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Leptin treatment prevents type I diabetic marrow adiposity but not bone loss in mice
Author(s) -
Motyl Katherine J.,
McCabe Laura R.
Publication year - 2009
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.21608
Subject(s) - leptin , endocrinology , medicine , bone marrow , diabetes mellitus , osteocalcin , resorption , bone resorption , osteoporosis , bone density , adipose tissue , bone remodeling , bone mineral , hormone , obesity , biology , alkaline phosphatase , biochemistry , enzyme
Leptin is a hormone secreted by adipocytes that is implicated in the regulation of bone density. Serum leptin levels are decreased in rodent models of type 1 (T1‐) diabetes and in diabetic patients. Whether leptin mediates diabetic bone changes is unclear. Therefore, we treated control and T1‐diabetic mice with chronic (28 days) subcutaneous infusion of leptin or saline to elucidate the therapeutic potential of leptin for diabetic osteoporosis. Leptin prevented the increase of marrow adipocytes and the increased aP2 expression that we observed in vehicle‐treated diabetic mice. However, leptin did not prevent T1‐diabetic decreases in trabecular bone volume fraction or bone mineral density in tibia or vertebrae. Consistent with this finding, markers of bone formation (osteocalcin RNA and serum levels) in diabetic mice were not restored to normal levels with leptin treatment. Interestingly, markers of bone resorption (TRAP5 RNA and serum levels) were decreased in diabetic mice by leptin treatment. In summary, we have demonstrated a link between low leptin levels in T1‐diabetes and marrow adiposity. However, leptin treatment alone was not successful in preventing bone loss. J. Cell. Physiol. 218: 376–384, 2009. © 2008 Wiley‐Liss, Inc.