Difference in glucose intolerance between C57BL/6J and ICR strain mice with streptozotocin/nicotinamide-induced diabetes

Shimizu, Ryo; Sakazaki, Fumitoshi; Okuno, Tomofumi; Nakamuro, Katsuhiko; Ueno, Hitoshi

doi:10.2220/biomedres.33.63

Cited by 26 publications

(25 citation statements)

References 15 publications

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“…3 was collected from ICR mice. ICR mice are w5 g heavier than equivalent agematched C57BL/6 mice, and there are established differences in glucose metabolism between the two strains, particularly in models of diabetes (Luo et al 1998, Burgess et al 2005, Shimizu et al 2012. Thus this is most likely due to variations in glucose metabolism between different mouse strains as mentioned previously (Andrikopoulos et al 2008, Berglund et al 2008, and reinforces the point that rodent strain is an important factor to be taken into consideration when comparing between studies.…”

Section: Route and Dose Of Glucose Administrationmentioning

confidence: 58%

METABOLIC PHENOTYPING GUIDELINES: Assessing glucose homeostasis in rodent models

Bowe

Franklin

Hauge-Evans

et al. 2014

Journal of Endocrinology

215

142

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The pathophysiology of diabetes as a disease is characterised by an inability to maintain normal glucose homeostasis. In type 1 diabetes, this is due to autoimmune destruction of the pancreatic b-cells and subsequent lack of insulin production, and in type 2 diabetes it is due to a combination of both insulin resistance and an inability of the b-cells to compensate adequately with increased insulin release. Animal models, in particular genetically modified mice, are increasingly being used to elucidate the mechanisms underlying both type 1 and type 2 diabetes, and as such the ability to study glucose homeostasis in vivo has become an essential tool. Several techniques exist for measuring different aspects of glucose tolerance and each of these methods has distinct advantages and disadvantages. Thus the appropriate methodology may vary from study to study depending on the desired end-points, the animal model, and other practical considerations. This review outlines the most commonly used techniques for assessing glucose tolerance in rodents and details the factors that should be taken into account in their use. Representative scenarios illustrating some of the practical considerations of designing in vivo experiments for the measurement of glucose homeostasis are also discussed.

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Section: Route and Dose Of Glucose Administrationmentioning

confidence: 58%

METABOLIC PHENOTYPING GUIDELINES: Assessing glucose homeostasis in rodent models

Bowe

Franklin

Hauge-Evans

et al. 2014

Journal of Endocrinology

215

142

View full text Add to dashboard Cite

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“…The toxin causes a reduction in insulin production and subsequent hyperglycemia with the severity depending on the strain of the rodent (Rodrigues et al, 1997, Shimizu et al, 2012) and the dose of STZ (Ventura-Sobrevilla et al, 2011). Typically induced between 11-week to 14-week of age in either mice or rats, STZ-T1D impedes normal bone mass accrual resulting in lower structural strength of cortical bone and reduced trabecular bone within several weeks as compared to non-diabetic controls (Nyman et al, 2011, Silva et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

Preserving and restoring bone with continuous insulin infusion therapy in a mouse model of type 1 diabetes

et al. 2017

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Those with type 1 diabetes (T1D) are more likely to suffer a fracture than age- and sex-matched individuals without diabetes, despite daily insulin therapy. In rodent studies examining the effect of bone- or glucose-targeting therapies on preventing the T1D-related decrease in bone strength, insulin co-therapy is often not included, despite the known importance of insulin signaling to bone mass accrual. Therefore, working toward a relevant pre-clinical model of diabetic bone disease, we assessed the effect of continuous subcutaneous insulin infusion (CSII) therapy at escalating doses on preserving bone and the effect of delayed CSII on rescuing the T1D-related bone deterioration in an established murine model of T1D. Osmotic minipumps were implanted in male DBA/2 J mice 2 weeks (prevention study) and 6 weeks (rescue study) after the first injection of streptozotocin (STZ) to deliver insulin at 0, 0.0625, 0.125, or 0.25 IU/day (prevention study; n = 4–5 per dose) and 0 or 0.25 IU/day (rescue study; n = 10 per group). CSII lasted 4 weeks in both studies, which also included age-matched, non-diabetic DBA/2 J mice (n = 8–12 per study). As the insulin dose increased, blood glucose decreased, body weight increased, a serum maker of bone resorption decreased, and a serum marker of bone formation increased such that each end-point characteristic was linearly correlated with dose. There were insulin dose-dependent relationships (femur diaphysis) with cross-sectional area of cortical bone and cortical thickness (micro-computed tomography) as well as structural strength (peak force endured by the mid-shaft during three-point bending). Likewise, trabecular bone volume fraction (BV/TV), thickness, and number (distal femur metaphysis) increased as the insulin dose increased. Delayed CSII improved glycated hemoglobin (HbA1c), but blood glucose levels remained relatively high (well above non-diabetic levels). Interestingly, it returned the resorption and formation markers to similar levels as those seen in non-T1D control mice. This apparent return after 4 weeks of CSII translated to a partial rescue of the structural strength of the femur mid-shaft. Delayed CSII also increased Tb.Th to levels seen in non-T1D controls but did not fully restore BV/TV. The use of exogenous insulin should be considered in pre-clinical studies investigating the effect of T1D on bone as insulin therapy maintains bone structure without necessarily lowering glucose below diabetic levels.

