Abstract
Ischemia is one of the main epidemic factors and characteristics of diabetic chronic wounds, and exerts a profound effect on wound healing. To explore the mechanism of and the cure for diabetic impaired wound healing, we established a type 2 diabetic rat model. We used an 8weeks high fat diet (HFD) feeding regimen followed by multiple injections of streptozotocin (STZ) at a dose of 10mg/kg to induce Wister rat to develop type 2 diabetes. Metabolic characteristics were assessed at the 5th week after the STZ injections to confirm the establishment of diabetes mellitus on the rodent model. A bipedicle flap, with length to width ratio 1.5, was performed on the back of the rat to make the flap area ischemic. Closure of excisional wounds on this bipedicle flap and related physiological and pathological changes were studied using histological, immunohistochemical, real time PCR and protein immunoblot approaches. Our results demonstrated that a combination of HFD feeding and a low dose of STZ is capable of inducing the rats to develop type 2 diabetes with noticeable insulin resistance, persistent hyperglycemia, moderate degree of insulinemia, as well as high serum cholesterol and high triglyceride levels. The excision wounds on the ischemic double pedicle flap showed deteriorative healing features comparing with non-ischemic diabetic wounds, including: delayed healing, exorbitant wound inflammatory response, excessive and prolonged ROS production and excessive production of MMPs. Our study suggested that HFD feeding combined with STZ injection could induce type 2 diabetes in rat. Our ischemic diabetic wound model is suitable for the investigation of human diabetic related wound repair; especically for diabetic chronic wounds.
Highlights
Type 2 diabetes mellitus is a complicated metabolic disorder characterized by abnormal glucose homeostasis due to anomalous insulin secretion and function [1]
During the first 4wks after STZ injection, rats showed a slight decrease in body weight (BW), while the rats of the control group continuously gained BW and had a higher BW than the high fat diet (HFD) rats 4wks after diabetes induction (Fig 1A)
Finding a diabetic chronic wound model that precisely mimics the pathological characteristics of diabetic wounds is in persistent demand
Summary
Type 2 diabetes mellitus is a complicated metabolic disorder characterized by abnormal glucose homeostasis due to anomalous insulin secretion and function [1]. Once a person gets diabetes, the risk that he may suffer from a diabetic foot ulcer could be as high as 25% [2]. The probability of diabetes-related lower leg amputations during their lifetime exceeds 84% [3,4]. Foot ulcers causes both emotional and physical pain which can lead to productivity and financial losses [2,5].
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