https://transhumanist.ru/index.php?action=history&feed=atom&title=GIPR 2026-06-25T02:25:16Z История изменений этой страницы в вики MediaWiki 1.43.6 https://transhumanist.ru/index.php?title=GIPR&diff=5699&oldid=prev 2021-05-12T13:55:54Z

<p>Новая страница: «Gastric inhibitory polypeptide receptor precursor (GIP-R) (Glucose-dependent insulinotropic polypeptide receptor) ==Publications== {{medline-entry |title=Impact...»</p> <p><b>Новая страница</b></p><div>Gastric inhibitory polypeptide receptor precursor (GIP-R) (Glucose-dependent insulinotropic polypeptide receptor)<br /> <br /> ==Publications==<br /> <br /> {{medline-entry<br /> |title=Impact of glucose-dependent insulinotropic peptide on age-induced bone loss.<br /> |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/18072880<br /> |abstract=[[GIP]] is an important hormonal link between nutrition and bone formation. We show for the first time that BMSCs express functional [[GIP]] receptors, that expression decreases with aging, and that elevations in [[GIP]] can prevent age-associated bone loss. We previously showed that C57BL/6 mice lose bone mass as they age, particularly between 18 and 24 mo of age. The mechanisms involved in this age-dependent induced bone loss are probably multifactorial, but adequate nutrition and nutritional signals seem to be important. Glucose-dependent insulinotropic peptide ([[GIP]]) is an enteric hormone whose receptors are present in osteoblasts, and [[GIP]] is known to stimulate osteoblastic activity in vitro. In vivo, [[GIP]]-overexpressing C57BL/6 transgenic ([[GIP]] Tg( )) mice have increased bone mass compared with controls. Bone histomorphometric data suggest that [[GIP]] increases osteoblast number, possibly by preventing osteoblastic apoptosis. However, potential [[GIP]] effects on osteoblastic precursors, bone marrow stromal cells (BMSCs), had not previously been examined. In addition, effects of [[GIP]] on age-induced bone loss were not known. Changes in BMD, biomechanics, biomarkers of bone turnover, and bone histology were assessed in C57BL/6 [[GIP]] Tg( ) versus Tg(-) (littermate) mice between the ages of 1 and 24 mo of age. In addition, age-related changes in [[GIP]] receptor ([[GIP]]R) expression and [[GIP]] effects on differentiation of BMSCs were also assessed as potential causal factors in aging-induced bone loss. We report that bone mass and bone strength in [[GIP]] Tg( ) mice did not drop in a similar age-dependent fashion as in controls. In addition, biomarker measurements showed that [[GIP]] Tg( ) mice had increased osteoblastic activity compared with wildtype control mice. Finally, we report for the first time that BMSCs express [[GIP]]R, that the expression decreases in an age-dependent manner, and that stimulation of BMSCs with [[GIP]] led to increased osteoblastic differentiation. Our data show that elevated [[GIP]] levels prevent age-related loss of bone mass and bone strength and suggest that age-related decreases in [[GIP]] receptor expression in BMSCs may play a pathophysiological role in this bone loss. We conclude that elevations in [[GIP]] may be an effective countermeasure to age-induced bone loss.<br /> |mesh-terms=* Aging<br /> * Animals<br /> * Gastric Inhibitory Polypeptide<br /> * Glucose<br /> * Male<br /> * Mice<br /> * Mice, Inbred C57BL<br /> * Mice, Transgenic<br /> * Osteoporosis<br /> <br /> |full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2669161<br /> }}</div>

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