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Androgenic status affects rat preadipocyte adipose conversion from two deep intra-abdominal (epididymal and perirenal) fat depots differently. The aim of this study was to establish whether these site-specific alterations of adipogenesis are related to altered expressions of the transcriptional factors regulating proliferation and differentiation of preadipocytes, c-myc and CCAAT/enhancer binding proteins (C/EBPs: C/EBPalpha and beta). The increased proliferation of epididymal and perirenal preadipocytes from castrated rats was not linked to variations in c-myc mRNA and protein levels. The expression of the early marker of adipogenesis, lipoprotein lipase (LPL), was decreased by androgenic deprivation in epididymal cells but remained insensitive to the androgenic status in perirenal preadipocytes. In contrast, LPL expression increased in subcutaneous preadipocytes from castrated rats, an effect which was partly corrected by testosterone treatment. Expression of C/EBPbeta was unaffected by androgenic status whatever the anatomical origin of the preadipocytes. In contrast, the mRNA and protein levels of C/EBPalpha were greatly decreased by androgenic deprivation in epididymal cells, an alteration which could not be corrected by in vivo testosterone administration. Altogether these results demonstrated that in preadipocytes androgenic deprivation affects site-specifically the expression of LPL, an early marker of adipogenesis and of C/EBPalpha, a master regulator of adipogenesis. These observations contribute to an explanation of why castration induces defective adipose conversion in rat epididymal preadipocytes specifically.
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ABSTRACT
The effects of castration and testosterone treatment on insulin- and phorbol ester (TPA)-stimulated lipogenic responses, phorbol dibutyrate-specific binding to protein kinase C (PKC) in the cytosol and the β-PKC isoform level quantified by immunoblotting were compared in rat fat cells from femoral subcutaneous (SC) and deep intra-abdominal (epididymal) fat deposits.
In control rats, the PKC content was lower in SC than in epididymal fat cells. After castration, the difference in PKC content between SC and epididymal fat cells was reduced and restored by testosterone treatment. However, androgenic status failed to modify the PKC content in SC fat cells. The lipogenic response to insulin was also differently regulated by the androgenic status in the two fat deposits. After castration, the response was increased in SC fat cells, while it was blunted in epididymal fat cells. These effects were corrected by testosterone administration.
These results demonstrate that, in white adipocytes, PKC is an additional biological parameter which varies according to the anatomical origin of the fat cells. They also provide evidence that PKC is controlled by androgens in vivo and emphasize the regional site specificity of such a control.
Journal of Endocrinology (1993) 138, 493–501
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Abstract
The effects of ovarian status on insulin- and phorbol 12-myristate 13-acetate (TPA)-stimulated lipogenic responses, phorbol ester-specific binding to protein kinase C (PKC) and immunoblot-quantified β- and ε-PKC isoform levels were compared in female rat fat cells from subcutaneous and deep intra-abdominal (parametrial) fat deposits.
In control rats, the cytosolic PKC content per cell was 70% lower in subcutaneous than in parametrial adipocytes. In subcutaneous and parametrial fat cells, the cytosolic PKC contents were reduced by ovariectomy and restored to normal by the administration of ovarian hormones (oestradiol plus progesterone). However, the lipogenic response to TPA was unaltered by ovarian status in both fat deposits, contrasting with the insulin-stimulated lipogenic response. This response increased in parametrial fat cells after ovariectomy and returned to normal after ovarian hormone treatment whereas, in subcutaneous fat cells, the insulin response was either unaltered by ovariectomy or increased by the administration of ovarian hormones. This study shows important site-related differences in fat cell PKC content but also reveals a similar modulation of this PKC by ovarian status, regardless of the anatomical localization of the fat cells. The physiological significance of these findings is discussed.
Journal of Endocrinology (1994) 140, 275–282
