2018
DOI: 10.1016/j.bj.2018.08.005
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The streptozotocin-high fat diet induced diabetic mouse model exhibits severe skin damage and alterations in local lipid mediators

Abstract: BackgroundType 2 diabetes (T2D) can go undiagnosed for years, leading to a stage where produces complications such as delayed skin wound healing. Animal models have been developed in the last decades to study the pathological progression in this disease. Streptozotocin (STZ), that has a selective pharmacological toxicity toward pancreatic β cells, in addition to high fat diet has been widely used to induce diabetes however no evidence has shown its effects on the skin integrity.MethodsEighteen C57BL/6J male mi… Show more

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Cited by 14 publications
(10 citation statements)
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References 19 publications
(20 reference statements)
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“…Hyperglycemia, insulin resistance, and β-cell failure are key characteristics of type 2 diabetes. In accordance with previous findings, compared to non-DM mice, our HFD/STZ-treated mice showed higher levels of fasting blood glucose and insulin resistance as demonstrated by the impaired glucose tolerance in an IPGTT test [18][19][20]. In addition, plasma insulin levels and the numbers of pancreatic insulin-secreting β-cells were markedly decreased in the HFD/STZ-treated DM mice compared to these values in non-DM mice.…”
Section: Discussionsupporting
confidence: 92%
“…Hyperglycemia, insulin resistance, and β-cell failure are key characteristics of type 2 diabetes. In accordance with previous findings, compared to non-DM mice, our HFD/STZ-treated mice showed higher levels of fasting blood glucose and insulin resistance as demonstrated by the impaired glucose tolerance in an IPGTT test [18][19][20]. In addition, plasma insulin levels and the numbers of pancreatic insulin-secreting β-cells were markedly decreased in the HFD/STZ-treated DM mice compared to these values in non-DM mice.…”
Section: Discussionsupporting
confidence: 92%
“…via single or multiple injections of varying dosages, ranging from 25 to 45 mg/kg BW in rats and 40 to 100 mg/kg BW in mice. [185][186][187][188][189] As an example, Mansor et al 183 191 At the end of the experimental protocol, the animals displayed frank hyperglycaemia (>300 mg/dl), marked dyslipidaemia, hepatic fibrosis and pancreatic β-cell dysfunction with subsequent insulinopenia. 191 Interestingly, in addition to signs of cardiovascular injury, these animals developed microvascular angiopathies, namely, nephropathy, retinopathy and behavioural signs of peripheral neuropathy.…”
Section: Prediabetesmentioning
confidence: 99%
“…192 These observations have been corroborated by other reports. 184,186,187 Finally, it should be emphasized that diet-induced regimens com- (Table 3). Furthermore, even in genetic animal models of NASH, diet acts as a secondary trigger for disease progression.…”
Section: Prediabetesmentioning
confidence: 99%
“…In this brief communication, Leguina-Ruzzi et al. [24] demonstrate that mice treated with streptozotocin, which selectively kills pancreatic beta cells, and fed a high fat diet show the typical skin lesions observed in diabetes, making this model particularly useful for studying this complication.…”
Section: Also In This Issuementioning
confidence: 99%