Clinically relevant experimental rodent models of diabetic foot ulcer

Wound Healing Impairment in Type 2 Diabetes Model of Leptin-Deficient Mice—A Mechanistic Systematic Review

“…The study aimed to address only the leptin-deficient murine model of T2DM. Thus, it lacks findings concerning diabetic wound healing on other rodent models such as Zucker diabetic Sprague Dawley rats, Zuker fatty rat, SHR/N-cp Rat, or JCR/LA-cp Rat [ 5 , 154 ]. In addition, the review did not cover dietary or pharmacologically induced T2DM models—such C57BL/6J mice fed with a high-fat diet [ 155 ] or low-dose streptazocin-treated animals [ 156 ].…”

“…However, small size, cost efficiency, obesity and hyperglycemia, easy availability of those mice, widespread use in wound healing research, and delayed healing are still advantages of the leptin-deficient murine model. The above-mentioned are counterbalanced with unfavourable traits such as loose and hairy skin, wound healing with contraction (overcome by wound splinting), difficulty in inducing partial thickness wounds, limited translational efficiency, and an immune response distinct from that of humans [ 154 ]. Additionally, the background strain of leptin-deficient mice influences the phenotype.…”

Type 2 Diabetes Mellitus: Pathogenic Features and Experimental Models in Rodents

“…характеризуются гипергликемией, вызванной ожирением, тяжелой гиперинсулинемией и резистентностью к инсулину как в мышечной, так и в жировой ткани, выраженными изменениями в панкреатических остров-ках -от гипертрофии и дегрануляции до фиброза и замещения их соединительной тканью [67][68][69][70]. Ряд работ, посвященных устранению симптомов СД2, изучению взаимосвязи ожирения и гомеостаза глюкозы, а также диабетических осложнений, сделаны с использованием полигенных моделей [71][72][73][74][75][76][77][78][79][80][81][82][83][84][85][86].…”

“…Polygenic models, namely KK and KK AY mice, OLETF rats, NZO mice, etc., are characterized by obesity-induced hyperglycemia, severe hyperinsulinemia, IR in both muscle and adipose tissue, and pronounced changes in the pancreatic islets: from hypertrophy and degranulation to fibrosis and their replacement by the connective tissue [ 67 , 68 , 69 , 70 ]. A number of works focused on the elimination of T2DM symptoms, analysis of the relationship between obesity and glucose homeostasis, as well as diabetic complications, have been done using polygenic models [ 71 , 72 , 73 , 74 , 75 , 76 , 77 , 78 , 79 , 80 , 81 , 82 , 83 , 84 , 85 , 86 ].…”

A review on contemporary nanomaterial-based therapeutics for the treatment of diabetic foot ulcers (DFUs) with special reference to the Indian scenario

“…1,2 There are many diabetes-related complications, such as diabetic ketoacidosis, nerve damage, hypoglycemia, mastopathy, kidney-related diseases, cardiovascular diseases, necrobiosis, retinopathy, hyperosmolar acidosis, and musculoskeletal conditions; however, the most prevalent is diabetic foot ulcers (DFUs). 3,4 Among the affected diabetic individuals worldwide, 20% of patients develop diabetic wounds (DWs). 5 A diabetic wound/foot ulcer infection is a critical complication in diabetic patients, which takes time to heal, resulting in the degradation of skin tissues and exposure of cellular layers.…”