Decreases in local hormone biosynthesis and c-fos gene expression accompany differentiation of porcine preadipocytes |
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Authors: | H Rex Gaskins Jong-Won Kim Gary J Hausman |
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Institution: | (1) Department of Foods and Nutrition, University of Georgia, 30602 Athens, Georgia;(2) United States Department of Agriculture, P. O. Box 5677, 30613 Athens, Georgia;(3) Present address: The Jackson Laboratory, 04609 Bar Harbor, Maine |
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Abstract: | Summary To better understand possible autocrine or paracrine mechanisms involved in adipose tissue development, we have studied the
biosynthesis of insulinlike growth factor I (IGF-I) and prostaglandin E2 (PGE2) by cultured porcine preadipocytes in response to factors known to modulate cell growth and differentiation. The expression
of c-fos was also monitored because of the potential role of that proto-oncogene in coordination of growth and differentiation. Preadipocytes
were grown to confluence and then maintained in one of three media treatments: a) standard medium supplemented with 10% fetal
bovine serum (FBS), b) FBS supplemented with dexamethasone (Dex), c) FBS supplemented with dibutryladenosine 3′–5′-cyclic
monophosphate. Indirect measurements of growth indicated that cell proliferation did not differ due to media type. Histochemical
and enzymatic measurements of adipocyte development revealed that differentiation occurred only in those cultures exposed
to Dex. The increase in adipocyte differentiation in response to Dex was associated with a decrease in c-fos and actin RNA expression whereas the decrease in c-fos RNA expression in response to Dex was small (approximately 40%); immunocytochemical analysis indicated that induction of
Fos protein occurred only in undifferentiated cells. Thus, the cells responsible for the decrease in c-fos RNA expression are possibly those signaled to differentiate into adipocytes. Expression of IGF-I RNA and secretion of IGF-I
and PGE2 were also decreased in response to Dex treatment. These data provide the first demonstration that biosynthesis of IGF-I by
preadipocytes can be modulated by a potent inducer of adipocyte differentiation. The combined results indicate that glucocorticoids
may stimulate adipocyte differentiation by suppressing intracellular and putative intercellular mitogenic signals.
This work was supported in part by grant HD 18447 from the National Institutes of Health, Bethesda, MD (G. J. H.).
Mention of a trade mark, proprietary product, or specific equipment does not constitute a guarantee or warranty by the U.
S. Department of Agriculture or University of Georgia and does not imply its approval to the exclusion of other products that
may be suitable. |
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Keywords: | c-fos insulinlike growth factor I prostaglandin E2 adipocyte differentiation |
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