Gastric inhibitory polypeptide as an endogenous factor promoting new bone formation after food ingestion.

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.

[Disorders of calcium metabolism during pregnancy and breast feeding]. / Zaburzenia gospodarki wapniowo-fosforanowej w ciazy i podczas laktacji.

Hypoparathyroidism following thyroidectomy or due to autoimmune process is the most common cause of hypocalcaemia. If untreated, maternal hypocalcaemia may stimulate fetal parathyroids which results in bone demineralization. Calcium supplementation may also reduce the risk of hypertension. Moreover, hypocalcaemia may inhibit the synthesis of calcium gene-related peptide (CGRP), which, in turn, decreases blood pressure and uterus contractions. In women of reproductive age hypercalcaemia is mostly due to hyperparathyroidism. The complications include toxemia, vomiting, and hypercalcaemic crisis. Maternal hypercalcaemia can suppress fetal parathyroid function and cause neonatal hypocalcaemia. The pharmacotherapy involves diuretics, fluids and oral phosphates. Bisphosphonates are contraindicated. Parathyroid surgery may be performed in the second trimester of pregnancy.

Congenital osteoclast deficiency in osteopetrotic (op/op) mice is improved by ovariectomy and orchiectomy.

We examined the changes in the appearance of osteoclasts in the femora of ovariectomized (OVX) or orchiectomized (ORX) op/op mice. Osteoclasts on the trabecular bone surface of the OVX or ORX op/op mice significantly increased in number seven or eight times in comparison with sham-operated op/op mice. Furthermore, TRAP-positive cells increased about four times in 100-week-old females and males, compared with sham-operated groups. These results have indicated that a sex hormone reduction due to OVX or ORX induces prominent recruitment of osteoclasts in op/op mice.