Burns are complex injuries that lead to hyperglycemia as a stress response. Diabetes Mellitus (DM) is a hormonal and metabolic disorder categorized by impaired insulin secretion and yielding to elevate plasma glucose levels and therefore complicates the therapy of burns, it is also developed via uncontrolled stress reaction to the burn. Also, DM will impact on nutrition and lifestyle of burn patients. This review provides pathophysiology, difficulties and managements of burns related to the patients with DM to offer evidence-based care to seriously ill people. Performing a treatment for diabetic burn patient is difficult for healthcare professionals. Traumatic burn in non-diabetic people may develop stress-induced hyperglycemia which ends up with DM due to endocrine complications from their injury. The higher risk for burn injuries is found in pre-existing DM. Special medical plan should be employed to control burns. Additionally, treatments for present burn must be reformed to avoid diabetes mellitus, management of glucose level, and help healing process in diabetic foot ulcer.

Increased intake of dietary fructose is markedly associated with multiple negative health outcomes and burdens. Insulin resistance (IR) and type 2 diabetes mellitus (T2DM) are the most common complications that present with conjugated cellular-biochemical abnormalities. This article explains the involvement of increased dietary fructose intake in the occurrence of IR and T2DM and addresses basic metabolic mechanisms. PubMed, Medline, Science Direct, ADI, and WHO databases were searched through June 2021. Current research predicts that over 350 million people may have diabetes by 2030. IR acts as an influencer promoter of T2DM development. IR can occur as a result of high fructose intake. Fructose metabolism results in de novo lipogenesis, while its decreasing effect of peroxisome proliferator-activated receptor (PPAR) activity elevates the levels of inflammatory cytokines, resulting in down-regulation of insulin receptor substrate-1 phosphorylation. Fructose stimulates oxidative stress by activating nicotinamide adenine dinucleotide phosphate oxidase and synthesis of advanced glycation end-products. Fructose also stimulates purine-induced uric acid synthesis and leptin resistance, which contributes to abnormal insulin action. It is crucial to understand the mechanisms of fructose-induced IR via induction of oxidative stress, inflammation, leptin resistance, and uric acid production. This helps prevent and control variable diseases, T2DM being the most.