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Effect of selenium on appetite in the selenium-deficient chick
The Journal of Nutrition
|April 1, 1980
Summary
Oral selenium supplementation, particularly seleno-DL-methionine, rapidly increased feed intake and activity in chicks. This essential trace element also boosted glucose levels and glutathione peroxidase activity, showing swift biological effects.
Area of Science:
- Animal nutrition
- Trace element metabolism
- Biochemistry
Background:
- Selenium is an essential trace element crucial for various physiological functions.
- Selenium deficiency can lead to impaired growth and specific health issues in poultry.
- Understanding the rapid effects of selenium is vital for optimizing animal health and productivity.
Purpose of the Study:
- To investigate the immediate physiological and biochemical responses to oral selenium administration in selenium-deficient chicks.
- To compare the onset of effects between different forms of selenium (seleno-DL-methionine and selenite).
- To differentiate the impact of selenium on appetite from its role in pancreatic health.
Main Methods:
- Selenium-deficient chicks were administered oral doses of seleno-DL-methionine or selenite.
- Feed consumption, spontaneous activity, body weight gain, and plasma glucose were monitored.
- The activity of selenium-dependent glutathione peroxidase in plasma and liver was measured.
- The onset of pancreatic atrophy was assessed in relation to feed intake.
Main Results:
- Seleno-DL-methionine increased feed consumption within 2-3 hours; selenite showed a significant effect at 3-4 hours.
- Spontaneous activity, body weight gain, and plasma glucose increased 6-8 hours post-administration.
- Selenium-dependent glutathione peroxidase activity increased in plasma (8 hours) and liver (24 hours).
- Pancreatic atrophy onset was independent of feed intake levels.
Conclusions:
- Oral selenium administration elicits rapid physiological and biochemical responses in chicks.
- Different selenium forms exhibit varying speeds of action.
- Selenium's appetite-stimulating effect appears separate from its role in preventing nutritional pancreatic atrophy.