Prenatal Dexamethasone Programs Expression of Genes in Liver and Adipose Tissue and Increased Hepatic Lipid Accumulation But Not Obesity on a High-Fat Diet

被引:85
作者
Drake, Amanda J. [1 ]
Raubenheimer, Peter J. [1 ]
Kerrigan, David [1 ]
McInnes, Kerry J. [1 ]
Seckl, Jonathan R. [1 ]
Walker, Brian R. [1 ]
机构
[1] Univ Edinburgh, Endocrinol Unit, Ctr Cardiovasc Sci, Queens Med Res Inst, Edinburgh EH16 4TJ, Midlothian, Scotland
基金
英国医学研究理事会;
关键词
IN-UTERO; INSULIN-RESISTANCE; METABOLIC SYNDROME; BIRTH-WEIGHT; GLUCOCORTICOID EXPOSURE; BLOOD-PRESSURE; GROWTH; CHILDREN; DISEASE; MODEL;
D O I
10.1210/en.2009-1088
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The association between low birth weight and cardiovascular disease is amplified by the development of obesity. We explored the effects of postnatal high-fat (HF) feeding in dexamethasone (Dex)-programmed rats, in which prenatal glucocorticoid overexposure is associated with reduced birth weight and adult glucose intolerance. Male Wistar rats exposed to Dex or vehicle (Veh) during the last week of gestation were weaned onto HF or control diets for 6 months. Dex-exposed animals were of lower birth weight and showed catch-up growth by 7 wk. There were no differences in obesity or hyperinsulinaemia between Dex-HF and Veh-HF animals. However, Dex-HF animals had increased hepatic triglyceride content compared with Veh-HF animals. mRNA transcript profiles in adipose tissue revealed depot-specific changes in the expression of genes involved in fatty acid esterification and triglyceride synthesis and storage with prenatal Dex exposure. Thus, antenatal glucocorticoid overexposure in rats does not confer increased sensitivity to HF diet-induced obesity, but increases susceptibility to fatty liver. This may be due to depot-specific-programmed alterations in fat metabolism in adipose tissue. (Endocrinology 151: 1581-1587, 2010)
引用
收藏
页码:1581 / 1587
页数:7
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