Ispectrum Magazine Ispectrum Magazine #06 - Page 34

A 1985 study published in the journal Endocrinology by HS Grunstein et al showed that hyperinsulinaemia suppresses glucose utilization in specific brain regions. In 2012 Lim and team in the Journal of Cell Physiology showed that hyperglycaemia induces apoptosis via CB1 activation through the decrease of FAAH 1 in retinal pigment cells. In 1982 AL McCall et al, in the journal Proceedings of the National Academy of Sciences, found that hyperglycaemia reduces glucose transport into the brain by 45% by reduction of the GLUT hexose transporters: “... These results suggest that chronic hyperglycaemia decreases the number of hexose carrier molecules available at the blood-brain barrier. Such an adaptation could operate to decrease the net flux of glucose into the brain during sustained hyperglycaemia...” In 2011 in the journal Metabolic Brain Disease, MS Ola and others demonstrated that insulin regulates glutamine synthetase in a time- and dose-dependent fashion -- increase in insulin suppresses glutamine synthetase in retinal glial cells. In 2009 X Shen and G Xu in a study in the journal Current Eye Research showed that the cytokine IL-1beta (which is increased by pathological microbiota during excess glucose in the gut) suppresses glutamine synthetase in retinal glial cells during conditions of high glucose concentration. Hyperinsulinism is a major risk factor for Alzheimer’s disease via the insulin degrading enzyme (IDE), which degrades both insulin and the amyloid-beta peptide (a significant contributing influence in this degenerative disease). Excess insulin would monopolise IDE and reduce the clearance and degradation of amyloid-beta peptide. In the absence of the ApoeE4 gene the mechanism would be exclusively sugar driven. A 2006 study by WQ Qui and MF Folstein examined this relationship and found: “It is intriguing to notice that both hyperinsulinaemia and IDE gene variations are related to the risk of AD when the ApolipoproteinE4 (ApoE4) allele, the major risk factor of late-onset AD, is not present. Further studies of the role of IDE in the pathogenesis of AD, which may uncover potential treatment targets, are much needed.” 33