0383 : Vascular programming of rats exposed in utero to maternal obesity

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• 作者：Cyrielle Payen¹ ; Maxime Gé ; rard² ; Jennifer Bourreau¹ ; Gé ; raldine Gascoin² ; Daniel Henrion¹ ; Celine Fassot ; ¹ ; ^{celine.fassot@inserm.fr" class="auth_mail" title="E-mail the corresponding author}
• 刊名：Archives of Cardiovascular Diseases Supplements
• 出版年：2016
• 出版时间：April 2016
• 年：2016
• 卷：8
• 期：3
• 页码：210
• 全文大小：47 K

文摘

Obesity in women of childbearing age is of particular concern since there is overwhelming evidence that being born to an obese mother increases the risk for the child of developing metabolic (obesity, insulin resistance) and cardiovascular (vascular dysfunction) disorders in later life. These findings suggest that the nutritional stress associated with maternal obesity has an impact on the longterm health of the offspring and could impact directly the fetal vascular function. However, current studies use animals in which vascular dysfunction and metabolic disorders are present simultaneously. Using a model of rats exposed in utero to maternal obesity, we aimed to determine if maternal obesity was able to directly re-program fetal vascular function or if development of such dysfunction was linked to metabolic abnormalities in offspring. Obese female rats (under hight-fat diet) were crossed with non-obese males. The metabolic status of male offspring from obese mothers (OMO) and mothers controls (CMO) was evaluated immediately after weaning (21j) and 2 months later by tolerance tests to insulin (ITT) and glucose (GTT), and plasmatic lipid profile. Vascular reactivity of the aorta was evaluated by myography (vascular reactivity in response to pharmacological agents). At weaning, GTT, ITT, plasmatic lipid profile as well as vascular reactivity of OMO were similar to those of CMO. At 3 months of age, although metabolic and lipid profiles are not modified, endotheliumdependant vasodilation was altered in OMO compared to CMO (acetylcholine dose-response curve EC₅₀: 2,46E-06±5,26E-07 vs 3,60E-07±5,01E-08 for OMO and CMO respectively, p<0,05). In presence of L-NAME, indomethacin (coxinhibitor) improved vasodilation showing that prostaglandins have a more important role in OMO than in CMO. Our results bring out a vascular dysfunction before the development of metabolic disorders and highlight a possible fetal vascular reprogramming in response to maternal obesity.

The author hereby declares no conflict of interest