Aging and the role of estrogen in calcium mobilization in the laying hen

Abstract

Although estrogen (E₂) is intimately involved in calcium homeostasis in a number of vertebrate species, it is traditionally not considered a calciotropic hormone because its influence on extracellular calcium appears to be more indirect. In avian species, calcium homeostasis is closely linked to the ovulatory cycle and reproductive hormones. Sexual maturity and the onset of egg-laying in White Leghorn chickens increase plasma E₂, total blood calcium and duodenal calcium absorption (Hurwitz et al., 1973; Elaroussi et al., 1993). These three (plasma E₂, total calcium, duodenal calcium absorption) have been shown to decrease with age (Al-Batshan et al., 1994; Mahmoud et al., 1996).

Three studies were conducted to investigate the mechanism of action of E₂ in various tissues involved in calcium homeostasis in the laying hen. Both plasma E₂ and in vitro duodenal calcium-transport (CaT) were negatively affected by increasing age from pre-pubertal (∼16 wk) to late-stage (>70 wk). However, skeletal integrity, as measured by bone mineral content (BMC) and bone mineral density (BMD), increased in older birds; a corresponding shift in calcium from structural to medullary bone and/or changes in the collagen matrix may explain this finding in spite of the well-documented bone fragility that occurs with age. Estrogen receptor-α (ERα) populations were localized by immunocytochemistry in the shellgland, kidney, duodenum, and hypothalamus; again, as hens aged, there was a clear decrease in ERα immunostaining. Western blot analysis of ERα in the shellgland, kidney and duodenum confirmed this decrease. The antiestrogen, tamoxifen, had no effect on hormone profiles; however, duodenal CaT was significantly increased. The presence of ERα in duodenum suggests a direct role for E₂ at that site. A breakdown in this receptor as hens age, rather than in the more indirect kidney receptor-cascade, may provide a plausible explanation for the various phenomena seen in skeletal and shell calcification as hens age. The results from the present studies could radically redirect current industry practices designed to prevent production-related osteoporosis in the hen.