The critical, hormone-like function of the active metabolite of Vitamin D3, calcitriol, in regulating the intestinal uptake of dietary calcium, which is the primary mechanism for maintaining serum calcium homeostasis and providing the essential mineral substrate for bone mineralization. Efficient calcium absorption, driven by adequate Vitamin D3 status, is non-negotiable for the proper function of the bone remodeling cycle and the prevention of skeletal disorders like osteomalacia and osteoporosis. This is a fundamental axis of skeletal health.
Origin
This term is foundational to nutritional endocrinology, recognizing Vitamin D3 not merely as a vitamin but as a prohormone whose active form, calcitriol, exerts systemic endocrine control. The discovery of its mechanism in the gut established its central role in calcium metabolism. The link between Vitamin D deficiency and rickets/osteomalacia underscores its importance.
Mechanism
Calcitriol binds to the Vitamin D Receptor on the enterocytes lining the small intestine, triggering a cascade of gene expression changes that increase the synthesis of calcium-binding proteins, such as calbindin, and calcium channels. This upregulation facilitates the active transport and passive diffusion of calcium across the intestinal wall into the bloodstream. This mechanism ensures that sufficient calcium is available to meet the demands of bone formation and systemic physiological needs.
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