Relationships among age, eggshell thickness and vitamin D metabolism and its expression in the laying hen

Abstract

Hens forming uncalcified shells synthesized less 1,25-hydroxycholecalciferol (1,25(OH) 2D 3) and less duodenal and eggshell gland (ESG) calbindin than normal laying hens. Hens forming thin shells had lower intestinal and ESG calbindin and its mRNA. Reducing ESG calcium (Ca 2+) transport by the carbonic anhydrase inhibitor acetazolamide, but not by dietary Ca 2+ restriction, reduced ESG calbindin and its mRNA. Two sub-populations of hens characterized by shell thickness (ST) maintained this characteristic throughout the whole production period. The differences between the two sub-populations increased with age. In old laying hens, the two sub-populations responded differently to dietary Ca 2+ restriction and to exogenous 1,25(OH) 2D 3. Those forming a thin shell responded to 1,25(OH) 2D 3 by a significant improvement in ST. The results suggest that: (a) the mechanism responsible for Ca 2+ transport to the egg shell consists of a vitamin D-dependent absorption of Ca 2+ and a multi-factor-dependent transfer of Ca 2+ to the shell; (b) both steps are, most likely, calbindin-mediated; however, the induction of calbindin gene expression in the ESG is predominantly calcium-dependent; and (c) the apparent defect in vitamin D metabolism or its expression in old hens is typical of, or even exclusive, to thin-shell-forming hens.