Lipoprotein lipase mass and activity in severe hypertriglyceridemia

Kobayashi, Junji; Hashimoto, Hideyuki; Fukamachi, Isamu; Tashiro, Jun; Shirai, Kohji; Saitō, Yasushi; Yoshida, Sho

doi:10.1016/0009-8981(93)90144-s

Cited by 126 publications

(76 citation statements)

References 12 publications

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“…Also, if either macrophages derived from peripheral blood monocytes or adipose tissue can be used as samples, differentiation from HTGL becomes unnecessary. If changes in the LPL protein level are involved, the immunological protein assay is effective and there have been a few reports on the use of ELISA in Japan [21][22][23] , which has been adopted as a general clinical laboratory test 21) . If the LPL activity is markedly reduced, and if the concentration of apolipoprotein C-, a critical cofactor of LPL, is normal or elevated, the diagnosis of this condition would be considered definite.…”

Section: D) Diagnosismentioning

confidence: 99%

Diagnosis and Management of Type I and Type V Hyperlipoproteinemia

Gotoda

Shirai

Ohta

et al. 2012

JAT

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Both type and type hyperlipoproteinemia are characterized by severe hypertriglyceridemia due to an increase in chylomicrons. Type hyperlipoproteinemia is caused by a decisive abnormality of the lipoprotein lipase (LPL)-apolipoprotein C-system, whereas the cause of type hyperlipoproteinemia is more complicated and more closely related to acquired environmental factors. Since the relationship of hypertriglyceridemia with atherosclerosis is not as clear as that of hypercholesterolemia, and since type and hyperlipoproteinemia are relatively rare, few guidelines for their diagnosis and treatment have been established; however, type and hyperlipoproteinemia are clinically important as underlying disorders of acute pancreatitis, and appropriate management is necessary to prevent or treat such complications. Against such a background, here we propose guidelines primarily concerning the diagnosis and management of type and hyperlipoproteinemia in Japanese.

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Section: D) Diagnosismentioning

confidence: 99%

Diagnosis and Management of Type I and Type V Hyperlipoproteinemia

Gotoda

Shirai

Ohta

et al. 2012

JAT

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“…At 1 month of age, venous blood was obtained by venipuncture just before infants were fed. Serum LPLm concentrations were measured by a sandwich enzyme-linked immunosorbent assay using a specific monoclonal antibody against LPL (Daiichi Pure Chemicals, Tokyo, Japan), as reported by Kobayashi et al (1993). Serum IGF-I concentrations were analyzed by immunoradiometric assay kit (FUJI-FILM RI Pharma Co., Ltd, Tokyo, Japan).…”

Section: Serum Assaysmentioning

confidence: 99%

“…Over the last decade, several studies showed that LPL mass in non-heparinized serum (LPLm) was a useful, physiologically relevant index of LPL-mediated lipolysis of plasma triacylglycerol (TG), because of low concentrations in LPL-deficient patients (Kern et al, 1990;Kobayashi et al, 1993) and significant relationships between serum LPLm, lipids, lipoproteins, and insulin resistance (Kobayashi et al, 1993(Kobayashi et al, , 2007Tornvall et al, 1995;Watanabe et al, 1999;Hanyu et al, 2007;Saiki et al, 2007). The aim of this study is to know the influence of LPL on neonatal subcutaneous fat growth.…”

Section: Introductionmentioning

confidence: 99%

Association between serum lipoprotein lipase mass concentration and subcutaneous fat accumulation during neonatal period

et al. 2010

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Background/Objectives: Subcutaneous adipose tissue grows rapidly during the first months of life. Lipoprotein lipase (LPL) has a quantitatively important function in adipose tissue fat accumulation and insulin-like growth factor-I (IGF-I) is a determinant of neonatal growth. Recent studies showed that LPL mass in non-heparinized serum (LPLm) was an index of LPL-mediated lipolysis of plasma triacylglycerol (TG). The objective was to know the influence of serum LPL and IGF-I on neonatal subcutaneous fat growth, especially on catch-up growth in low birth weight infants. Subjects/Methods: We included 47 healthy neonates (30 males, 17 females), including 7 small for gestational age. We measured serum LPLm and IGF-I concentrations at birth and 1 month, and analyzed those associations with subcutaneous fat accumulation. Results: Serum LPLm and IGF-I concentrations increased markedly during the first month, and positively correlated with the sum of skinfold thicknesses both at birth (r ¼ 0.573, P ¼ 0.0001; r ¼ 0.457, P ¼ 0.0035) and at 1 month (r ¼ 0.614, Po0.0001; r ¼ 0.787, Po0.0001, respectively). In addition, serum LPLm concentrations correlated inversely to very low-density lipoprotein (VLDL)-TG levels (r ¼ À0.692, Po0.0001 at birth; r ¼ À0.429, P ¼ 0.0052 at 1 month). Moreover, the birth weight Z-score had an inverse association with the postnatal changes in individual serum LPLm concentrations (r ¼ À0.639, Po0.0001). Conclusions: Both serum LPLm and IGF-I concentrations were the determinants of subcutaneous fat accumulation during the fetal and neonatal periods. During this time, LPL-mediated lipolysis of VLDL-TG may be one of the major mechanisms of rapid growth in subcutaneous fat tissue. Moreover, LPL, as well as IGF-I, may contribute to catch-up growth in smaller neonates.

