Breed differences in adult animals are determined during fetal development. If interventions are to be developed that influence growth of muscle and fat, it is important to know at which time during gestation breed differences appear and are fixed. The objective of this study was to characterize fetal development in cattle of different breeds. Pregnant cows of 4 cattle breeds with different growth impetus and muscularity were slaughtered under normal processing conditions and the fetuses were removed. German Angus, a typical beef cattle; Galloway, a smaller, environmentally resistant beef type; Holstein Friesian, a dairy type; and Belgian Blue, an extreme type for muscle growth were used. Fetuses of each breed were investigated at 3, 6, and 9 mo of gestation. Fetuses were weighed and dissected into carcass, organs, and muscles. Body fat weight was obtained using the Soxhlet extraction method. Fetal weight increased most rapidly in the third trimester of gestation mainly due to the accelerated muscle and fat deposition. The organ weight to body weight (BW) ratios decreased and the muscle and fat weight to BW ratios increased. At 3 mo of gestation, Galloway fetuses had the significantly smallest BW, half-carcass weight, leg weight, organ weight, muscle weight and shortest leg length. In contrast, Holstein fetuses had the significantly greatest BW, liver, kidney, and lung weights and significantly longest leg length among the 4 breeds, but no differences between Holstein Friesian and Belgian Blue were detected in half-carcass and leg weight. Indeed, Belgian Blue fetuses had the significantly greatest half-carcass weight, leg weight, and muscle weight at 9 mo of gestation, and Galloway had a significantly greater body fat to BW ratio than Holstein Friesian and Belgian Blue. These differences were not evident at 3 and 6 mo of gestation. These data show that the profound increase of tissue and organ weights occurred in later gestation in cattle fetuses even though breed differences were evident as early as 3 mo of gestation. Depending on the tissue of interest, impacting fetal growth likely needs to occur early in gestation before the appearance of breed-specific differences.

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Urinary citrate is an important inhibitor of calcium stone formation. Most of citrate reabsorption in the proximal tubule is thought to occur via a dicarboxylate transporter NaDC1 located in the apical membrane. OK cells, an established opossum kidney proximal tubule cell line, transport citrate but the characteristics change with extracellular calcium such that low calcium solutions stimulate total citrate transport as well as increase the apparent affinity for transport. The present studies address several fundamental properties of this novel process: the polarity of the transport process, the location of the calcium-sensitivity and whether NaDC1 is present in OK cells. OK cells grown on permeable supports exhibited apical > basolateral citrate transport. Apical transport of both citrate and succinate was sensitive to extracellular calcium whereas basolateral transport was not. Apical calcium, rather than basolateral, was the predominant determinant of changes in transport. Also 2,3-dimethylsuccinate, previously identified as an inhibitor of basolateral dicarboxylate transport, inhibited apical citrate uptake. Although the calcium-sensitive transport process in OK cells is functionally not typical NaDC1, NaDC1 is present in OK cells by Western blot and PCR. By immunolocalization studies, NaDC1 was predominantly located in discrete apical membrane or subapical areas. However by biotinylation, apical NaDC1 decreases in the apical membrane with lowering calcium. In sum, OK cells express a calcium-sensitive/regulated dicarboxylate process at the apical membrane which responds to variations in apical calcium. Despite the functional differences of this process compared to NaDC1, NaDC1 is present in these cells, but predominantly in subapical vesicles.