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Status: In Stock SZ-R006017 Mol. Status: Custom Synthesis SZ-R006018 Mol. Status: In Stock SZ-R006019 Mol. Status: In Stock SZ-R006021 Mol. Status: Custom Synthesis SZ-R006022 Mol. Status: Under Synthesis SZ-R006023 Mol. Status: Out of Stock SZ-R006024 Mol. Status: Custom Synthesis SZ-R006025 Mol. Status: Custom Synthesis SZ-R006026 Mol. Status: Custom Synthesis SZ-R006027 Mol. Status: Custom Synthesis SZ-R006028 Mol. Status: Custom Synthesis SZ-R006030 Mol.

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Upgrade your browser today or install Google Chrome Frame to better experience this site. Osteoporosis is a well-known disease and caused 9 million osteoporotic fractures worldwide in the year 2000 (1).

Osteoporotic fractures occurring at the spine and the forearm are associated with significant morbidity, but the most serious consequences arise in patients with hip fractures. Among those who survive this period, 1 in 5 requires nursing home care (3).

Thus, osteoporosis is associated with not only morbidity, but also decline in the quality of life. Osteoporosis is classified as primary osteoporosis induced by menopause or aging and secondary osteoporosis. Well-known causes of secondary osteoporosis include, endocrine disorders, such as Cushing's syndrome, hypogonadism, hyperthyroidism, hyperparathyroidism and diabetes mellitus (4). Gastrointestinal diseases, such as inflammatory bowel disease (5), rheumatoid arthritis (6) and myeloma bone disease (7), also induce osteoporosis.

In addition, the incidence of osteoporosis following gastrectomy has become a clinical issue. Although numerous studies have examined bone metabolic disorders following gastrectomy since it was first reported by Sarasin (8), the pathophysiology and the treatment of these disorders have not been fully elucidated.

Based on experimental results using rat models, general nutritional deficiencies (9), calcium malabsorption (10), vitamin D deficiency (11), loss of gastric acid (12) and secondary hyperparathyroidism (13) have been suggested as possible causes of bone metabolic disorder following gastrectomy. However, fully understanding the morbidity and developing clinical therapies for skeletal disorders is critical for improving patient quality of life. Recent epidemiological studies have shown that long-term therapy with proton pump inhibitors (PPIs) significantly increases the risk of osteoporosis and pathological hip fracture in patients with gastroesophageal reflux disease (14).

It is thought that PPIs reduce the production and secretion of hydrochloric acid in stomach, increase the pH in the stomach and inhibit absorption of insoluble calcium in the small intestine, thus leading to malabsorption of calcium phosphate and bone metabolism disorder (15,16).

PPIs also reportedly inhibit bone resorption by osteoclasts (17,18). However, the irreversible PPI mediated by the PPIs requires a specific pH environment. PPIs are all prodrugs that require two sequential protonation steps for activation (19). In the first step, a pyridine radical is activated, and in the second step, a benzimidazole radical is activated. The first step is required for accumulation of the PPI in the intracellular secretory canaliculus, and the second step is necessary for binding of the PPI with the proton pump.

This suggests that rabeprazole can efficiently combine with the proton pump to produce an immediate effect (21). For the two sequential protonation steps, the proton pump inhibitory action of the PPIs is extremely site-specific. In addition to the secretory canaliculi of the gastric parietal cells, the osteoclastic resorption vacuole may be the only other place in which proton pump inhibition by PPIs is known to occur.

Clinical studies have supported the theory that the short-term use of a PPI reduces bone resorption markers (18,22).

There are conflicting data regarding the effect of PPIs on bone metabolism, with little known concerning the effects of PPIs on osteoclasts and bone resorption. Therefore, the present study analyzed the effect of PPIs on bone metabolism following total gastrectomy (TG) in a rat model of osteoporosis. Using the rat TG model, poor calcium absorption that is observed during gastric anacidity was reproduced and the confounding antisecretory activity of the PPI was excluded to determine the specific effect of a PPI on osteoclasts.

In total, 75 male Wistar rats (Charles River Laboratories Japan, Inc. The rats were provided a standard solid chow, CRF-1 (Charles River Laboratories Japan, Inc. The animal welfare committee of Kanazawa University approved the experiments.