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Dietary Copper Improves Intestinal Morphology via Modulating Intestinal Stem Cell Activity in Pigs
Lanmei Yin1, Qing Yang1, Yiming Zhang1,2
1Laboratory of Animal Nutrition and Human Health, Hunan Provincial Key Laboratory of Animal Intestinal Function and Regulation, Hunan International Joint Laboratory of Animal Intestinal Ecology and Health, College of Life Sciences, Hunan Normal University, Changsha 410081, China.
Dietary copper supplementation in piglets promotes intestinal development by enhancing intestinal stem cell activity and proliferation. This study reveals copper
Area of Science:
- Animal Nutrition
- Gastroenterology
- Developmental Biology
Background:
- Copper (Cu) is a vital micronutrient for animal health.
- Dietary copper's impact on piglet growth and intestinal health is known, but mechanisms are unclear.
- Intestinal stem cells (ISC) are crucial for intestinal epithelium development and renewal.
Purpose of the Study:
- To investigate the hypothesis that dietary copper influences piglet intestinal development by modulating ISC activity.
- To explore the underlying mechanisms of copper's effects on the intestine.
Main Methods:
- A study involving 85 piglets fed varying dietary copper sulfate (CuSO4) concentrations (25-125 mg/kg) in two phases.
- Analysis of intestinal morphology, including villus width and height, and Ki67-positive cell counts.
- In vitro experiments assessing copper sulfate's effects on ISC activity, including organoid budding efficiency and crypt development.
Main Results:
- Increased dietary copper decreased villus width but increased Ki67-positive cells (cell proliferation) in phase 1.
- Higher copper levels (125 mg/kg) in phase 2 significantly increased villus height.
- In vitro, copper sulfate enhanced organoid budding efficiency, crypt depth, and crypts per organoid, indicating improved ISC activity.
Conclusions:
- Dietary copper supplementation improves intestinal morphology in finishing pigs.
- Copper promotes intestinal development through enhanced cell proliferation and modulation of intestinal stem cell activity.
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