Heparin-Released Plasma Lipases in Chronic Renal Failure and after Renal Transplantation

1979 ◽  
Vol 57 (2) ◽  
pp. 155-165 ◽  
Author(s):  
G. A. Crawford ◽  
E. Savdie ◽  
J. H. Stewart

1. Post-heparin plasma from normal subjects, patients with chronic renal failure and recipients of renal allografts were subjected to affinity chromatography on heparin—agarose (Sepharose 4B) columns to separate two fractions representing hepatic lipase and lipoprotein lipase respectively. 2. The optimum conditions for assay of each fraction were determined for both normal and uraemic plasma. 3. Normal males had activities of hepatic lipase which were higher, and activities of lipoprotein lipase which were lower, than normal females. There was no consistent relationship to age for either enzyme. 4. Thirty patients with chronic renal failure untreated by dialysis had significantly elevated serum triacylglycerol concentrations, and significantly lowered lipoprotein lipase activities when compared with control groups with similar ages for each sex. However, only in uraemic males was hepatic lipase activity significantly reduced. 5. In a study of female patients with chronic renal failure, there were no significant differences in activities of hepatic lipase or lipoprotein lipase or concentrations of serum triacylglycerols between eight patients receiving dialysis treatment and eight untreated by dialysis. 6. Although serum triacylglycerol concentrations were raised in the group of 15 renal transplant recipients, lipase activities were not diminished. The only significant change was elevation of hepatic lipase activity in female graft recipients. 7. No relationship was found between the enzyme activities and fasting serum triacylglycerol concentrations in any group. However, there was a weak inverse correlation between serum creatinine and hepatic lipase in female patients from both renal failure and transplant groups. 8. Similar results were obtained when the enzymes were assayed with, as substrate, a laboratory-prepared emulsion of 14C-labelled triolein in water with soya-bean lecithin as emulsifier, or commercially prepared soya-bean oil in water, emulsified with egg-yolk lecithin and containing glycerol (Intralipid).

1995 ◽  
Vol 269 (1) ◽  
pp. G103-G109 ◽  
Author(s):  
M. Klin ◽  
M. Smogorzewski ◽  
S. G. Massry

Chronic renal failure (CRF) is associated with increased Ca2+ content of liver and reduced hepatic lipase activity. This has been attributed to a rise in cytosolic Ca2+ ([Ca2+]i) of the hepatocytes, but data on this issue are lacking. We examined the [Ca2+]i and ATP content of hepatocytes as well as the activity of Na(+)-K(+)-adenosinetriphosphatase (Na(+)-K(+)-ATPase), Ca(2+)-ATPase, and Na+/Ca2+ exchanger of hepatic membrane vesicles from normal rats, animals with 6 wk of CRF, CRF normocalcemic parathyroidectomized (CRF-PTX) rats, and CRF and normal animals treated with verapamil (CRF-V, normal-V). [Ca2+]i in hepatocytes of CRF rats was higher (281 +/- 7.4 nM) and ATP lower (6.4 +/- 1.8 nmol/mg protein) than in normal (209 +/- 5.3 nM; 12.5 +/- 0.89 nmol/mg protein), CRF-PTX (212 +/- 1.0 nM; 13.7 +/- 0.79 nmol/mg protein), normal-V (215 +/- 2.3 nM; 14.2 +/- 0.77 nmol/mg protein), and CRF-V rats (209 +/- 7.4 nM; 14.8 +/- 0.72 nmol/10(6) cells). The Na(+)-K(+)-ATPase, the maximal velocity of Ca(2+)-ATPase, and the activity of the Na+/Ca2+ exchanger were reduced, whereas the Michaelis constant of Ca(2+)-ATPase was increase in CRF rats compared with the other four groups of rats. The values in the latter groups were not different.(ABSTRACT TRUNCATED AT 250 WORDS)


1984 ◽  
Vol 30 (9) ◽  
pp. 1568-1570 ◽  
Author(s):  
C Ehnholm ◽  
E A Nikkilä ◽  
P Nilsson-Ehle

Abstract We compared two methods for the direct selective measurement of hepatic lipase and lipoprotein lipase activities in human plasma after intravenous administration of heparin. Except for the emulsifier (gum arabic vs lecithin), the two assay media for hepatic lipase are essentially similar. Results for hepatic lipase by these two assays correlate well (r = 0.99). The assays for lipoprotein lipase in the two procedures differ in the way that hepatic lipase activity is eliminated (immunological inhibition vs a specific substrate emulsion), and also with regard to the emulsifier. The substrate emulsion stabilized by gum arabic (immunological assay) consistently yielded about three times higher enzymic activity than the specific substrate stabilized by lecithin. Experiments in which purified enzymes were used demonstrated that this systematic difference can be accounted for by the different emulsifiers. The satisfactory correlation (r = 0.92) between the two lipoprotein lipase assays, however, demonstrates that they measure the same enzymic activity.


