title: Effects of a high-salt diet on adipocyte glucocorticoid receptor and 11-beta hydroxysteroid dehydrogenase 1 in salt-sensitive hypertensive rats.
abstract: High-salt diets decrease insulin sensitivity in salt-sensitive hypertensive rats, and glucocorticoids promote adipocyte growth and may have pathophysiological roles in the metabolic syndrome. The aim of this study was to clarify the relationship between high-salt diet and the adipocyte glucocorticoid hormones in salt-sensitive hypertensive rats. Six-week-old Dahl salt-sensitive (DS) hypertensive rats and salt-resistant (DR) rats were fed a high-salt diet or a normal-salt diet for 4 weeks. Fasting blood glucose (FBG), serum adiponectin, plasma insulin, and corticosterone in plasma and in visceral adipose tissues, 11beta-hydroxysteroid dehydrogenase 1 (11beta-HSD1) activities in adipose tissues and glucose uptake in isolated muscle were measured. Animals underwent an oral glucose tolerance test (OGTT). The expression of mRNA for glucocorticoid receptor (GR), 11beta-HSD1 and tumor necrosis factor-alpha (TNF-alpha) in adipose tissues were measured using a real-time PCR. A high-salt diet did not influence FBG; however, decreased 2-deoxy glucose uptake and plasma insulin during OGTT in DS rats. The high-salt diet increased significantly adipose tissue corticosterone concentration and 11beta-HSD1 activities, gene expression for GR, 11beta-HSD1 and TNF-alpha in adipose tissues in DS rats compared with DR rats (p<0.05). The high-salt diet did not influence plasma corticosterone and serum adiponectin concentration in DS and DR rats. These results suggest that changes in GR and 11beta-HSD1 in adipose tissue may contribute to insulin sensitivity in salt-sensitive hypertensive rats.
authors: Division of Endocrinology and Hypertension, Department of Internal Medicine, Graduate School of Medical Science, Kanazawa University, 13-1 Takara-machi, Kanazawa 920-8641, Japan.
authors: Mikiya
authors: M
authors: Usukura
authors: Aoshuang
authors: A
authors: Zhu
authors: Takashi
authors: T
authors: Yoneda
authors: Shigehiro
authors: S
authors: Karashima
authors: Kunimasa
authors: K
authors: Yagi
authors: Masakazu
authors: M
authors: Yamagishi
authors: Yoshiyu
authors: Y
authors: Takeda
mesh_terms: D043205:11-beta-Hydroxysteroid Dehydrogenase Type 1 / Q000235:genetics*; D017667:Adipocytes / Q000187:drug effects* / Q000378:metabolism*; D000818:Animals; D004032:Diet; D005786:Gene Expression Regulation / Q000187:drug effects; D005947:Glucose / Q000378:metabolism; D006801:Humans; D006973:Hypertension / Q000235:genetics / Q000378:metabolism / Q000473:pathology*; D008297:Male; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D011965:Receptors, Glucocorticoid / Q000235:genetics*; D012965:Sodium Chloride / Q000494:pharmacology*; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics
chemical_list: D012333:RNA, Messenger; D011965:Receptors, Glucocorticoid; D014409:Tumor Necrosis Factor-alpha; D012965:Sodium Chloride; D043205:11-beta-Hydroxysteroid Dehydrogenase Type 1; D005947:Glucose