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Hypertension and metabolic disorders are multi-factorial and caused by both genetic and environmental factors. However, recent epidemiological and experimental studies indicate an inverse relationship between birth weight and blood pressure suggesting that pre-natal or in-utero insults may program chronic disease in adult life; particularly high blood pressure, renal disease, obesity and type II diabetes. Low birth weight is a crude marker of an unhealthy environment during fetal growth. The highest rates of low birth weight and also the highest rates of hypertension and obesity are both localized in the Southern part of United States, with Mississippi ranking first.
To investigate the mechanisms linking low birth weight and hypertension and metabolic disorders, we use a unique model of placental insufficiency to generate low birth weight rat offspring. In adult male offspring, the renin angiotensin system and male sex hormone are potential mediators, but the exact link and mechanisms have not been clearly expounded. Sex differences are observed in this model of low birth weight-programmed hypertension as the female low birth weight rat does not share the common pathway of high blood pressure with the male low birth weight rat. The mechanisms which this sex difference in fetal programmed chronic disease need to be elucidated. Moreover, the effect of a mismatch of pre- and post-natal events or examination of the post-natal factors that modify prenatal-programmed hypertension and metabolic disorder is still unknown. Thus, understanding the complexity of the developmental programming of adult disease may useful to develop therapies for early prevention, detection and treatment options for increased cardiovascular and metabolic risk that occurs in response to an adverse fetal environment.
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