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Gastric Inhibitory Polypeptide as an Endogenous Factor Promoting New Bone Formation after Food Ingestion
Author(s) -
Katsushi Tsukiyama,
Yuichiro Yamada,
Chizumi Yamada,
Norio Harada,
Yukiko Kawasaki,
Masahito Ogura,
Kazuhisa Bessho,
Minqi Li,
Norio Amizuka,
Masahiro Sato,
Nobuyuki Udagawa,
Naoyuki Takahashi,
Kiyoshi Tanaka,
Yutaka Oiso,
Yutaka Seino
Publication year - 2006
Publication title -
molecular endocrinology
Language(s) - English
Resource type - Journals
eISSN - 1944-9917
pISSN - 0888-8809
DOI - 10.1210/me.2005-0187
Subject(s) - endocrinology , calcium , medicine , biology , ingestion , osteoporosis , calcium in biology , bone resorption , bone remodeling , calcium metabolism
Calcium plays a fundamental role as second messenger in intracellular signaling and bone serves as the body's calcium reserve to tightly maintain blood calcium levels. Calcium in ingested meal is the main supply and inadequate calcium intake causes osteoporosis and bone fracture. Here, we describe a novel mechanism of how ingested calcium is deposited on bone. Meal ingestion elicits secretion of the gut hormone gastric inhibitory polypeptide (GIP) from endocrine K cells in the duodenum. Bone histomorphometrical analyses revealed that bone formation parameters in the mice lacking GIP receptor (GIPR(-/-)) were significantly lower than those of wild-type (GIPR(+/+)) mice, and that the number of osteoclasts, especially multinuclear osteoclasts, was significantly increased in GIPR(-/-) mice, indicating that GIPR(-/-) mice have high-turnover osteoporosis. In vitro examination showed the percentage of osteoblastic cells undergoing apoptosis to be significantly decreased in the presence of GIP. Because GIPR(-/-) mice exhibited an increased plasma calcium concentration after meal ingestion, GIP directly links calcium contained in meal to calcium deposition on bone.

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