The cld mutation on mouse chromosome 17 causes combined lipase deficiency, leading to severe hypertriglyceridemia and early postnatal lethality, providing a model for studying lipid metabolism.
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Establishes cld mice as a model of lethal hyperchylomicronemia; leaves open applicability to human lipase deficiencies.
Two triglyceride lipases, lipoprotein lipase and hepatic triglyceride lipase, participate in the metabolism of plasma lipoproteins. A single recessive mutation, cld, on mouse chromosome 17 causes an apparent deficiency of both lipoprotein lipase and hepatic triglyceride lipase activities. Mice homozygous for this defect develop lethal hyperchylomicronemia within 2 days postpartum as a consequence of nursing. Plasma triglyceride values in affected mice often reach 20,000 milligrams per deciliter (100 times higher than that in normal littermates), and total lipase activity in plasma or tissues is 5 to 20 percent of that in controls.
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Paterniti et al. (1983) studied this question.
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