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Antenatal glucocorticoid at clinically relevant doses alter glucose tolerance in the adult offspring in sheep
Author(s) -
Figueroa Jorge P.,
Massmann Angela G,
Zhang Jie,
Rose James C
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1196.1
Subject(s) - medicine , endocrinology , hyperinsulinemia , leptin , insulin resistance , offspring , adipose tissue , insulin , glucose tolerance test , betamethasone , gestation , glucocorticoid , glucose homeostasis , carbohydrate metabolism , pregnancy , biology , obesity , genetics
Exposure to glucocorticoids (GC) in the perinatal period is associated with alterations in glucose tolerance and hypertension in adult life. The aim of the present study was to study the effects of clinically relevant doses of GC on glucose tolerance and adipose tissue leptin expression. Pregnant sheep were treated with two IM doses of betamethasone (BM, 0.17 mg/kg) or vehicle 24‐hours apart at 80 days gestational age (term 145) and allowed to deliver at term. Adult offspring (12–18 months of age) of both sexes were chronically instrumented under general anesthesia to place intravascular catheters. Insulin sensitivity was evaluated both by iv glucose tolerance test (IVGTT) and euglycemic clamp (HEC) techniques. Leptin mRNA expression was determined by RPA in perirenal, omental and subcutaneous fat. Data Mean±SEM were analyzed by two way ANOVA and/or t test. A significant time and treatment (BM) effect was observed in plasma glucose during the IVGTT. BM also was associated with higher insulin plasma levels, but did not reach statistical significance. Leptin expression was significantly higher in perirenal but not omental adipose tissue of BM exposed sheep [0.28±0.1 vs 0.88±0.2;0.60±0.2 vs 1.0±0.2]. Exposure to a single course of GC at 0.55 gestation has longterm effects on glucose metabolism regulation. BM‐exposed sheep exhibit alterations in glucose tolerance, hyperinsulinemia and insulin resistance. HL 68728.