To the Editor:
In their recent paper, Reseland et al.(1) studied the leptin transcription, translation, and secretion in primary cultures of human osteoblasts (HO). Leptin, the obese gene (OB) product, which is synthesized and secreted mainly by adipocytes, is becoming a relevant factor for bone-formation regulation,(2–5) in addition to its role as a hormonal regulator of body weight.(6) Although leptin action on osteoblasts has been described via hypothalamus,(2) we have started a study on a possible direct action of the hormone on HO in primary culture. The first step in our work has been to analyze if human osteoblasts in primary culture express OB-R, mainly OB-R L (isoform receptor with intracellular signal-transducing capabilities).(7) In concordance with the results reported by Reseland et al.(1) we detected, by reverse-transcription polymerase chain reaction (RT-PCR), transcripts corresponding to the isoform OB-R L of the leptin receptor in HO, obtained from two men and two women. However, Ducy et al.(2) could not detect OB-R L in human osteoblasts. To ensure that this finding is reliable, in our analysis we included samples obtained from other tissues such as kidney and skeletal muscle as negative controls. No signal was found in either of the tissues, verifying the true positivity of the OB-R L in the osteoblasts and reinforcing the validity of the findings obtained both by Reseland et al.(1) and by ourselves. This is important because other authors using nonquantitative PCR detected these transcripts in a large number of different tissues.(8) OB-R S isoform was detected in all samples. In summary, although our results strongly suggest OB-R L expression by osteoblasts, we believe that further functional studies showing the signal transduction by this receptor in HO are necessary.