PubMed · 7361817
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J R Snyder, J R Newland. 1980. Hematology problem.. https://pubmed.ncbi.nlm.nih.gov/7361817/
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Severe fasting hypertriglyceridaemia (5 to 126 mmol/litre) and anaemia (packed cell volume < 11 per cent) was observed in 12 litters of kittens around the time of weaning; the entire litter was usually affected, with significant mortality. Lipid analysis revealed marked increases in chylomicrons and moderate increases in very low density lipoproteins. Supportive measures for the treatment of anaemia and weaning on to a low fat diet resulted in rapid resolution of the clinical signs, anaemia and hypertriglyceridaemia. On recovery, plasma was collected from kittens from five of the affected litters, plus a number of closely related cats and unrelated cats living in the same environment. The lipoprotein lipase (LPL) activity was mildly but significantly lower in the previously affected kittens, their parents and unaffected siblings, than in the unrelated cats. The cats had normal apolipoprotein C-II function, normal heparin binding activity and no evidence of a circulating inhibitor to LPL. They did not have the LPL gene mutation reported previously in LPL-deficient cats from New Zealand.
The mCAT-1 gene encodes a basic amino acid transporter that also acts as the receptor for murine ecotropic leukemia viruses. Targeted mutagenesis in embryonic stem cells has been used to introduce a germ-line null mutation into this gene. This mutation removes a domain critical for virus binding and inactivates amino acid transport activity. Homozygous mutant pups generated from these cells were approximately 25% smaller than normal littermates, very anemic, and died on the day of birth. Peripheral blood from homozygotes contained 50% fewer red blood cells, reduced hemoglobin levels, and showed a pronounced normoblastosis. Histological analyses of bone marrow, spleen, and liver showed a decrease in both erythroid progenitors and mature red blood cells. Mutant fetal liver cells behaved normally in in vitro hematopoietic colony-forming assays but generated an anemia when transplanted into irradiated C.B.-17 SCID mice. Furthermore, reconstitution of the white cell compartment of SCID mice by mutant fetal liver cells was less complete than that observed with a mixed population of wild-type and heterozygous fetal liver cells. Primary embryo fibroblasts from mutant mice were completely resistant to ecotropic retrovirus infection. Thus, mCAT-1 not only appears to be the sole receptor for a group of murine ecotropic retroviruses associated with hematological disease but also plays a critical role in both hematopoiesis and growth control during mouse development.