-Acute nutrient ingestion leads to a rapid inhibition of bone resorption while effects on makers of bone formation are less marked or absent, suggesting that there is a transient shift toward skeletal accretion in the immediate postprandial period. The cellular bases for these effects are not clear. Glucose-dependent insulinotropic peptide (GIP), a known modulator of glucose-induced insulin secretion, is secreted from intestinal endocrine cells in response to nutrient ingestion. In addition to the effect of GIP on pancreatic ␤-cells, GIP receptors are expressed by osteoblastic cells in bone, suggesting a role for this incretin hormone in bone formation. To determine whether GIP also plays a role in the anti-resorptive effect of nutrient ingestion, osteoclasts were analyzed for the presence of GIP receptors by PCR, immunohistochemical and immunocytochemical analyses of bone tissue, and freshly isolated mature osteoclasts and osteoclast-like cells cultured in vitro. Osteoclast function was assessed by fetal long bone resorption assay and by use of the Osteologic disc assay. Our results demonstrate that GIP receptor transcripts and protein are present in osteoclasts. In addition, with the use of an in vitro organ culture system and mature osteoclasts, GIP was found to inhibit bone resorption in the organ culture system and the resorptive activity of mature osteoclasts. These data are consistent with the hypothesis that GIP inhibits bone breakdown through a direct effect on osteoclast-resorptive activity and suggest one mechanism for the postprandial reduction in markers of bone breakdown. nutrition; bone breakdown; incretin SERUM AND URINE MARKERS OF bone breakdown have been shown to decrease after a meal or an oral glucose tolerance test, suggesting that nutrient-induced elevations of a gastrointestinal factor are capable of inhibiting bone resorption (1). Although postprandial elevations in insulin were initially felt to be involved in preventing bone breakdown and have an impact on bone turnover (1,7,9,22), subsequent insulin clamp studies have shown that insulin had no effect on bone turnover if blood sugar was maintained constant (9), suggesting that other gastrointestinal factors play a role in suppressing bone turnover (7, 9). Two gut-secreted hormones known to be important modulators of glucose-induced insulin secretion ("incretin" hormones) are glucose-dependent insulinotropic peptide (GIP) and glucagon-like peptide-1 (GLP-1) (13).Our laboratory has previously reported that GIP receptors are present on osteoblasts, osteocytes, and chondrocytes and that addition of GIP to osteoblast-like cells leads to an increase in collagen type I expression and alkaline phosphatase activity, consistent with an anabolic effect (3). In addition, intermittent injection of GIP was shown to prevent bone loss in an ovariectomized rat model (2), while absence of the GIP receptor in GIP receptor knockout mice resulted in decreased bone formation, increased bone breakdown, and significantly lower bone mass (24,25). To further eva...

Although the manual placement of the cup resulted in 27% of outliers from the intended CA, the CA technique significantly reduced the dislocation after primary THA.

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Since a cementless stem has little version adjustability in the femoral canal, these findings are useful for surgeons in preoperative planning and to achieve proper component placement in THA.

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