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Dietary and pharmacological compounds altering intestinal calcium absorption in humans and animals

并行传输 吸收(声学) 钙代谢 骨化三醇 抗氧化剂 化学 内科学 内分泌学 生物化学 生物 医学 声学 磁导率 物理
作者
Vanessa Areco,María A. Rivoira,Valeria Rodríguez,Ana Maria Estivalete Marchionatti,Ágata R. Carpentieri,Nori Tolosa de Talamoni
出处
期刊:Nutrition Research Reviews [Cambridge University Press]
卷期号:28 (2): 83-99 被引量:61
标识
DOI:10.1017/s0954422415000050
摘要

The intestine is the only gate for the entry of Ca to the body in humans and mammals. The entrance of Ca occurs via paracellular and intracellular pathways. All steps of the latter pathway are regulated by calcitriol and by other hormones. Dietary and pharmacological compounds also modulate the intestinal Ca absorption process. Among them, dietary Ca and P are known to alter the lipid and protein composition of the brush-border and basolateral membranes and, consequently, Ca transport. Ca intakes are below the requirements recommended by health professionals in most countries, triggering important health problems. Chronic low Ca intake has been related to illness conditions such as osteoporosis, hypertension, renal lithiasis and incidences of human cancer. Carbohydrates, mainly lactose, and prebiotics have been described as positive modulators of intestinal Ca absorption. Apparently, high meat proteins increase intestinal Ca absorption while the effect of dietary lipids remains unclear. Pharmacological compounds such as menadione, dl-butionine-S,R-sulfoximine and ursodeoxycholic acid also modify intestinal Ca absorption as a consequence of altering the redox state of the epithelial cells. The paracellular pathway of intestinal Ca absorption is poorly known and is under present study in some laboratories. Another field that needs to be explored more intensively is the influence of the gene × diet interaction on intestinal Ca absorption. Health professionals should be aware of this knowledge in order to develop nutritional or medical strategies to stimulate the efficiency of intestinal Ca absorption and to prevent diseases.
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