Streptozotocin‐Induced Diabetic Models in Mice and Rats

Abstract

Streptozotocin (STZ) is an antibiotic that causes pancreatic islet β‐cell destruction and is widely used experimentally to produce a model of type 1 diabetes mellitus (T1DM). Detailed in this article are protocols for producing STZ‐induced insulin deficiency and hyperglycemia in mice and rats. Also described are protocols for creating animal models for type 2 diabetes using STZ. These animals are employed for assessing the pathological consequences of diabetes and for screening potential therapies for the treatment of this condition. © 2021 The Authors.

Protective Role of Recombinant Human Thrombomodulin in Diabetes Mellitus

“…In type 2 DM, initial compensatory islet hyperplasia occurs in response to insulin resistance followed by a progressive β-cell dysfunction leading to hyperglycemia, increased oxidative stress, and infiltration of pancreatic islets by macrophages and T-cells [31,33,41,42]. Isletitis is also observed in STZ-induced DM [43,44]. In agreement with previous observations, we found decreased infiltration of macrophages in diabetic mice treated with rhTM compared to their untreated counterpart mice.…”

Emerging Roles of Myeloid-Derived Suppressor Cells in Diabetes

“…Afterward, in the fourth week, the proportion of MDSC in the peripheral blood experienced the change from low to high, which may be due to the differentiation of MDSC ( Hsieh et al, 2018 ). As for in the bone marrow, initially, the number of MDSC appeared to decrease and subsequently (about 2 weeks later) return to normal levels ( Furman, 2015 ; Hsieh et al, 2018 ; Kim et al, 2018 ). In addition, a significant increase was noted in the number of MDSC in other organs.…”

Streptozotocin-induced hyperglycemia alters the cecal metabolome and exacerbates antibiotic-induced dysbiosis

“…STZ has been used to replicate both type-1 and type-2 diabetic phenotypes in animals since the mid-1960s ( Deeds et al, 2011 ; Eleazu et al, 2013 ). Models of STZ administration vary widely in their dosage concentration, injection frequency, and inclusion or exclusion of high-fat feed typically due to differences in research goals ( Deeds et al, 2011 ; Furman, 2021 ). Because STZ does not perfectly mimic type-2 diabetes, the inclusion of a high-fat feeding period before injection was recently proposed as a method to induce hyperinsulinemia and insulin resistance in STZ-treated animals ( Furman, 2021 ; Chao et al, 2018 ).…”

“…Models of STZ administration vary widely in their dosage concentration, injection frequency, and inclusion or exclusion of high-fat feed typically due to differences in research goals ( Deeds et al, 2011 ; Furman, 2021 ). Because STZ does not perfectly mimic type-2 diabetes, the inclusion of a high-fat feeding period before injection was recently proposed as a method to induce hyperinsulinemia and insulin resistance in STZ-treated animals ( Furman, 2021 ; Chao et al, 2018 ). Regardless, STZ consistently induces the characteristic symptoms of HG, insulin deficiency, polydipsia, and polyurea ( Furman, 2021 ; Kolb, 1987 ).…”

“…Because STZ does not perfectly mimic type-2 diabetes, the inclusion of a high-fat feeding period before injection was recently proposed as a method to induce hyperinsulinemia and insulin resistance in STZ-treated animals ( Furman, 2021 ; Chao et al, 2018 ). Regardless, STZ consistently induces the characteristic symptoms of HG, insulin deficiency, polydipsia, and polyurea ( Furman, 2021 ; Kolb, 1987 ). Although there is conservation of immunological responses to β cell ablation ( Eleazu et al, 2013 ), one must consider that microbiome-related phenotypes derived from STZ-induced HG are likely specific to the submodel and may not readily translate across studies.…”