牛奶热
亚临床感染
钙
冰崩解
牧群
钾
酸中毒
酮症
甲状旁腺激素
哺乳期
动物科学
低钙血症
医学
化学
生物
内分泌学
内科学
怀孕
遗传学
有机化学
糖尿病
作者
Jesse P. Goff,R.L. Horst
出处
期刊:PubMed
日期:2003-01-01
卷期号:97: 145-7
被引量:20
摘要
Strategies for the prevention of milk fever in the United States have made several 180 degree changes over the last several decades. During the 1950's and 1960's evidence suggested that low calcium diets could be utilized to stimulate the parathyroid prior to calving to initiate calcium homeostasis prior to the onset of lactation. High calcium diets were avoided and the strategy worked--for a while, until more concentrated farming practices changed the cation composition of the forages. Although Norwegian scientists presented evidence of a role for cations and anions in milk fever during the late 1960's, recent studies have more precisely defined the physiological link between high diet potassium and tissue sensitivity to parathyroid hormone as a leading cause of milk fever. Manipulation of dietary cation-anion balance has been growing rapidly as a means of controlling not only milk fever but sub-clinical hypocalcemia as well. A recent United States survey found that 45% of dairy operations feed dry cows a "low potassium diet" to reduce milk fever. In addition some use anionic salts. About 27% of dairy farms feed dry cows a diet with added anions to induce a compensated metabolic acidosis which has proved effective in reducing subclinical hypocalcemia. These diets are often high in calcium.
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