Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.24.3 (collagenase)
 18,340 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the present study, hypertriglyceridemia was induced by feeding S. D. rats with high carbohydrate diet (carbohydrate accounting for 80% of total calorie) for 5 days. Rat liver parenchymal cells (PC) and non-parenchymal cells (NPC) were prepared by collagenase method. Human plasma LDL, VLDL and HDL were isolated by density gradient ultracentrifugation method. 125I-LDL was labelled by ICI method. 125I-LDL binding to rat liver PC and NPC were measured by Goldstein and Brown's method. The results showed that both rat liver PC and NPC had LDL receptors to bind, uptake and degradate 125I labelled human plasma LDL. The Bmax of 125I-LDL binding to NPC was 7-fold higher than that of PC (P < 0.01), but the Kd values remained unchanged. The Bmax of 125I-LDL binding to liver NPC from hypertriglyceridemic rats was significantly higher than that of NPC from the normal diet (carbohydrate accounting for 60% of total calorie) rats (435.4 + 100.0 vs 307.1 +/- 76.8 ng/mg cell protein, n = 6, P > 0.05), but there was no difference in Kd between the HTG rats and normal rats (18.1 +/- 4.1 vs 17.2 +/- 4.0 micrograms/ml n = 6, P > 0.05). These results suggest that the increase in fractional catabolic rate of LDL in patients with hypertriglyceridemia reported by Vega and Grundy might be induced by the increase in number of LDL receptor on liver non-parenchymal cells.
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PMID:[Study on LDL receptors of liver non-parenchymal cells in hypertriglyceridemic rats induced by high carbohydrate diet]. 858 86