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“…30) The ICR mouse strain with experimental diabetes induced by NA/STZ-treatment is more sensitive to hyperglycemia under diabetic conditions than the C57BL/6J strain. 17) Using the NA/STZ-induced diabetic mouse model, the objective was to elucidate the protective effects of supplementary SeMet on oxidative stress in pancreatic islets under insufficient and physiological Se levels because this selenocompound improves pancreatic GPX1 activity the most in mice with insufficient dietary Se status.…”

Section: Discussionmentioning

confidence: 99%

“…Here, we demonstrated that the ICR mouse strain mildly induced by nicotinamide (NA) and streptozotocin (STZ) was an appropriate model of diabetes. 17) There are conflicting reports on the relevance between supplementary Se or the physiological status and the prevalence of type 2 diabetes. Previous studies demonstrate that Se status of diabetic patients are physiologically insufficient compared with healthy individuals.…”

mentioning

confidence: 99%

Effect of Seleno-L-methionine on Oxidative Stress in the Pancreatic Islets of a Short-Term Induced Diabetic Mouse Model in Insufficient Selenium Status

Ueno

Shimizu

Okuno

et al. 2018

Biological & Pharmaceutical Bulletin

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The protective effects of seleno-L-methionine (SeMet) on oxidative stress in pancreatic islets were investigated with a short-term nicotinamide (NA) and streptozotocin (STZ)-induced diabetic mouse model. ICR mice were intraperitoneally injected twice with 100 mg/kg STZ and 120 mg/kg NA at a 1-d interval and were then orally administered 158 µg Se/kg SeMet with free access to a selenium-deficient diet for 5 weeks. Administration of SeMet significantly improved the levels of glycated hemoglobin (HbA1c), non-fasting and oral glucose tolerance-tested (OGTT) blood glucose, plasma adiponectin and hepatic glycogen that deteriorated by NA/STZ treatment. However, supplementary SeMet did not restore non-fasting plasma insulin levels in NA/STZ treatment group and significantly suppressed OGTT plasma insulin levels in the control group. Although SeMet significantly suppressed 8-hydroxy-2′-deoxyguanosine density in pancreatic islets, SeMet did not restore insulin density. The hepatic and pancreatic mRNA levels of glutathione peroxidase 1 (GPX1) increased by NA/STZ treatment or SeMet administration. These results suggest that although a physiological level of SeMet improves glucose tolerance by exhibiting insulin-mimetic activity in a short-term induced diabetic mouse model under insufficient Se status, the suppression of pancreatic oxidative stress with the induction GPX1 by SeMet supplementation is unlikely to restore insulin storage and secretion.Key words selenium; diabetes; insulin; glutathione peroxidase 1; seleno-L-methionine; oxidative stress Selenium (Se) is one of the essential micronutrients for human and animals and exerts as a key component of selenoproteins to regulate many physiological functions.1) The families of glutathione (GSH) peroxidase (GPX) and thioredoxin reductase (TR) are the well-known Se-dependent antioxidant enzymes.2,3) GPX1 is particularly important because the antioxidant enzyme has the higher affinity than catalase for hydrogen peroxide (H 2 O 2 ) 4) that is formed by superoxide dismutase from superoxide anions 5) or directly generated by oxidative stress in cytoplasm. Therefore, Se deficiency induces some pathological conditions including cancer and cardiovascular disease.6) The patients with Se-deficiency syndrome, Keshan disease cause cardiomyopathy with the pancreatic atrophy and degeneration.7) The fragility for the oxidative stress in pancreas may be responsible for the pathogenesis. 8)The early stages of type 2 diabetes is characterized by postprandial hyperglycemia by insufficient secretion of insulin from pancreatic β-cells and by the poor response on the target organs.9,10) As the etiology of type 2 diabetes is linked to genetic and lifestyle factors, 11,12) the onset is preventable through the improvements of dietary habits and lifestyle.13) However, deteriorations in dietary habits and lifestyle are involved with oxidative stress 14) and thereby connected with the onset of diabetes.15) Increased generation of reactive oxygen species (ROS) promotes a functional disorder in pancreat...

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Difference in glucose intolerance between C57BL/6J and ICR strain mice with streptozotocin/nicotinamide-induced diabetes

Cited by 26 publications

References 15 publications

METABOLIC PHENOTYPING GUIDELINES: Assessing glucose homeostasis in rodent models

METABOLIC PHENOTYPING GUIDELINES: Assessing glucose homeostasis in rodent models

Preserving and restoring bone with continuous insulin infusion therapy in a mouse model of type 1 diabetes

Effect of Seleno-L-methionine on Oxidative Stress in the Pancreatic Islets of a Short-Term Induced Diabetic Mouse Model in Insufficient Selenium Status

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