Comparing rat’s to human’s age: How old is my rat in people years?
(Impact Factor: 2.93).
07/2005; 21(6):775-7. DOI: 10.1016/j.nut.2005.04.002
Available from: Alexandra N Garcia
- "Animals were randomly assigned to one of eight treatment groups as illustrated in Fig. 1 to test different timings and durations of hormone treatment based on those used in the WHI, in which the women experienced an average 12-year delay in treatment relative to the last menstrual period. We calculated based upon the rats' life cycle compared to humans, that 3 months to an adult rat is equal to about 5 years in a woman (Sengupta, 2013; Quinn, 2005). Capsules containing either 100% cholesterol (Veh) or 5% 17b- estradiol/95% cholesterol (E 2 ) were implanted subcutaneously between the shoulder blades at the time of surgery. "
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ABSTRACT: The current study tested the "critical window" hypothesis of menopause that postulates that the timing and duration of hormone treatment determine their potential outcomes. Our focus was genes in the rat hypothalamus involved in social and affiliative behaviors that change with aging and/or estradiol (E2): Avp, Avpr1a, Oxt, Oxtr, and Esr2 in the paraventricular nucleus (PVN) and supraoptic nucleus (SON). Rats were reproductively mature or aging adults, ovariectomized, given E2 or vehicle treatment of different durations, with or without a post-OVX delay. Our hypothesis was that age-related changes in gene expression are mitigated by E2 treatments. Contrary to this, PVN Oxtr increased with E2, and Avpr1a increased with age. In the SON, Avpr1a increased with age, Oxtr with age and timing, and Avp was by duration. Thus, chronological age and E2 have independent actions on gene expression, with the "critical window" hypothesis supported by the observed timing and duration effects.
Available from: onlinelibrary.wiley.com
- "7 Furthermore, the progression and timeline of aging in humans are not equivalent to that in rodents. Quinn (2005) determined that the ratio of rat to human life span is 1 to 30, making the age of the host species an important factor to consider in the study design. 8 Moreover, rats reach mature skeletal size much earlier than humans. "
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ABSTRACT: Background: A variety of experimental animal models are used extensively to study mechanisms underlying cancer cachexia, and to identify potential treatments. The important potential confounding effect of dietary composition and intake used in many preclinical studies of cancer cachexia is frequently overlooked. Dietary designs applied in experimental studies should maximize the applicability to human cancer cachexia, meeting the essential requirements of the species used in the study, matched between treatment and control groups as well as also being generally similar to human consumption. Methods: A literature review of scientific studies using animal models of cancer and cancer cachexia with dietary interventions was performed. Studies that investigated interventions using lipid sources were selected as the focus of discussion. Results: The search revealed a number of nutrient intervention studies (n=44), with the majority including n-3 fatty acids (n=16), mainly eicosapentaenoic acid and/or docosahexaenoic acid. A review of the literature revealed that the majority of studies do not provide information about dietary design; food intake or pair-feeding is rarely reported. Further, there is a lack of standardization in dietary design, content, source, and overall composition in animal models of cancer cachexia. A model is proposed with the intent of guiding dietary design in preclinical studies to enable comparisons of dietary treatments within the same study, translation across different study designs, as well as application to human nutrient intakes. Conclusion: The potential for experimental endpoints to be affected by variations in food intake, macronutrient content, and diet composition is likely. Diet content and composition should be reported, and food intake assessed. Minimum standards for diet definition in cachexia studies would improve reproducibility of pre-clinical studies and aid the interpretation and translation of results to humans with cancer.
Available from: Maya Frankfurt
- "Following a one-week acclimation period during which animals were allowed to adjust to the new housing conditions, male and female adolescent subjects (Andreollo et al., 2012; Kwekel et al., 2010; Quinn, 2005), now aged 6 weeks, were randomly assigned to either a control (vehicle only) or experimental group (BPA exposed). BPA (N99% purity grade) was obtained from Sigma-Aldrich Corp (St. "
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ABSTRACT: We have previously demonstrated that adolescent exposure of rats to bisphenol-A (BPA), an environmental endocrine disrupter, increases anxiety, impairs spatial memory, and decreases dendritic spine density in the CA1 region of the hippocampus (CA1) and medial prefrontal cortex (mPFC) when measured in adolescence in both sexes. The present study examined whether the behavioral and morphological alterations following BPA exposure during adolescent development are maintained into adulthood. Male and female, adolescent rats received BPA, 40μg/kg/bodyweight, or control treatments for one week. In adulthood, subjects were tested for anxiety and locomotor activity, spatial memory, non-spatial visual memory, and sucrose preference. Additionally, stress-induced serum corticosterone levels and dendritic spine density in the mPFC and CA1 were measured. BPA-treated males, but not females, had decreased arm visits on the elevated plus maze, but there was no effect on anxiety. Non-spatial memory, object recognition, was also decreased in BPA treated males, but not females. BPA exposure did not alter spatial memory, object placement, but decreased exploration during the tasks in both sexes. No significant group differences in sucrose preference or serum corticosterone levels in response to a stress challenge were found. However, BPA exposure, regardless of sex, significantly decreased spine density of both apical and basal dendrites on pyramidal cells in CA1 but had no effect in the mPFC. Current data are discussed in relation to BPA dependent changes, which were present during adolescence and did, or did not, endure into adulthood. Overall, adolescent BPA exposure, below the current reference safe daily limit set by the U.S.E.P.A., leads to alterations in some behaviors and neuronal morphology that endure into adulthood.
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