ABSTRACT There is evidence to suggest that an individual’s susceptibility to cardiovascular disease cannot be entirely explained by differences in adult environment (life style factors ie. low physical activity, high fat/salt diet), or by genetic causes, but may also be influenced by factors encountered in utero. Epidemiological studies have pointed to a correlation between low birth weight for gestational age (an index of suboptimal intrauterine environment) and increased incidence of adult-onset of cardiovascular and metabolic diseases (hypertension, non-insulin dependent diabetes mellitus, and hyperlipidaemia - known as Syndrome X). It has been proposed that an adverse intrauterine environment during a critical stage of development may permanently alter, or ‘program’ the development of fetal tissues, which enables the fetus to survive, but with adverse consequences in postnatal life. Many animal models in which intrauterine environment was altered by underutrition or by steroid treatment during entire gestation or during different parts of gestation demonstrated long- term (programming) effects on health of an adult. We have shown that brief dexamethasone exposure during early gestation in sheep programmed hypertension independently of insulin resistance of glucose or amino acid metabolism. Interestingly, it led to increased insulin sensitivity to the inhibition of lipolysis, which may increase susceptibility to the development of obesity postnatally. This review will mainly focus on the possible role of the renin-angiotensin system and hippocampal-hypothalamo-pituitary-adrenal axis in programming of adult cardiovascular disease. It will also raise some questions for future research.
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