Francis A. Kallfelz

Dietary taurine deficiency and dilated cardiomyopathy in the fox

Taurine deficiency has been implicated as a potential cause of dilated cardiomyopathy. However, the relationship between taurine and myocardial function is presently unclear. The purpose of this study was to determine whether dilated cardiomyopathy in the fox is associated with dietary taurine deficiency. A total of 68 foxes from farms with a history of death caused by dilated cardiomyopathy and 14 foxes from a farm with no history of dilated cardiomyopathy were studied. Dilated cardiomyopathy was diagnosed by echocardiography in 48% of the foxes from one farm with a positive history and in none of the foxes from the control farm. Foxes less than 9 months of age were more commonly affected than older foxes (p = 0.03). Plasma taurine concentrations were significantly less (p less than 0.01) in foxes that had dilated cardiomyopathy (26.8 +/- 16.4 nmol/ml) than in the control foxes (99.3 +/- 60.2 nmol/ml). A significantly higher (p less than 0.01) incidence of dilated cardiomyopathy was present in foxes with a history of a sibling or offspring that died of dilated cardiomyopathy than in foxes without a family history of cardiac death. In one fox with dilated cardiomyopathy that was tested, the myocardial taurine concentration was lower (1.7 mumol/gm wet weight) than that of control foxes (7.3 +/- 1.6 mumol/gm wet weight). Hepatic cysteinesulfinic acid decarboxylase activity was significantly less (p less than 0.001) in foxes with dilated cardiomyopathy (0.97 +/- 0.2 nmol/mm.mg protein) than in control foxes (2.11 +/- 0.07 nmol CO2/mm.mg protein).(ABSTRACT TRUNCATED AT 250 WORDS)

Humeral skeletal development and plasma constituent changes in fetuses of ewes maintained on a low calcium diet from 60 days of gestation.

SummaryThe objective of this study was to evaluate the effects of a long-term, low-calcium diet on fetal calcium metabolism and fetal skeleton skeleton development in ewes. Eleven pregnant sheep were assigned to two groups, fed either a diet low in calcium (0.26% total dry matter) or normal in calcium (0.8% total dry matter) for 2 months, starting at 60 days gestational age. The ewes fed the low calcium diet showed lower plasma levels of calcium and higher plasma levels of hydroxyproline, parathyroid hormone, and 1,25 (OH)2D compared with the ewes fed the normal calcium diet. There were no differences in these variables between the two groups of fetuses. These observations suggest that the plasma components of calcium homeostasis measured in the fetal lamb in the present study are independent of the ewe and are not significantly affected by the presence of lowere maternal calcium for many weeks during pregnancy. Despite the ability of the fetus of the ewe on the low calcium diet to maintain relatively normal circulating plasma components of calcium homeostasis, long-term maternal hypocalcemia delayed fetal skeletal ossification as shown by histological examination of the fetal humerus. The fetal humerus from low calcium-fed ewes showed a lower proportion of bone versus cartilage (45.6±5.9 versus 57.4±4.6%, mean ±SD) lower ash content (15.4±1.5 versus 17.4±1.0%), and lower specific gravity (1.19±0.2 versus 1.22±0.02) (P<0.05) than the humerus from fetuses of normal calcium-fed ewes. This study shows that the long-term calcium intake of the ewe does affect fetal skeletal development, despite a lack of observable effects on fetal plasma concentrations of calcium or known calcium regulating hormones such as 1,25(OH)2D or parathyroid hormone.

Osteochondrosis in fetuses of ewes overfed calcium.

SummaryEwes were fedad libitum (up to maximum of 2.5 kg/day) a complete feed containing either 1.52% calcium (High Ca) or 0.59% calcium (Normal Ca) on a dry matter basis from day 50 of pregnancy, and the fetuses were removed at 133–135 days. Thyroid C cells, identified by indirect immunofluorescence, were more numerous (P<0.001) and plasma levels of 24,25-dihydroxycholecalciferol [24,25(OH)2D] were higher (P<0.09) in fetuses of High Ca ewes. These fetuses also had retarded cartilage differentiation in the proximal humeral epiphysis and metaphysis as well as transverse trabeculation in the epiphysis. These entities are two of the hallmarks of osteochondrosis. It was shown that feeding high dietary calcium to pregnant ewes caused osteochondrosis in their fetuses. Hypercalcitoninism and/or an adverse effect of supraphysiological levels of 24,25-dihydroxycholecalciferol may have been contributory to the skeletal abnormalities.

Calcium and 24,25-dihydroxyvitamin D: Inverse relation in cows with parturient paresis

SummaryRecent work suggests a role for 24,25-dihydroxyvitamin D in inhibiting mobilization of bone. This study was undertaken to investigate its possible role in the etiology of parturient paresis, a hypocalcemic condition of dairy cows occurring at the onset of lactation. This metabolic disease was chosen to serve as a model of impaired mineral homeostasis. The animals examined were parturient Holstein cows with (N=6) and without (N=7) parturient paresis. Determinations of serum 1,25-dihydroxyvitamin D, serum 24,25-dihydroxyvitamin D, and serum calcium were used to evaluate the 2 groups. The hormones were isolated using methylene chloride:methanol extraction, Sephadex LH-20 chromatography, and high-pressure liquid chromatography (HPLC). Quantitation was by competitive protein binding assays. Serum 1,25-dihydroxyvitamin D levels of affected cows were not significantly different from those of normal cows. The 24,25-dihydroxyvitamin D levels of paretic cows (3.48±0.27 ng/ml) were significantly higher than in the normal cows (2.03±0.34 ng/ml) (p<0.01). Linear regression analysis of the data from the paretic cows revealed an inverse relationship between serum calcium and 24,25-dihydroxyvitamin D (r=−0.94). This negative correlation between serum 24,25-dihydroxyvitamin D and serum total calcium in a naturally occurring hypocalcemic disease of dairy cattle may provide evidence that this metabolite is of significance in the etiology and pathogenesis of this syndrome.