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Identification of Functional Prolactin (PRL) Receptor Gene Expression: PRL Inhibits Lipoprotein Lipase Activity in Human White Adipose Tissue

Department of Physiology (C.L., L.S., S.E., H.B.), The Wallenberg Laboratory (B.O.), and Department of Obstetrics and Gynecology (B.W., B.E.), Sahlgrenska University Hospital, Göteborg University, 405 30 Göteborg, Sweden

Address all correspondence and requests for reprints to: Dr. Håkan Billig, Department of Physiology, Göteborg University, P.O. Box 434, SE 405 30 Göteborg, Sweden. E-mail: hakan.billig{at}fysiologi.gu.se.

During lactation serum levels of prolactin (PRL) are elevated, and the activity of lipoprotein lipase (LPL) is decreased in the adipose tissue and increased in the mammary gland. However, PRL has been suggested to affect the adipose tissue in an indirect fashion during lactation. In the present study, we demonstrated expression of four PRL receptor (PRLR) mRNA isoforms (L, I, S1_a, and S1_b) in human sc abdominal adipose tissue and breast adipose tissue using RT-PCR/Southern blot analysis. In addition, L-PRLR [relative molecular mass (M_r) 90,000] and I-PRLR (M_r 50,000) protein expression was detected in human sc abdominal adipose tissue and breast adipose tissue using immunoblot analysis. Two additional protein bands with the molecular weight M_r 40–35,000 were also detected. The direct effect of PRL on the regulation of LPL activity in human abdominal adipose tissue cultured in vitro was investigated. PRL (500 ng/ml) reduced the LPL activity in human adipose tissue to 31 ± 7.7%, compared with control. GH (100 ng/ml) also reduced the LPL activity, to 45 ± 8.6%, compared with control. In agreement with previous studies, cortisol increased the LPL activity and GH inhibited cortisol-induced LPL activity. Furthermore, we found that PRL also inhibited the cortisol-induced LPL activity. Taken together, these results demonstrate a direct effect of PRL, via functional PRLRs, in reducing the LPL activity in human adipose tissue, and these results suggest that LPL might also be regulated in this fashion during lactation.

This work was supported by Grants 10380 and 13550 from the Swedish Medical Research Council and grants from The Royal Society of Arts and Sciences in Göteborg, The Swedish Society for Medical Research, and Assar Gabrielsson’s research fund.

C.L. and L.S. were equal contributors to this work.

Abbreviations: BMI, Body mass index; I, intermediate prolactin receptor isoform; L, long prolactin receptor isoform; M_r, relative molecular mass; LPL, lipoprotein lipase; PRL, prolactin; PRLR, PRL receptor; S1_a and S1_b, PRLR isoforms.

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