Abstract
Wuleen and Bahrs (l-3) first demonstrated the “stiffness syndrome” in guinea pigs. Van Wagtendonk and coworkers (4-7) reported studies of the metabolic changes resulting from the deficiency of the fat-soluble factor involved. The isolation of the active factor from raw cream and cane juice has been described by van Wagtendonk and Wulzen (8, 9). However, several investigators have been unable to demonstrate the characteristic deficiency symptoms in guinea pigs (10, 11). Using a diversity of diets, we were able to produce deficiency symptoms in guinea pigs which were apparently identical with those described by the Oregon State College group. Several synthetic diets, the skim milk diet of van Wagtendonk (4), and a commercial type of pelleted diet, were used for the study of this deficiency disease. The syndrome appeared the most rapidly and severely on the pellet diet. This is partly due to the poor growth and physical condition of the animals fed the synthetic or skim milk diets and partly to some property of the pellet diet which markedly induces a severe deficiency. This phenomenon may be caused by the presence in this diet of the “antagonistic factor” mentioned by van Wagtendonk and Wulzen (9).
Highlights
Since ergostanyl acetate appeared to be more active than the free sterol, our attention was mainly directed to this derivative
It cannot be said that any one of the pure compounds which we have found active is identical with the crystalline ‘Lantistiffness” factor isolated by van Wagtendonk and Wulzen, since we have not isolated any material from a natural source and the chemical nature of their active substance has not been revealed
The degree of structural specificity exhibited by the series of compounds tested is of considerable interest and has been discussed above
Summary
The skim milk diet of van Wagtendonk [4], and a commercial type of pelleted diet, were used for the study of this deficiency disease. The syndrome appeared the most rapidly and severely on the pellet diet This is partly due to the poor growth and physical condition of the animals fed the synthetic or skim milk diets and partly to some property of the pellet diet which markedly induces a severe deficiency. This phenomenon may be caused by the presencein this diet of the “antagonistic factor” mentioned by van Wagtendonk and Wulzen [9]. Some animals were already deficient when we received them, indicating that the previous dietary history of the animals is an important factor in determining the time of onset of the diseasein any given experiment
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