Martin J, Timofeeva E. Intermittent access to sucrose increases sucroselicking activity and attenuates restraint stress-induced activation of the lateral septum. Am J Physiol Regul Integr Comp Physiol 298: R1383-R1398, 2010. First published March 3, 2010 doi:10.1152/ajpregu.00371.2009.-Intermittent access to palatable food can attenuate anorectic and hormonal responses to stress in rats. The neuronal mechanisms of modulation of stress response by diets are not fully understood. The present study was conducted to create rat models with intermittent access to sucrose that demonstrate resistance to stress-induced hypophagia, to study the pattern of sucrose consumption by these rat models, and to investigate in which brain structures intermittent sucrose regimens modify stressinduced neuronal activation. The obtained results demonstrate that 6-wk intermittent access to sucrose without food restriction (4 day/wk ad libitum access to sucrose in addition to chow, and following 3 day/wk exclusive feeding of chow; SIA rats) and combined with food restriction (4 day/wk access to chow and sucrose restricted to 2 h/day, and following 3 days/wk on unrestricted chow; SIR rats) increased sucrose-licking activity. The alterations in the rats' feeding behavior were accompanied by a resistance of their body weight gain and food intake to 1-h restraint stress applied once per week. The chronic intermittent sucrose consumption significantly lowered, in the SIA and SIR rats, the levels of expression of corticotropin-releasing factor type 2 receptor and restraint stress-induced expression of c-fos mRNA in the medioventral part of the lateral septum. Conversely, the levels of the corticotropin-releasing factor type 2 receptor transcript in the ventromedial hypothalamic nucleus were decreased only in the foodrestricted SIR rats. The lower stress-induced neuronal activation in the medioventral part of the lateral septum may contribute to the attenuated anorectic stress response in the rats maintained on intermittent sucrose regimens. restraint stress; c-fos; corticotropin-releasing factor; hypothalamicpituitary-adrenal axis; corticotropin-releasing factor type 2 receptor ACCUMULATED EVIDENCE STRONGLY suggests that palatable diets can modify the effects of stress. Thus a feeding regimen with an option of eating palatable sucrose and lard may attenuate hypophagic responses to restraint stress (48). Restraint stress applied acutely and repeatedly usually promotes anorectic effects in rats fed regular chow (24,74,77). The anorectic effect of restraint stress apparently depends on the brain corticotropin-releasing factor (CRF) system, since the central application of the nonspecific CRF antagonist ␣-helical CRF considerably reversed restraint stress-induced anorexia (77). CRF is a key neuropeptide-regulating activity of the hypothalamic-pituitary-adrenal (HPA) axis. Activation of the HPA axis in response to stress has been extensively characterized. Briefly, exposure to stress activates the neurons in the parvocellular part of the paraventr...

The results of this study show the presence of a positive association of TSH-FT4 at the time of delivery, which may be modulated by the amount of iodine consumed by the mother during pregnancy.

Estrogen-related receptor ␣ (ERR␣), a member of the nuclear receptor superfamily, is closely related to the estrogen receptors (ER␣ and ER␤). The ERR␣ gene is estrogen-responsive in several mouse tissues and cell lines, and a multiple hormone-response element (MHRE) in the promoter is an important regulatory region for estrogen-induced ERR␣ gene expression. ERR␣ was recently shown to be a negative prognostic factor for breast cancer survival, with its expression being highest in cancer cells lacking functional ER␣. The contribution of ERR␣ in breast cancer progression remains unknown but may have important clinical implications. In this study, we investigated ERR␣ gene expression and chromatin structural changes under the influence of 17␤-estradiol in both ER-positive MCF-7 and ER-negative SKBR3 breast cancer cells. We mapped the nucleosome positions of the ERR␣ promoter around the MHRE region and found that the MHRE resides within a single nucleosome. Local chromatin structure of the MHRE exhibited increased restriction enzyme hypersensitivity and enhanced histone H3 and H4 acetylation upon estrogen treatment. Interestingly, estrogen-induced chromatin structural changes could be repressed by estrogen antagonist ICI 182 780 in MCF-7 cells yet were enhanced in SKBR3 cells. We demonstrated, using chromatin immunoprecipitation assays, that 17␤-estradiol induces ERR␣ gene expression in MCF-7 cells through active recruitment of co-activators and release of co-repressors when ERR␣ and AP1 bind and ER␣ is tethered to the MHRE. We also found that this estrogen effect requires the MAPK signaling pathway in both cell lines.Estradiol (E 2 ) 2 is required for the development and function of multiple tissue types and physiological systems in mammals, and it has been implicated in a range of pathological conditions, including the initiation and progression of breast cancer (Refs.

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