Chronic maternal feed restriction impairs growth but increases adiposity of the fetal guinea pig
Date
2005
Authors
Kind, K.
Roberts, C.
Sohlstrom, A.
Katsman, A.
Clifton, P.
Robinson, J.
Owens, J.
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Journal article
Citation
American Journal of Physiology. Regulatory Integrative and Comparative Physiology, 2005; 288(1):R119-R126
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Karen L. Kind, Claire T. Roberts, Annica I. Sohlstrom, Arkadi Katsman, Peter M. Clifton, Jeffrey S. Robinson, and Julie A. Owens
Conference Name
Abstract
Small size at birth has been associated with an increased risk of central obesity and reduced lean body mass in adult life. This study investigated the time of onset of prenatally induced obesity, which occurs after maternal feed restriction, in the guinea pig, a species that, like the human, develops substantial adipose tissue stores before birth. We examined the effect of maternal feed restriction [70% ad libitum intake from 4 wk before to midpregnancy, then 90% until day 60 gestation (term ~69 days)] on fetal growth and body composition in the guinea pig. Maternal feed restriction reduced fetal (–39%) and placental (–30%) weight at 60 days gestation and reduced liver, biceps muscle, spleen, and thymus weights, relative to fetal weight, while relative weights of brain, lungs, and interscapular and retroperitoneal fat pads were increased. In the interscapular depot, maternal feed restriction decreased the volume density of multilocular fat and increased that of unilocular fat, resulting in an increased relative weight of interscapular unilocular fat. Maternal feed restriction did not alter the relative weight of perirenal fat or the volume density of adipocyte populations within the depot but increased unilocular lipid locule size. Maternal feed restriction in the guinea pig is associated with decreased weight of major organs, including liver and skeletal muscle, but increased adiposity of the fetus, with relative sparing of unilocular adipose tissue. If this early-onset obesity persists, it may contribute to the metabolic and cardiovascular dysfunction that these offspring of feed-restricted mothers develop as adults.
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Copyright © 2005 by the American Physiological Society