1994 ◽  
Vol 140 (2) ◽  
pp. 203-209 ◽  
Author(s):  
K Vikman-Adolfsson ◽  
J Oscarsson ◽  
P Nilsson-Ehle ◽  
S Edén

Abstract Lipoprotein lipase and hepatic lipase are involved in the degradation and cellular uptake of lipids in peripheral tissues and the liver. These enzymes seem to be influenced by gonadal steroids in the rat as well as in man. Since gonadal steroids have been shown to influence the secretory pattern of GH and since the effect of gonadal steroids on several metabolic functions may be dependent upon their effects on GH secretion, the present study was undertaken to investigate the developmental regulation of heparin-releasable lipoprotein lipase and hepatic lipase activities in female and male rats, and to study the effects of gonadal steroids and different modes of GH administration to hypophysectomized rats on these enzyme activities. Female and male Sprague–Dawley rats from 20 to 65 days of age were studied. Hypophysectomy was performed at 50 days of age and these rats were given replacement therapy with thyroxine and cortisone. Groups of hypophysectomized rats were treated with either oestradiol valerate (0·1 mg/kg per day) or testosterone enanthate (1 mg/kg per day). Bovine GH (1 mg/kg per day) was given to groups of hypophysectomized rats either by two daily subcutaneous injections or by continuous infusion using osmotic minipumps. Hormone treatment was given for 1 week. Lipoprotein lipase and hepatic lipase activities were measured in heparinized plasma. There was no difference in lipoprotein lipase activity between male and female rats at 20 to 45 days of age. Lipoprotein lipase activity decreased between 45 and 65 days of age in male rats but not in females and, at 65 days of age, lipoprotein lipase activity was higher in females compared with males. Hepatic lipase activity increased from 20 to 45 days of age in both female and male rats but at 45 and 65 days of age it was higher in female than in male rats. Hypophysectomy decreased lipoprotein lipase and hepatic lipase activity in female rats. Neither oestradiol nor testosterone treatment had any effects in hypophysectomized rats. Treatment with bovine GH increased both lipoprotein lipase and hepatic lipase activities irrespective of its mode of administration and these effects were not influenced by additional treatment with oestradiol or testosterone. After the last injection of GH, lipoprotein lipase activity was increased for 12 h. Hepatic lipase activity was increased at 2 and 4 h after the last GH injection but after 12 h the activity had decreased, indicating that the time-course for the effects of GH on lipoprotein lipase and hepatic lipase may be different. It is concluded that GH markedly influences post-heparin lipoprotein lipase and hepatic lipase activities. The lack of effects of gonadal steroids on these activities in hypophysectomized rats suggests that the gonadal steroids influence these lipases via their influence on GH release. Journal of Endocrinology (1994) 140, 203–209


1988 ◽  
Vol 41 (2) ◽  
pp. 215
Author(s):  
RK Tume ◽  
RF Thornton ◽  
G WJohnson

Lipoprotein lipase and hepatic lipase have been shown to be present in the post-heparin plasma of sheep. Intravenous injection of heparin into sheep produced a rapid increase in the free fatty acid concentration and lipolytic enzyme activity of the plasma, both peaking within 5-15 min and then falling to pre-heparin levels within 30-60 min. Lipolytic activity was not detected in plasma before heparin treatment. Two distinct lipolytic activities were separated from the plasma by chromatography on heparin-Sepharose 6B. Lipoprotein lipase was identified on the basis that the lipolytic activity was dependent upon the addition of plasma, inhibited by 1M NaCI, and inhibited by a specific antiserum against lipoprotein lipase. The second lipolytic activity of plasma was identified as hepatic lipase, as it was not dependent upon plasma for activity, nor was it inhibited by 1M NaCI or antiserum against lipoprotein lipase. Its properties were identical to the lipase extracted from the liver of sheep. Lipoprotein-lipase activity, but not hepatic-lipase activity, was dependent upon the nutritional state of the sheep at the time of heparin injection. However, hepatic lipase comprised a significant proportion of the total lipolytic activity.


2006 ◽  
Vol 290 (2) ◽  
pp. F262-F272 ◽  
Author(s):  
N. D. Vaziri

Chronic renal failure (CRF) results in profound lipid disorders, which stem largely from dysregulation of high-density lipoprotein (HDL) and triglyceride-rich lipoprotein metabolism. Specifically, maturation of HDL is impaired and its composition is altered in CRF. In addition, clearance of triglyceride-rich lipoproteins and their atherogenic remnants is impaired, their composition is altered, and their plasma concentrations are elevated in CRF. Impaired maturation of HDL in CRF is primarily due to downregulation of lecithin-cholesterol acyltransferase (LCAT) and, to a lesser extent, increased plasma cholesteryl ester transfer protein (CETP). Triglyceride enrichment of HDL in CRF is primarily due to hepatic lipase deficiency and elevated CETP activity. The CRF-induced hypertriglyceridemia, abnormal composition, and impaired clearance of triglyceride-rich lipoproteins and their remnants are primarily due to downregulation of lipoprotein lipase, hepatic lipase, and the very-low-density lipoprotein receptor, as well as, upregulation of hepatic acyl-CoA cholesterol acyltransferase (ACAT). In addition, impaired HDL metabolism contributes to the disturbances of triglyceride-rich lipoprotein metabolism. These abnormalities are compounded by downregulation of apolipoproteins apoA-I, apoA-II, and apoC-II in CRF. Together, these abnormalities may contribute to the risk of arteriosclerotic cardiovascular disease and may adversely affect progression of renal disease and energy metabolism in CRF.


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