The protective mechanisms of microglia cells help to maintain central nervous system (CNS) homeostasis and function.1 Microglia are innate immune cells that constantly survey their surrounding CNS microenvironment for pathogens, damaged cells, and inflammatory molecules. Sugars from our diet, including glucose and fructose, combine with endogenous proteins non-enzymatically and form advanced glycation-end products (AGEs).2 AGEs are shown to produce reactive oxygen species, leading to inflammation and cellular damage that may be mediated by microglia.3 Fructose consumption has become increasingly prevalent within the American diet, as it is a lower cost sweetener.4 Microglia become activated and phagocytic in the presence of high levels of glucose, but the effects of fructose are not yet fully understood.3 The reactivity of fructose within the body and it’s long-term health implications remain unclear.
Blackley, Regina; Stryker, Matthew; DeNapoli, Susan; and Lull, Melinda E., "The differential effects of fructose and glucose on advanced glycation end-product formation and cellular damage in vitro" (2014). Doctoral External Publications. Paper 2.
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