| 包装 | 价格(元) |
| 10mM (in 1mL DMSO) | 电议 |
| 50mg | 电议 |
Cell lines | The white preadipocyte cell line 3T3-L1 and the brown preadipocyte cell line T37i |
Preparation Method | Three hours before stimulation, the differentiated cells were starved in starvation medium: DMEM (for 3T3-L1) or DMEM/F12 with 20 mM HEPES (for T37i) supplemented with P/S and 0.2% dextran-coated charcoal-treated FBS. Subsequently, the cells were stimulated for 24 hours in starvation medium containing 1 μL/mL ethanol vehicle control, 1 μM corticosterone, 0.2 μM insulin, or 1 μM corticosterone and 0.2 μM insulin. |
Reaction Conditions | 1 μM for 15min |
Applications | Corticosterone treatment altered many aspects of WAT and BAT morphology and function with some clear differences between male and female mice. The visceral depot gWAT had a substantially greater mass in vehicle-treated male mice than in vehicle-treated female mice. This sex-dependent pattern disappeared after corticosterone treatment, as corticosterone-treated male and female mice had a comparable gWAT mass. Two subcutaneous depots, iWAT and aWAT, also gained more mass upon corticosterone treatment, but there was no significant sex difference. Corticosterone treatment noticeably elevated the total WAT mass (the sum of the aforementioned WAT masses) without a significant sex difference. |
Animal models | Female BALB/c mice |
Preparation Method | The mice (three-to-four-week-old) were randomly divided into control group and Corticosterone group. Each mouse in the treatment group was injected with Corticosterone. Corticosterone was dissolved in DMSO to reach a concentration 0.2 mg/μL. The control group was injected with the same volume of DMSO. The treatment procedures were briefly presented as follows: On the first day at 7:00 a.m., mice were injected with 10 IU of PMSG. The control group (n = 40) and the test group (n = 40) were injected with 5 μL of DMSO and 5 μL of Corticosterone (0.2 mg/μL) every 8 hours. |
Dosage form | 0.2 mg/μL |
Applications | Corticosterone group's weight gain of the (1 mg/mouse) was slowed down, the action was slow, and the coat color was dull, compared with the control group. The ovary at each stage was weighed and the organ index was calculated. The results are shown in Figure 1. At 48 h, the gain of body weight in the Corticosterone group was significantly lower than that of the control group. Ovarian weight and ovarian index in the Corticosterone group was significantly lower than that of the control group. At 55 h, the gain of body weight, ovarian weight and ovarian index of the Corticosterone group were significantly lower than those of the control group. |
| 文献引用 | |
| 产品描述 | Corticosterone (17 deoxycortisol) is a glucocorticoid with oral activity and produced by adrenal cortex, which plays an important role in regulating the neuronal function of limbic system (including hippocampus, prefrontal cortex and amygdala). Corticosterone increased Rab mediated AMPAR membrane trafficking through SGK induced phosphorylation of GDI[1]. Corticosterone has been shown to cause hippocampal damage in a number of ways; altering dendritic tree of hippocampal neurons, apoptosis of hippocampal neurons[2]and inhibition of adult neurogenesis in dentate gyrus[3]. Firstly, high concentrations of Corticosterone were required to induce neuronal death in mouse hippocampal neurons, and secondly, glial cells in cultures were refractory to Corticosterone -induced apoptosis. Corticosterone induced apoptosis in primary cultures of hippocampal neurons in a dose dependent manner. Significant apoptosis started to be seen with 50 µM Corticosterone, and the number of apoptotic cells increased with increase in Corticosterone concentration[4]. Corticosterone-treated male mice were more severe whole-body insulin resistance in the, the high blood insulin concentrations upon corticosterone treatment resulted in lower glucose production in male mice but not in female mice. Because GCs stimulate and insulin suppresses hepatic gluconeogenesis, it is hard to separate the contribution of these two factors in the control of EGP. Quinn et al[5]have shown that female mice have a higher hepatic susceptibility to GCs. Thus, more pronounced actions of GCs in female mice might overrule the inhibitory effect of insulin on EGP or, alternatively, the FBG levels of corticosterone-treated mice were at their lowest limit, which requires EGP to prevent symptomatic hypoglycemia. Corticosterone treatment had opposite effects on GCR in male and female mice. GCR tended to increase in female mice but tended to decrease in male mice. These findings confirm that peripheral insulin resistance was more severe in corticosterone-treated males than in corticosterone-treated females because the elevated insulin levels by corticosterone treatment should have increased GCR substantially in both sexes. Altogether, The sex-differential effects of high-dose corticosterone treatment on insulin sensitivity were mainly driven by the more pronounced insulin resistance of peripheral tissues in male mice[6]. References: |
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