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Increased hypothalamic-pituitary-adrenal axis activity and hepatic insulin resistance in low-birth-weight rats.

Increased hypothalamic-pituitary-adrenal axis activity and hepatic insulin resistance in low-birth-weight rats. Research Abstract Details 

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  • Increased hypothalamic-pituitary-adrenal axis activity and hepatic insulin resistance in low-birth-weight rats. Abstract Text:

    esben s buhlEsben S Buhl,susanne neschenSusanne Neschen,shin yonemitsuShin Yonemitsu,joerg rossbacherJoerg Rossbacher,dongyan zhangDongyan Zhang,katsutaro morinoKatsutaro Morino,allan flyvbjergAllan Flyvbjerg,pascale perretPascale Perret,varman samuelVarman Samuel,jung kimJung Kim,gary w clineGary W Cline,kitt falk petersenKitt Falk Petersen,esben s buhlEsben S Buhl,susanne neschenSusanne Neschen,shin yonemitsuShin Yonemitsu,joerg rossbacherJoerg Rossbacher,dongyan zhangDongyan Zhang,katsutaro morinoKatsutaro Morino,allan flyvbjergAllan Flyvbjerg,pascale perretPascale Perret,varman samuelVarman Samuel,jung kimJung Kim,gary w clineGary W Cline,kitt falk petersenKitt Falk Petersen,

    Individuals born with a low birth weight (LBW) have an increased prevalence of type 2 diabetes, but the mechanisms responsible for this association are unknown. Given the important role of insulin resistance in the pathogenesis of type 2 diabetes, we examined insulin sensitivity in a rat model of LBW due to intrauterine fetal stress. During the last 7 days of gestation, rat dams were treated with dexamethasone and insulin sensitivity was assessed in the LBW offspring by a hyperinsulinemic euglycemic clamp. The LBW group had liver-specific insulin resistance associated with increased levels of PEPCK expression. These changes were associated with pituitary hyperplasia of the ACTH-secreting cells, increased morning plasma ACTH concentrations, elevated corticosterone secretion during restraint stress, and an approximately 70% increase in 24-h urine corticosterone excretion. These data support the hypothesis that prenatal stress can result in chronic hyperactivity of the hypothalamic-pituitary-adrenal axis, resulting in increased plasma corticosterone concentrations, upregulation of hepatic gluconeogenesis, and hepatic insulin resistance.

    Increased hypothalamic-pituitary-adrenal axis activity and hepatic insulin resistance in low-birth-weight rats. Publishing Authors By Initials

    es buhlES Buhl,s neschenS Neschen,s yonemitsuS Yonemitsu,j rossbacherJ Rossbacher,d zhangD Zhang,k morinoK Morino,a flyvbjergA Flyvbjerg,p perretP Perret,v samuelV Samuel,j kimJ Kim,gw clineGW Cline,kf petersenKF Petersen,es buhlES Buhl,s neschenS Neschen,s yonemitsuS Yonemitsu,j rossbacherJ Rossbacher,d zhangD Zhang,k morinoK Morino,a flyvbjergA Flyvbjerg,p perretP Perret,v samuelV Samuel,j kimJ Kim,gw clineGW Cline,kf petersenKF Petersen,

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    Increased hypothalamic-pituitary-adrenal axis activity and hepatic insulin resistance in low-birth-weight rats. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: American journal of physiology. Endocrinology and

    VOLUME: 293

    Page Numbers: E1451-8

    Journal Abbreviation: Am. J. Physiol. Endocrinol. Me

    ISSN: 0193-1849

    DAY: 25

    MONTH: 09

    YEAR: 2007

    Increased hypothalamic-pituitary-adrenal axis activity and hepatic insulin resistance in low-birth-weight rats. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 100901226

    Increased hypothalamic-pituitary-adrenal axis activity and hepatic insulin resistance in low-birth-weight rats. Keywords Mesh Terms:

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    Chemical & Substance for Abstract: Increased hypothalamic-pituitary-adrenal axis activity and hepatic insulin resistance in low-birth-weight rats. Information

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    Grant and Affiliation Information for Increased hypothalamic-pituitary-adrenal axis activity and hepatic insulin resistance in low-birth-weight rats.

    AFFILIATION: Department of Pharmacology, Faculty of Health Sciences, Medical Department M, University of Aarhus, Aarhus, Denmark.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NIDDK

    GRANT: R01 DK40936

    ACRONYM: DK

    MEDLINETA: Am J Physiol Endocrinol Metab

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