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  • American Diabetes Association  (3)
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  • American Diabetes Association  (3)
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  • 1
    Online Resource
    Online Resource
    Insulin and Leptin Resistance With Hyperleptinemia in Mice Lacking Androgen Receptor
    American Diabetes Association ; 2005
    In:  Diabetes Vol. 54, No. 6 ( 2005-06-01), p. 1717-1725
    Details
    In: Diabetes, American Diabetes Association, Vol. 54, No. 6 ( 2005-06-01), p. 1717-1725
    Abstract: Epidemiological evidence suggests that sex differences exist in type 2 diabetes. Men seem to be more susceptible than women to the consequences of obesity and sedentary lifestyle, possibly because of differences in insulin sensitivity and regional body fat deposition. Thus, lacking androgen receptor (AR) in male individuals may promote insulin resistance. To determine whether lacking AR in male individuals contributes to in vivo insulin resistance, an AR knockout model (AR−/y) was used to study the correlation between AR and insulin resistance. Progressive reduced insulin sensitivity and impaired glucose tolerance were seen in AR−/y mice with advancing age. Aging AR−/y mice displayed accelerated weight gain, hyperinsulinemia, and hyperglycemia, and loss of AR contributes to increased triglyceride content in skeletal muscle and liver. Leptin is higher in serum of AR−/y mice. Treatment with exogenous leptin fails to stimulate weight loss in AR−/y mice in advanced age, suggesting leptin resistance in the AR−/y/ mice. Exogenous dihydrotestosterone replacement fails to reverse the metabolic abnormalities and insulin resistance in AR−/y mice. Our in vivo studies demonstrate that androgen-AR plays key roles in the development of insulin and leptin resistance, which may contribute to the development of type 2 diabetes and cardiovascular disease.
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/diabetes.54.6.1717
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2005
    detail.hit.zdb_id: 1501252-9
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    Online Resource
  • 2
    Online Resource
    Online Resource
    Neuronal Androgen Receptor Regulates Insulin Sensitivity via Suppression of Hypothalamic NF-κB–Mediated PTP1B Expression
    American Diabetes Association ; 2013
    In:  Diabetes Vol. 62, No. 2 ( 2013-02-01), p. 411-423
    Details
    In: Diabetes, American Diabetes Association, Vol. 62, No. 2 ( 2013-02-01), p. 411-423
    Abstract: Clinical investigations highlight the increased incidence of metabolic syndrome in prostate cancer (PCa) patients receiving androgen deprivation therapy (ADT). Studies using global androgen receptor (AR) knockout mice demonstrate that AR deficiency results in the development of insulin resistance in males. However, mechanisms by which AR in individual organs coordinately regulates insulin sensitivity remain unexplored. Here we tested the hypothesis that functional AR in the brain contributes to whole-body insulin sensitivity regulation and to the metabolic abnormalities developed in AR-deficient male mice. The mouse model selectively lacking AR in the central nervous system and AR-expressing GT1-7 neuronal cells were established and used to delineate molecular mechanisms in insulin signaling modulated by AR. Neuronal AR deficiency leads to reduced insulin sensitivity in middle-aged mice. Neuronal AR regulates hypothalamic insulin signaling by repressing nuclear factor-κB (NF-κB)–mediated induction of protein-tyrosine phosphatase 1B (PTP1B). Hypothalamic insulin resistance leads to hepatic insulin resistance, lipid accumulation, and visceral obesity. The functional deficiency of AR in the hypothalamus leads to male mice being more susceptible to the effects of high-fat diet consumption on PTP1B expression and NF-κB activation. These findings suggest that in men with PCa undergoing ADT, reduction of AR function in the brain may contribute to insulin resistance and visceral obesity. Pharmacotherapies targeting neuronal AR and NF-κB may be developed to combat the metabolic syndrome in men receiving ADT and in elderly men with age-associated hypogonadism.
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/db12-0135
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2013
    detail.hit.zdb_id: 1501252-9
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  • 3
    Online Resource
    Online Resource
    Androgen Receptor Roles in Insulin Resistance and Obesity in Males: The Linkage of Androgen-Deprivation Therapy to Metabolic Syndrome
    American Diabetes Association ; 2014
    In:  Diabetes Vol. 63, No. 10 ( 2014-10-01), p. 3180-3188
    Details
    In: Diabetes, American Diabetes Association, Vol. 63, No. 10 ( 2014-10-01), p. 3180-3188
    Abstract: Prostate cancer (PCa) is one of the most frequently diagnosed malignancies in men. Androgen-deprivation therapy (ADT) is the first-line treatment and fundamental management for men with advanced PCa to suppress functions of androgen/androgen receptor (AR) signaling. ADT is effective at improving cancer symptoms and prolonging survival. However, epidemiological and clinical studies support the notion that testosterone deficiency in men leads to the development of metabolic syndrome that increases cardiovascular disease risk. The underlying mechanisms by which androgen/AR signaling regulates metabolic homeostasis in men are complex, and in this review, we discuss molecular mechanisms mediated by AR signaling that link ADT to metabolic syndrome. Results derived from various AR knockout mouse models reveal tissue-specific AR signaling that is involved in regulation of metabolism. These data suggest that steps be taken early to manage metabolic complications associated with PCa patients receiving ADT, which could be accomplished using tissue-selective modulation of AR signaling and by treatment with insulin-sensitizing agents.
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/db13-1505
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2014
    detail.hit.zdb_id: 1501252-9
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