Burn injury insulin resistance and central nervous system complications: A review

摘要: Abstract Insulin resistance is a major underlying and preexisting event in chronic metabolic disorders. However, this also an acute, de novo condition critical burn survivors other emergency episodes. Irrespective to its proximal trigger pathology, peripheral insulin results from impaired receptor’s signaling accurately transduce the hormonal message, leading hyperglycemia, hypermetabolism catabolia. Elevation of stress hormones, pro-inflammatory cytokines, along with spillover mitochondria-derived free radicals lead receptor impairment that counteracts anabolic actions. These post-burn metabolic-inflammatory disorders could last for years embraces central nervous system. The persistence these events may suggest existence memory beyond described diabetes, which involvement epigenetic mechanisms remains be investigated. brain target organ multiple complications seem set forth through peripheral/central inflammation, nitric oxide imbalance, oxidative stress, ultimately neuronal insufficient glucose utilization. From neuroses dementia neurological are as clinical expression degeneration, apoptosis, synapsis rupture. All represent collapse neuroprotective actions due failed axis. Although mechanistically determined by different players, both scenarios, mitochondria appear energy homeostasis failure. This review includes most recently identified pathogenic drivers on resistance, whereas it reveals breaches translate future therapeutic interventions.