Lipoprotein lipase in the kidney: activity varies widely among animal species

Ruge, Toralph; Neuger, Lucyna; Sukonina, Valentina; Wu, Gengshu; Barath, Stefan; Gupta, Jitendra; Frankel, Barbara J.; Christophersen, Bjørn O.; Nordstoga, K.; Olivecrona, Thomas; Olivecrona, Gunilla

doi:10.1152/ajprenal.00089.2004

Cited by 19 publications

(22 citation statements)

References 35 publications

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“…This enzyme is primarily expressed in tissues that use fatty acids for fuel or store large amounts of TGs, such as parenchymal cells of the adipose tissue, skeletal muscle, heart, and kidney cortex, and is secreted to the endothelium of local blood vessels (53). Previous studies by Olivecrona's group (46) demonstrated that LPL is present in mouse kidney proximal tubular epithelial cells; however, the regulation of LPL enzyme activity or its expression during acute kidney injury has not been previously examined. We found that similar to the effects of reducing epididymal white adipose tissue mass and LPL activity, cisplatin also inhibited the expression and enzyme activity of kidney LPL.…”

Section: Discussionmentioning

confidence: 99%

Reduced kidney lipoprotein lipase and renal tubule triglyceride accumulation in cisplatin-mediated acute kidney injury

Li¹,

Nagothu²,

Ranganathan

et al. 2012

American Journal of Physiology-Renal Physiology

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Peroxisome proliferator-activated receptor-α (PPARα) activation attenuates cisplatin (CP)-mediated acute kidney injury by increasing fatty acid oxidation, but mechanisms leading to reduced renal triglyceride (TG) accumulation could also contribute. Here, we investigated the effects of PPARα and CP on expression and enzyme activity of kidney lipoprotein lipase (LPL) as well as on expression of angiopoietin protein-like 4 (Angptl4), glycosylphosphatidylinositol-anchored-HDL-binding protein (GPIHBP1), and lipase maturation factor 1 (Lmf1), which are recognized as important proteins that modulate LPL activity. CP caused a 40% reduction in epididymal white adipose tissue (WAT) mass, with a reduction of LPL expression and activity. CP also reduced kidney LPL expression and activity. Angptl4 mRNA levels were increased by ninefold in liver and kidney tissue and by twofold in adipose tissue of CP-treated mice. Western blots of two-dimensional gel electrophoresis identified increased expression of a neutral pI Angptl4 protein in kidney tissue of CP-treated mice. Immunolocalization studies showed reduced staining of LPL and increased staining of Angptl4 primarily in proximal tubules of CP-treated mice. CP also increased TG accumulation in kidney tissue, which was ameliorated by PPARα ligand. In summary, a PPARα ligand ameliorates CP-mediated nephrotoxicity by increasing LPL activity via increased expression of GPHBP1 and Lmf1 and by reducing expression of Angptl4 protein in the proximal tubule.

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Section: Discussionmentioning

confidence: 99%

Reduced kidney lipoprotein lipase and renal tubule triglyceride accumulation in cisplatin-mediated acute kidney injury

Li¹,

Nagothu²,

Ranganathan

et al. 2012

American Journal of Physiology-Renal Physiology

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“…Third, the availability of apoC-I, apoC-II, apoC-III, and apoE, which are added to VLDL during assembly in the liver or are transferred to VLDL from HDL in the circulation, can affect the lipolytic activity [27,28,29,30,31], and a relative deficiency in apoC-II and increase in apoC-I and apoC-III has been reported in VLDL of subjects with CKD [31,32,33]. In addition, the kidney expresses both lipoprotein lipase and VLDL receptor [34,35]; therefore, CKD may affect the clearance of VLDL-TG and VLDL particles directly.…”

Section: Discussionmentioning

confidence: 99%

Very Low Density Lipoprotein Metabolism in Patients with Chronic Kidney Disease

Wang

Belani²,

Coyne³

et al. 2012

Cardiorenal Med

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Background: Hypertriglyceridemia is a common metabolic complication of chronic kidney disease (CKD) and an important risk factor for coronary heart disease in this patient population. The mechanisms responsible for the development of hypertriglyceridemia in subjects with CKD are not clear. Methods: We studied very low density lipoprotein triglyceride (VLDL-TG) and VLDL-apolipoprotein B-100 (VLDL-apoB-100) kinetics in vivo in 6 subjects with non-dialysis-dependent CKD (CKD-ND), 6 subjects with CKD treated with peritoneal dialysis (CKD-PD) and 24 sex-, age- and body mass index-matched control subjects with normal renal function (12 control subjects each matched with the CKD-ND and CKD-PD group, respectively). Results: The secretion rates of VLDL-TG and VLDL-apoB-100 into plasma were not different between CKD-ND or CKD-PD and their respective control groups. The mean residence times of VLDL-TG and VLDL-apoB-100 in plasma, which represents the time VLDL-TG and VLDL-apoB-100 spend in the circulation after secretion by the liver, tended to be greater in subjects with CKD-ND than in control subjects (222 ± 38 vs. 143 ± 21 min, p = 0.07, and 352 ± 102 vs. 200 ± 20 min, p = 0.06, respectively) and were about two-fold greater in subjects with CKD-PD compared with their control group (248 ± 51 vs. 143 ± 21 min and 526 ± 116 vs. 182 ± 16 min, respectively; both p ≤ 0.01). Conclusion: Impaired plasma clearance of VLDL-TG and VLDL-apoB-100 is the major abnormality associated with hypertriglyceridemia in patients with either CKD-ND or CKD-PD.

