Early changes in the adaptation to a low calcium diet in the chick
Related Experiment Videos
Insights
Dietary calcium restriction in chicks rapidly impacts growth and hormone levels. Early hormonal and mineral metabolism adjustments help counteract calcium deficiency until longer-term adaptations occur.
Area of Science:
- Animal Physiology
- Endocrinology
- Mineral Metabolism
Background:
- Dietary calcium is crucial for chick growth and development.
- Calcium homeostasis involves complex hormonal and metabolic regulation.
- Understanding acute responses to calcium deficiency is vital for poultry health.
Purpose of the Study:
- To investigate the immediate effects of dietary calcium reduction on chick physiology.
- To examine the roles of growth hormone, prolactin, and vitamin D metabolism in response to low calcium.
- To elucidate the interplay between hormonal and mineral adjustments during calcium deficiency.
Main Methods:
- 3-week-old chicks were fed a diet with 0.1% calcium, a reduction from 1%.
- Measurements included growth rate, plasma hormone levels (growth hormone, prolactin), and renal hydroxylase activity.
- Bone calcium incorporation was assessed using 47Ca tracer.
Main Results:
- A low calcium diet (0.1% Ca) led to decreased growth rate and growth hormone levels within 12 hours.
- Renal 25-hydroxicholecalciferol-24-hydroxylase activity increased, and 47Ca bone incorporation decreased acutely.
- Over 2.5 days, renal 1-hydroxylase activity increased, plasma prolactin decreased, and other parameters normalized, suggesting adaptation.
Conclusions:
- Early hormonal and mineral metabolic adjustments in chicks can counteract acute dietary calcium shortage.
- These rapid responses precede longer-term adaptive changes for sustained calcium deficiency.
- Renal hydroxylase activities were not directly regulated by circulating growth hormone or prolactin levels.
Abstract:
Twelve hours after the diet of 3-week-old chicks was changed from a 1% to a 0.1% concentration of calcium (Ca), the growth rate and circulating levels of growth hormone had fallen while renal 25-hydroxecholecalciferol-24-hydroxylase had risen. The amount of 47Ca incorporated into bone from an injection given 18 h previously was lower than in the control birds. Over the following 2 1/2 days on the low Ca diet, the renal 1-hydroxylase activity rose and the plasma prolactin level fell, but the other parameters moved back toward the control level. It was concluded that early adjustments in hormonal and mineral metabolism counteract the acute effects of a dietary Ca shortage until longer-term adaptive changes begin to compensate for a continuing Ca deficiency. The renal hydroxylase activities were not directly influenced by the level of circulating growth hormone or prolactin.