Hyperlipoproteinemia in Renal Insufficiency

Heuck, Claus-Christian; Ritz, Eberhard

doi:10.1159/000181745

Cited by 56 publications

(24 citation statements)

References 36 publications

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“…In contrast to these studies, Cattram et al (35) (Figs. 1 and 2); therefore, hyperlipidemia in uremia is solely due to defect(s) in clearance as previously suggested (1)(2)(3)(4)(5)(33)(34)(35).…”

Section: Discussionmentioning

confidence: 55%

“…Increased lipid production, reduced peripheral tissue removal, or a combination of both could contribute to hyperlipidemia in uremia (1,2). It is presently well established that abnormalities of lipoprotein lipase, the tissue enzyme system that mediates triglyceride removal, exist in uremia (3)(4)(5).…”

Section: Discussionmentioning

confidence: 99%

“…The precise mechanism(s) causing hypertriglyceridemia in renal failure remains unknown (1,2). It could be due to either increased triglyceride production by liver and/or reduced peripheral removal.…”

Section: Introductionmentioning

confidence: 99%

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Insulin resistance in uremia. Characterization of lipid metabolism in freshly isolated and primary cultures of hepatocytes from chronic uremic rats.

F¹,

Lanza-Jacoby²

1983

J. Clin. Invest.

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A B S T R A C T We have studied the mechanism(s) of hyperlipidemia and liver insulin sensitivity in a rat model of severe chronic uremia (U).Basal lipid synthesis was decreased in freshly isolated hepatocytes from U when compared with shamoperated ad lib.-fed controls (alfC). Basal lipid synthesis in pair-fed controls (pfC) was in between U and alfC. Similarly, the activity of liver acetyl CoA carboxylase, fatty acid synthetase, citrate cleavage enzyme, malate dehydrogenase, and glucose-6-phosphate dehydrogenase was diminished in U. Muscle and adipose tissue lipoprotein lipase was also decreased.Insulin stimulated lipid synthesis in freshly isolated hepatocytes from alfC. Hepatocytes from U and pfC were resistant to this effect of insulin. To ascertain if the insulin resistance in U was due to starvation (chow intake 50% of alfC) or to uremia itself, the U and pfC were intragastrically fed an isocaloric diet via a Holter pump the last week of the experimental period. Hepatocytes from orally fed U and pfC were also cultured for 24 h in serum-free medium. While freshly isolated and cultured U hepatocytes remained insulin resistant, those from pfC normalized, in vivo and in vitro, when they were provided with enough nutrients.Conclusions

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Section: Discussionmentioning

confidence: 55%

Section: Discussionmentioning

confidence: 99%

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Insulin resistance in uremia. Characterization of lipid metabolism in freshly isolated and primary cultures of hepatocytes from chronic uremic rats.

F¹,

Lanza-Jacoby²

1983

J. Clin. Invest.

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“…It is well known, that the most frequently described lipid abnormality in uremia is hypertriglyceridemia [6, 7]. An inverse correlation can be found between triglyceride and HDL levels [22].…”

Section: Discussionmentioning

confidence: 99%

“…Chronic renal failure is frequently associated with disturbances in lipoprotein transport, alterations in lipoprotein concentration, and abnormalities in lipid and apoprotein composition of lipoproteins [6, 7, 8, 9]. The activities of key enzymes in the lipoprotein metabolism (lipoprotein lipase, hepatic lipase, lecithin-cholesterol acyltransferase) may be diminished [10, 11, 12].…”

Section: Introductionmentioning

confidence: 99%

The Serum Paraoxonase Activity in Patients with Chronic Renal Failure and Hyperlipidemia

Paragh¹,

Serés²,

Balogh³

et al. 1998

Nephron

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Human serum paraoxonase is physically associated with an apolipoprotein (Apo-A₁) and clusterin-containing high-density lipoprotein (HDL) and prevents low-density lipoprotein from lipid peroxidation. The aim of our study was to determine whether paraoxonase activity or phenotype is altered in patients with chronic renal failure and in hyperlipidemic subjects without renal insufficiency and to compare the values with those of healthy controls. We investigated the serum paraoxonase activity and polymorphism in 119 hemodialyzed uremic patients, 107 patients with primary hyperlipoproteinemia, and in 110 healthy control subjects. The serum paraoxonase activity was significantly decreased both in hyperlipidemic (p < 0.01) and uremic patients (p < 0.001) as compared with controls. On comparison, the serum paraoxonase activity was significantly lower (p < 0.001) in uremic than in hyperlipoproteinemic patients. The HDL and Apo-A₁ levels were as follows: uremic < hyperlipidemic < control. To assess whether the observed reduction in paraoxonase activity was due to HDL and Apo-A₁ level decreases, we standardized the enzyme activity for HDL and Apo-A₁ concentrations. We found that the standardized paraoxonase activity (paraoxonase/HDL ratio) was also lower in the uremic patients (103.3 ± 69.5) as compared with hyperlipidemic patients (137.64 ± 81.0) and controls (194.45 ± 94.45). The standardized values for Apo-A₁ showed a similar tendency: paraoxonase/Apo-A₁ ratio in uremic patients 89.64 ± 47.8, in hyperlipidemic patients 128.12 ± 69.83, and in controls 161.40 ± 47.35. The phenotypic distribution of paraoxonase (AA, AB, BB) did not change significantly in the patient groups. These results suggest that HDL concentration and phenotypic distribution of paraoxonase may not be the only determining factors, but that other as yet undetermined factors could be involved in the enzyme activity changes.

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Organ and Metabolic Complications: Lipids/Atherosclerosis

Ritz

Nowicki²,

Wiȩcek³

Replacement of Renal Function by Dialysis

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Hyperlipoproteinemia in Renal Insufficiency

Cited by 56 publications

References 36 publications

Insulin resistance in uremia. Characterization of lipid metabolism in freshly isolated and primary cultures of hepatocytes from chronic uremic rats.

Insulin resistance in uremia. Characterization of lipid metabolism in freshly isolated and primary cultures of hepatocytes from chronic uremic rats.

The Serum Paraoxonase Activity in Patients with Chronic Renal Failure and Hyperlipidemia

Organ and Metabolic Complications: Lipids/Atherosclerosis

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