Streptozotocin‐Induced Diabetic Models in Mice and Rats

Wu, Kenneth K.; Huan, Youming

doi:10.1002/0471141755.ph0547s40

Cited by 274 publications

(228 citation statements)

References 27 publications

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“…The rats were divided into two groups: a nondiabetic healthy control group and an STZ-induced T1D group. After 1 week of acclimatization, T1D was induced in the latter group by injection of a single dose (60 mg STZ kg 21 ) of freshly prepared STZ (Sigma) administered via the intraperitoneal cavity, according to a previously described method (Wu & Huan, 2008). Glucose levels were measured in triplicate using a Contour Next glucometer (Bayer) in blood samples collected from a tail vein each week.…”

Section: Methodsmentioning

confidence: 99%

Streptozotocin-induced type-1-diabetes disease onset in Sprague–Dawley rats is associated with an altered intestinal microbiota composition and decreased diversity

et al. 2015

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There is a growing appreciation that microbiota composition can significantly affect host health and play a role in disease onset and progression. This study assessed the impact of streptozotocin (STZ)-induced type-1-diabetes (T1D) on intestinal microbiota composition and diversity in Sprague-Dawley rats, compared with healthy controls over time. T1D was induced by injection of a single dose (60 mg STZ kg "1 ) of STZ, administered via the intraperitoneal cavity. Total DNA was isolated from faecal pellets at weeks 0 (pre-STZ injection), 1, 2 and 4 and from caecal content at week 5 from both healthy and T1D groups. High-throughput 16S rRNA sequencing was employed to investigate intestinal microbiota composition. The data revealed that although intestinal microbiota composition between the groups was similar at week 0, a dramatic impact of T1D development on the microbiota was apparent post-STZ injection and for up to 5 weeks. Most notably, T1D onset was associated with a shift in the Bacteroidetes : Firmicutes ratio (P,0.05), while at the genus level, increased proportions of lactic acid producing bacteria such as Lactobacillus and Bifidobacterium were associated with the later stages of T1D progression (P,0.05). Coincidently, T1D increased caecal lactate levels (P,0.05). Microbial diversity was also reduced following T1D (P,0.05). Principle co-ordinate analyses demonstrated temporal clustering in T1D and control groups with distinct separation between groups. The results provide a comprehensive account of how T1D is associated with an altered intestinal microbiota composition and reduced microbial diversity over time.

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Section: Methodsmentioning

confidence: 99%

Streptozotocin-induced type-1-diabetes disease onset in Sprague–Dawley rats is associated with an altered intestinal microbiota composition and decreased diversity

et al. 2015

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“…Diabetes was induced by multiple low-dose STZ (MLDS) [24]. Eight-week-old male wild-type C57BL/6 or TRPM2 − / − mice were injected intraperitoneally (i.p) with STZ prepared in 0.1 M sodium citrate buffer, pH 5.0, for five consecutive days at a dose of 40 mg · kg − 1 body weight.…”

Section: Induction Of Diabetes With Streptozotocin and Glucose Assaysmentioning

confidence: 99%

TRPM2-mediated intracellular Zn2+ release triggers pancreatic β-cell death

Manna

Munsey

Abuarab

et al. 2015

Biochemical Journal

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Reactive oxygen species (ROS) can cause pancreatic β-cell death by activating transient receptor potential (melastatin) 2 (TRPM2) channels. Cell death has been attributed to the ability of these channels to raise cytosolic Ca 2 + . Recent studies however revealed that TRPM2 channels can also conduct Zn 2 + , but the physiological relevance of this property is enigmatic. Given that Zn 2 + is cytotoxic, we asked whether TRPM2 channels can permeate sufficient Zn 2 + to affect cell viability. To address this, we used the insulin secreting (INS1) β-cell line, human embryonic kidney (HEK)-293 cells transfected with TRPM2 and pancreatic islets. H 2 O 2 activation of TRPM2 channels increases the cytosolic levels of both Ca 2 + and Zn 2 + and causes apoptotic cell death. Interestingly, chelation of Zn 2 + alone was sufficient to prevent β-cell death. The source of the cytotoxic Zn 2 + is intracellular, found largely sequestered in lysosomes. Lysosomes express TRPM2 channels, providing a potential route for Zn 2 + release. Zn 2 + release is potentiated by extracellular Ca 2 + entry, indicating that Ca 2 + -induced Zn 2 + release leads to apoptosis. Knockout of TRPM2 channels protects mice from β-cell death and hyperglycaemia induced by multiple low-dose streptozotocin (STZ; MLDS) administration. These results argue that TRPM2-mediated, Ca 2 + -potentiated Zn 2 + release underlies ROS-induced β-cell death and Zn 2 + , rather than Ca 2 + , plays a primary role in apoptosis.

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“…Animals with a fasting blood glucose level 41.5 g L À1 on day 7 after injection were considered diabetic (Wu & Huan, 2008) and were included in the study.…”

Section: Hypoglycemic and Antihyperglycemic Effectsmentioning

confidence: 99%

Evaluation of antidiabetic properties of cactus pear seed oil in rats

Berraaouan

Ziyyat

Mekhfi

et al. 2014

Pharmaceutical Biology

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Context: Cactus pear (Opuntia ficus-indica (L.) Mill. (Cactaceae)) is a medicinal plant widely used to treat diabetes. Objective: This work investigates the hypoglycemic and antihyperglycemic effect of cactus pear seed oil (CPSO), its mechanism of action, and any toxic effects. Materials and methods: The hypoglycemic effect of CPSO was evaluated in groups of six healthy Wistar rats given 1 or 2 ml kg À1 orally and compared with groups receiving glibenclamide (2 mg kg À1 ) or water. Glycemia was determined after 30, 60, 120, 240, and 360 min. The antihyperglycemic effect of CPSO was determined in healthy rats and in streptozotocin-induced diabetic rats (STZ); normal rats received 0.8 ml kg À1 CPSO, while diabetic rats received 1 ml kg À1 CPSO, their controls received water or 2 mg kg À1 glibenclamide. For the antihyperglycemic effect evaluation, all the animals were fasted for 16 h before treatment and received glucose orally at 1 g kg À1 30 min after treatment; blood was taken after 30, 90, 150, and 210 min. Intestinal glucose absorption was estimated in rat jejunum perfused with a solution containing 5.55 mmol l À1 glucose. Acute toxicity was determined in albino mice that received oral or intraperitoneal doses of 1, 3, or 5 ml kg À1 CPSO. Results: CPSO (p.o.) decreased postprandial hyperglycemia (60 min after glucose loading), 40.33% and 16.01%, in healthy and STZ-diabetic glucose-loaded rats, respectively. CPSO, also, significantly decreased intestinal glucose absorption by 25.42%. No adverse effects were seen in mice administered CPSO at up to 5 ml kg À1. Conclusion: CPSO is antihyperglycemic. The effect can be explained partly by inhibition of intestinal glucose absorption.

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Streptozotocin‐Induced Diabetic Models in Mice and Rats

Cited by 274 publications

References 27 publications

Streptozotocin-induced type-1-diabetes disease onset in Sprague–Dawley rats is associated with an altered intestinal microbiota composition and decreased diversity

Streptozotocin-induced type-1-diabetes disease onset in Sprague–Dawley rats is associated with an altered intestinal microbiota composition and decreased diversity

TRPM2-mediated intracellular Zn2+ release triggers pancreatic β-cell death

Evaluation of antidiabetic properties of cactus pear seed oil in rats

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