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Liang, K. et al.

Role of secondary hyperparathyroidism in the genesis of hypertriglyceridemia and VLDL receptor deficiency in chronic renal failure.

Recent studies have revealed marked down-regulation of hepatic lipase ( HL), lipoprotein lipase ( LPL) and very low density lipoprotein-receptor (VLDL-R) expressions in animals with chronic renal failure (CRF). Acquired deficiency of these proteins, which together play an important role in catabolism of triglyceride-rich lipoproteins, is involved in the pathogenesis of CRF hypertriglyceridemia. Down-regulation of HL and LPL expressions in CRF can be completely reversed by parathyroidectomy (PTx), suggesting the role of excess parathormone ( PTH). However, the role of hyperparathyroidism in the pathogenesis of CRF-induced VLDL-R deficiency has not been investigated before, and was studied here. To this end, VLDL-R mRNA (Northern analysis) and VLDL-R protein (Western analysis) of the fat pad and soleus muscle were compared in CRF (5/6 nephrectomized) rats, CRF animals with PTx (CRF-PTx) and sham-operated control animals. The CRF animals exhibited marked hypertriglyceridemia coupled with significant reductions in skeletal muscle and adipose tissue VLDL-R mRNA abundance and protein mass. Parathyroidectomy resulted in a significant, but partial, amelioration of CRF hypertriglyceridemia. However, in contrast to its effect on HL and LPL expressions, PTx did not improve VLDL-R expression, suggesting a PTH-independent mechanism for the latter abnormality. The differential effect of PTx on HL and LPL on the one hand and VLDL-R on the other can, in part, account for partial as opposed to complete correction of the associated hypertriglyceridemia with PTx in the CRF animals.[1]

References

Role of secondary hyperparathyroidism in the genesis of hypertriglyceridemia and VLDL receptor deficiency in chronic renal failure. Liang, K., Oveisi, F., Vaziri, N.D. Kidney Int. (1998) [Pubmed]

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