title: Changes in insulin sensitivity during GnRH agonist treatment in premenopausal women with leiomyoma.
abstract: OBJECTIVE
  The purpose of this study was to determine (1) the influence of estrogen deficiency induced by gonadotropin-releasing hormone (GnRH) agonist administration on insulin sensitivity as well as hormones and factors related to insulin resistance and (2) the differences in the influence for these parameters by the degree of basal insulin sensitivity.
  
  
  METHODS
  Thirty-five women diagnosed with leiomyoma were enrolled in this study. Serum levels of fasting glucose, insulin, sex steroid hormones, sex hormone-binding globulin (SHBG), vascular inflammatory markers and cytokines before and at 6months after commencement of GnRH agonist administration were examined.
  
  
  RESULTS
  In all women, levels of insulin, glucose and homeostasis model assessment of insulin resistance (HOMA-IR) were not significantly changed. However, in women who had a low HOMA-IR before treatment, levels of insulin, glucose and HOMA-IR showed significant increases and total testosterone level showed a significant decrease. In women who had a high HOMA-IR, levels of insulin, HOMA-IR and SHBG were significantly decreased and levels of highly sensitive C-reactive protein, soluble intercellular adhesion molecule-1, E-selectin and monocyte chemoattractant protein-1 were significantly increased.
  
  
  CONCLUSIONS
  Change in insulin sensitivity caused by GnRH agonist administration for premenopausal women with leiomyoma differs depending on baseline insulin sensitivity before treatment.
authors.affiliation: Department of Obstetrics and Gynecology, Institute of Health Biosciences, The University of Tokushima Graduate School, Japan. sumika87@clin.med.tokushima-u.ac.jp
authors.forename: Sumika
authors.initials: S
authors.lastname: Matsui
authors.forename: Toshiyuki
authors.initials: T
authors.lastname: Yasui
authors.forename: Anna
authors.initials: A
authors.lastname: Tani
authors.forename: Kotaro
authors.initials: K
authors.lastname: Kunimi
authors.forename: Hirokazu
authors.initials: H
authors.lastname: Uemura
authors.forename: Satoshi
authors.initials: S
authors.lastname: Yamamoto
authors.forename: Akira
authors.initials: A
authors.lastname: Kuwahara
authors.forename: Toshiya
authors.initials: T
authors.lastname: Matsuzaki
authors.forename: Naoko
authors.initials: N
authors.lastname: Tsuchiya
authors.forename: Mitsutoshi
authors.initials: M
authors.lastname: Yuzurihara
authors.forename: Yoshio
authors.initials: Y
authors.lastname: Kase
authors.forename: Minoru
authors.initials: M
authors.lastname: Irahara
mesh_terms: D000328:Adult; D018931:Antineoplastic Agents, Hormonal / Q000627:therapeutic use*; D001786:Blood Glucose / Q000032:analysis; D015992:Body Mass Index; D002097:C-Reactive Protein / Q000378:metabolism; D018932:Chemokine CCL2 / Q000378:metabolism; D016207:Cytokines / Q000097:blood; D019040:E-Selectin / Q000378:metabolism; D005260:Female; D007987:Gonadotropin-Releasing Hormone / Q000819:agonists*; D006801:Humans; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D007889:Leiomyoma / Q000188:drug therapy*; D016729:Leuprolide / Q000627:therapeutic use*; D008875:Middle Aged; D017697:Premenopause; D012738:Sex Hormone-Binding Globulin / Q000378:metabolism; D013739:Testosterone / Q000097:blood; D014594:Uterine Neoplasms / Q000188:drug therapy*
chemical_list: D018931:Antineoplastic Agents, Hormonal; D001786:Blood Glucose; D018932:Chemokine CCL2; D016207:Cytokines; D019040:E-Selectin; D007328:Insulin; D012738:Sex Hormone-Binding Globulin; D018799:Intercellular Adhesion Molecule-1; D007987:Gonadotropin-Releasing Hormone; D013739:Testosterone; D002097:C-Reactive Protein; D016729:Leuprolide