ArticleActa cirurgica brasileira2021
Combination of cafeteria diet with intraperitoneally streptozotocin in rats. A type-2 diabetes model.
Article in Acta cirurgica brasileira, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 7 citations in OpenAlex.
- A novel mouse model for studying complications related to type 2 diabetes using a medium-fat diet, fructose, and streptozotocin.Scientific reports · 2025Article
- The efficacy of using metformin and/or quercetin for amelioration of gamma-irradiation induced tongue toxicity in diabetic rats.BMC oral health · 2024Article
- Novel Approaches in Chronic Renal Failure without Renal Replacement Therapy: A Review.Biomedicines · 2023Review
- Analysis of high-intensity interval training on bone mineral density in an experimental model of type 2 diabetes.Acta cirurgica brasileira · 2022Article
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Authors and funding
11 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
purposeTo develop a model of induction of type-2 diabetes (DM2) by combining low doses of streptozotocin (STZ) and a cafeteria diet.
methodsForty male Wistar rats (200 g) were allocated into four groups: control (non-diabetic, n = 10); STZ 30 mg/kg (diabetic, n = 10); STZ 35 mg/kg (diabetic,n = 10); and STZ 40 mg/kg (diabetic, n = 10). DM2 was induced with a single intraperitoneal injection of STZ after four weeks of cafeteria diet in the three diabetic groups. All animals were evaluated as for anthropometric, and biochemical analyses, as well as liver, kidney and pancreas histological analyses.
resultsLower weight gain, higher water intake, higher Lee index, hyperglycemia and modified total protein, urea, alpha-amylase, as well as insulin resistance, hepatic steatosis, pancreas, and kidney injury were observed in animals treated with 35 and 40 mg/kg of STZ.
conclusionsThe results show that the experimental model using cafeteria diet associated with 35 mg/kg of STZ is a low-cost model and efficient in order to develop DM2, confirmed by the presence of polydipsia, hyperglycemia, altered biochemical tests, insulin resistance and damages to the liver, pancreas and kidney, which is similar to the disease found in humans.
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