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Gastric Inhibitory Polypeptide as an Endogenous Factor Promoting New Bone Formation after Food Ingestion

Departments of Diabetes and Clinical Nutrition (K.Ts., Y.Y., C.Y., N.H., Y.K., M.O., Y.S.) and Oral and Maxillofacial Surgery (K.B.), Kyoto University Graduate School of Medicine, Kyoto 606-8507, Japan; Division of Oral Anatomy (M.L., N.A.), Department of Oral Biological Science, Niigata University Graduate School for Medical and Dental Sciences, Center for Transdisciplinary Research, Niigata University, Niigata 951-8514, Japan; Department of Biochemistry (M.S., N.U.) and Institute for Oral Science (N.T.), Matsumoto Dental University, Nagano 399-0781, Japan; Department of Nutrition (K.Ta.), Kyoto Women’s University, Kyoto 605-8501, Japan; Department of Endocrinology and Diabetology (K.Ts., Y.O.), Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan; and Kansai Electric Power Hospital (Y.S.), Osaka 553-0003, Japan

Address all correspondence and requests for reprints to: Dr. Yuichiro Yamada, Department of Diabetes and Clinical Nutrition, Kyoto University Graduate School of Medicine, 54 Shogoin-Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan. E-mail: yamada{at}metab.kuhp.kyoto-u.ac.jp.

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.