Abstract
Perinatal iron deficiency (PID) adversely programs offspring resulting in alterations in adult cardiometabolic function. Increased visceral adiposity is the proposed culprit for these sequelae, and may be potentiated by decreased physical activity. Herein, we determined (i) the effect of PID on visceral adipose tissue (VAT) and locomotor activity, and (ii) whether increased VAT is associated with blood pressure responsiveness to increased dietary sodium. Dams were fed a low iron diet (<10 mg/kg Fe) prior to and throughout gestation. From 12 to 35 weeks of age, locomotor activity (assessed by radiotelemetry) in PID offspring was 25% lower compared with control offspring (P<0.001). At 36 weeks of age, PID offspring had 15% more VAT than controls (P<0.05). Furthermore, the elevation of mean arterial pressure (by radiotelemetry) in response to increased sodium intake was approximately twofold greater in the PID offspring (P<0.05). PID results in increased visceral adiposity, which was associated with enhanced blood pressure responsiveness to dietary salt, perhaps due to programmed sedentary behavior.
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