Perinatal iron deficiency results in increased visceral adiposity in male Wistar rats

Abstract

Perinatal iron deficiency (ID) has adverse programming effects in adult offspring manifested as alterations in cardiovascular function as well as glucose and lipid metabolism. Given the importance of increased visceral adipose tissue (VAT) as a likely mediator of these sequalae, in the present study we determined the effect of perinatal ID on VAT in male wistar rats, and its association with other obesity‐related disturbances, such as salt sensitive arterial pressure (AP). Dams were fed a low iron diet (<10ppm Fe) prior to and throughout gestation. At delivery, dams were fed a normal iron diet (270ppm Fe). ID offspring had lower body weights (−11%) and markedly reduced hematocrits (−40%) at birth compared to controls. At 16 weeks of age, these animals had 20% more VAT (normalized to body weight) than controls. Furthermore, the elevation of AP (assessed by radiotelemetry) in response to increased sodium intake was 79% greater in the ID offspring compared to controls. In summary, perinatal ID resulted in a persistent increase in visceral adiposity associated with an enhanced hypertensive response to dietary salt. Supported by the Canadian Institutes of Health Research and the Bickell Foundation of Canada.