J. Anim Sci.
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J. Anim Sci. 1983. 56:579-583.
© 1983 American Society of Animal Science
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Lipogenesis and Pancreatic Insulin Release in Fetal Pigs1

T. R. Kasser2, G. J. Hausman3, D. R. Campion3 and R. J. Martin2

University of Georgia,2, Athens 30602 and and US Department of Agriculture,3, Athens, GA 30613

Abstract

Body composition, liver and adipose lipogenesis, and pancreatic insulin release were examined in intact and decapitated fetal pigs on d 110 of gestation. Decapitation was on d 45 of gestation. Decapitated fetuses deposited more body lipid and less body ash compared with intact fetuses. Body weight, water, dry matter and protein remained similar in intact and decapitated fetuses. Hepatic fatty acid esterification and synthesis were two- and threefold greater, respectively, in decapitated than in intact fetuses. Fatty acid synthesis in subcutaneous adipose tissue of decapitated fetuses was three times greater than values obtained in intact fetuses. The data supported the concept that substrate availability from the dam was not the rate-limiting step in fetal pig lipid synthesis and storage. High growth hormone levels in normal fetal pigs may be responsible for inhibiting lipogenesis, while fetal decapitation would remove this inhibition and be associated with greater lipid deposition. However, pancreatic insulin release was greater in decapitated than in intact fetuses; an indication that elevated lipid deposition may also be due to greater fetal insulin secretion.

Footnotes

1 This research was supported by the Univ. of Georgia Exp. Sta. Project H666 and by NIH Grants HD15064 and AM00716.

2 Dept. of Foods and Nutr.

3 Anim. Physiol. Res. Units, Richard B. Russell Agricultural Res. Center, SEA, Agricultural Res.






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Copyright © 1983 by the American Society of Animal Science.