It has been shown that ingestion of
glucose,
amino acids,
protein or mixed meals tends to increase serum and salivary
cortisol concentrations in healthy adults. Recently, it has been demonstrated that morning
glucose ingestion stimulates pulsatile
cortisol and
adrenocorticotropic hormone (
ACTH) secretion, thus elevating their mean concentrations. In light of the above, a question arises: could the frequent food--and specifically
glucose--consumption lead to
hypercortisolism with possible clinical implications? And can the human body, under normal conditions raise defence mechanisms against the transient
hypercortisolism caused by the frequent
glucose consumption? Studies have revealed novel mechanisms, which are implicated in the
glucocorticoid receptor (GR)-mediated action, providing a kind of
glucocorticoid resistance. This
glucocorticoid resistance could be mediated through both enhancing acetylation (via, among others, regulation of essential clock genes such as Per) and inhibiting deacetylation of GR (via possible regulation of
sirtuin activity). Interestingly, the acetylation/deacetylation processes seem to be regulated by
glucose. Thus,
glucose apart from causing increased
cortisol secretion can, simultaneously, counter-regulate this
hypercortisolism, by promoting directly and/or indirectly a
glucocorticoid resistance state. Undoubtedly, before extracting conclusions regarding the clinical significance of the increased
cortisol secretion following
glucose ingestion, we should first thoroughly investigate the 'defence' mechanisms provided by 'nature' to handle this
hypercortisolism.