STAT5A has an antilipogenic function in adipocytes by directly repressing fatty acid synthase expression in response to prolactin, which may contribute to the regulation of energy balance.
Should not inform clinical practice; leaves open STAT5A's role in systemic energy balance.
Growth hormone (GH) diminishes adipose tissue mass in vivo and decreases expression and activity of fatty acid synthase (FAS) in adipocytes. GH and prolactin (PRL) are potent activators of STAT5 and exert adipogenic and antiadipogenic effects in adipocytes. In this study, we demonstrate that GH and PRL decrease the mRNA and protein levels of FAS in 3T3-L1 adipocytes. We present evidence that indicates that FAS is repressed at the level of transcription. In addition, PRL responsiveness was shown to exist between -1,594 and -700 of the rat FAS promoter. Moreover, responsiveness to PRL was abolished with mutation of a site at position -908 to -893, which we have shown to bind STAT5A in a PRL-dependent manner. Taken together, these data strongly suggest that PRL directly represses expression of FAS in adipocytes through STAT5A binding to the -908 to -893 site. Furthermore, our results indicate that STAT5A has an antilipogenic function in adipocytes and may contribute to the regulation of energy balance.
No takes yet. Share an insight, caveat, or question.
Hogan et al. (2005) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: