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