ECTS2013 Poster Presentations Osteoporosis: pathophysiology and epidemiology (49 abstracts)
1Hospital Rio Hortega, Valladolid, Spain; 2Hospital Marques de Valdecilla, Reticef, Santander, Spain.
Background: Surgical treatment of type 2 diabetes, specially in obese patients, has provided good results in the control of blood glucose and Hb1Ac although its effect on bone health is not clear. The aim of this study was to evaluate gene expression of bone remodelling markers in type 2 diabetic Goto-Kakizaki (GK) non-obese rats after gastrojejunal bypass and sleeve gastroplasty, and their relationship with hormonal parameters.
Materials and methods: We designed an experimental study in GK rats non operated, rats with gastrojejunal bypass and sleeve gastroplasty. Gene expression of markers of bone remodeling was measured. Levels of insulin, leptin, and glucagon-like peptide-1 (GLP-1) were determined.
Results: GK rats had decreased levels of osteocalcine expression, a marker of bone formation, compared with Wistar rats. Gene expression of markers of bone remodeling in GK rats was similar in the three groups studied (control, gastrojejunal bypass, and gastroplasty) although there was a trend to decreased RANKL in gastroplasty group. Significant differences in the osteocalcin: RANKL ratio were observed between controls and gastrojejunal bypass rats compared with gastroplasty rats. The behaviour of gastrointestinal hormones was antagonistic between both techniques as expected (GLP-1 gastrojejunal bypass 1.54±0.24 ng/ml vs GLP-1 gastroplasty 0.673±0.09, P=0.0001; leptin gastrojejunal bypass 1178±0.474 pg/ml vs leptin gastroplasty 7391±4054 pg/ml, P=0.002). There was a reduction in leptin in the bypass group associated with an increase in gastrectomized rats. In gastrectomized rats there was an inverse relationship between leptin and RANKL (r=−0771, P=0.072).
Conclusion: Our results show a more favourable profile of sleeve gastroplasty on bone remodelling. There was a trend to an increase in the expression of the osteocalcin gene, which is probably mediated by increased expression of leptin that inhibits the expression of RANKL.