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“…The specific immunolocalization with anti-LPL antibodies by using immunohistochemistry is expressed in the glomerular endothelial, parietal epithelial, and tubular epithelial cells, where ectopic lipid deposition is observed in HSFD-fed minipigs with Oil Red O staining. However, there are conflicting reports that LPL is expressed by different types of renal cells, and its mRNA, mass and activity in kidneys vary widely among different species, such as human, mink, mouse, rat and Chinese hamster [11,12,30-33]. Mesangial cells, but not epithelial cells, express LPL mRNA in human and rat [11].…”

Section: Discussionmentioning

confidence: 99%

“…Mesangial cells, but not epithelial cells, express LPL mRNA in human and rat [11]. Immunostaining for kidney LPL indicates that the enzyme is present in tubular epithelial cells of mouse and mink [12] and vascular endothelium of glomeruli in guinea pig [34]. To our knowledge, the present study is the first to report that the expression and activity of LPL are evaluated in the kidney of Chinese Bama minipigs, and down-regulated by HSFD for 5 months.…”

Section: Discussionmentioning

confidence: 99%

“…Considering tissue-specific regulation and effects of LPL in lipid metabolism [10], the question arises whether LPL is involved in the mechanism of DN. LPL is expressed in mesangial and/or tubular epithelial cells, and localizes to the endothelial cells as in the blood vessels [11,12]. LPL enhances VLDL binding to glomerular mesangial cells and induces proliferation and platelet-derived growth factor (PDGF) expression independent of LPL's familiar role in triglyceride hydrolysis [13].…”

Section: Introductionmentioning

confidence: 99%

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Preventive effect of Ibrolipim on suppressing lipid accumulation and increasing lipoprotein lipase in the kidneys of diet-induced diabetic minipigs

Liu

Wang

et al. 2011

Lipids Health Dis

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BackgroundThe role of renal lipoprotein lipase (LPL) per se in kidney diseases is still controversial and obscure. The purpose of this study was to observe the preventive effects of Ibrolipim, a LPL activator, on lipid accumulation and LPL expression in the kidneys of minipigs fed a high-sucrose and high-fat diet (HSFD).MethodsMale Chinese Bama minipigs were fed a control diet or HSFD with or without 0.1 g/kg/day Ibrolipim for 5 months. Body weight, plasma glucose, insulin, lipids, LPL activity, and urinary microalbumin were measured. Renal tissue was obtained for detecting LPL activity and contents of triglyceride and cholesterol, observing the renal lipid accumulation by Oil Red O staining, and examining the mRNA and protein expression of LPL by real time PCR, Western Blot and immunohistochemistry.ResultsFeeding HSFD to minipigs caused weight gain, hyperglycemia, hyperinsulinemia, hyperlipidemia and microalbuminuria. HSFD increased plasma LPL activity while it decreased the mRNA and protein expression and activity of LPL in the kidney. The increases in renal triglyceride and cholesterol contents were associated with the decrease in renal LPL activity of HSFD-fed minipigs. In contrast, supplementing Ibrolipim into HSFD lowered body weight, plasma glucose, insulin, triglyceride and urinary albumin concentrations while it increased plasma total cholesterol and HDL-C. Ibrolipim suppressed the renal accumulation of triglyceride and cholesterol, and stimulated the diet-induced down-regulation of LPL expression and activity in the kidney.ConclusionsIbrolipim exerts renoprotective and hypolipidemic effects via the increase in renal LPL activity and expression, and thus the increased expression and activity of renal LPL play a vital role in suppressing renal lipid accumulation and ameliorating proteinuria in diet-induced diabetic minipigs.

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Lipoprotein lipase in the kidney: activity varies widely among animal species

Cited by 19 publications

References 35 publications

Reduced kidney lipoprotein lipase and renal tubule triglyceride accumulation in cisplatin-mediated acute kidney injury

Reduced kidney lipoprotein lipase and renal tubule triglyceride accumulation in cisplatin-mediated acute kidney injury

Very Low Density Lipoprotein Metabolism in Patients with Chronic Kidney Disease

Preventive effect of Ibrolipim on suppressing lipid accumulation and increasing lipoprotein lipase in the kidneys of diet-induced diabetic minipigs

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