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“…The plasma LPL mass was measured by a sandwich ELISA with commercial reagent kits (Daiichi Kagaku). 29 The EC-LPL level was calculated by subtraction of the preheparin LPL concentration from the postheparin LPL concentration.…”

Section: Tfpi and Lpl Antigen Determinationmentioning

confidence: 99%

Intravascular Free Tissue Factor Pathway Inhibitor Is Inversely Correlated With HDL Cholesterol and Postheparin Lipoprotein Lipase but Proportional to Apolipoprotein A-II

Kawaguchi¹,

Miyao²,

Noguchi³

et al. 2000

ATVB

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Abstract-To elucidate the distribution and clinical implications of tissue factor pathway inhibitor (TFPI) concentrations, we measured TFPI levels consisting of preheparin free, lipoprotein-bound (Lp-bound), and endothelial cell-anchor pools in 156 patients with coronary artery disease (average age, 61.2Ϯ9.1 years; range, 32 to 78 years) by heparin infusion (50 IU/kg) and compared them with the preheparin TFPI levels of 229 healthy subjects (average age, 59.6Ϯ9.4 years; range, 41 to 80 years). The patients had lower preheparin free TFPI and lower HDL cholesterol (HDL-C) levels than the healthy subjects with equivalent Lp-bound forms (free TFPI, 15.9Ϯ6.5 versus 19.2Ϯ8.1 ng/mL). In a partial correlation analysis, the preheparin free TFPI levels were shown to be inversely correlated with the HDL-C concentrations in both the patients (rϭϪ0.454, PϽ0.001) and the healthy subjects (rϭϪ0.136, PϽ0.05). As determined by comparison of preheparin and postheparin plasma, the patients generally showed preheparin free TFPI Ͻ10%, Lp-bound TFPI at 30%, and endothelial cell-anchor TFPI at 60%. When the patients were divided into 4 categories by their LDL cholesterol (LDL-C, 130 mg/dL) and HDL-C (40 mg/dL) levels to specify their coronary risks, the low-HDL-C groups had significantly increased preheparin and postheparin free TFPI levels and decreased postheparin LPL levels, whereas the high-LDL-C groups showed increased levels of Lp-bound TFPI. In a partial correlation analysis, we found a proportional relation between postheparin free TFPI and apolipoprotein A-II (rϭ0.5327) and between HDL-C and LPL (rϭ0.4906), whereas postheparin free TFPI was inversely correlated with HDL-C (rϭϪ0.4280) and postheparin LPL (rϭϪ0.4791). The inverse relationship between TFPI and LPL suggests that increased free TFPI concentrations as a compensatory response of the endothelium to prevent atherothrombotic processes compete with and displace LPL on endothelial surface, resulting in reduced LPL and low HDL-C. T issue factor pathway inhibitor (TFPI) plays an important role in the antithrombotic properties of vessel walls by inhibiting extrinsic coagulation processes. 1,2 Intravascular TFPI consists of free and lipoprotein-bound (Lp-bound) forms. 3 The free form includes 2 subfractions except in platelets, 4 ie, a circulating free TFPI fraction without carrier in preheparin plasma and a heparin-releasable TFPI fraction from endothelial cells. 5 Exogenous administration of recombinant TFPI to experimental animals prevents thrombosis, 6 whereas increased TFPI levels have been observed in patients with acute myocardial infarction. 7 Although the alteration of serum lipids by cholesterol-lowering therapy influences Lpbound TFPI profiles, 8 -11 little is known about the clinical implications of the TFPI level and its regulation in relation to lipid risk profiles.In the present study, we compared TFPI subfractions in preheparin plasmas of normal healthy subjects and patients with coronary artery disease (CAD). Significant negative correlations were observed ...

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Lipoprotein lipase mass and activity in severe hypertriglyceridemia

Cited by 126 publications

References 12 publications

Diagnosis and Management of Type I and Type V Hyperlipoproteinemia

Diagnosis and Management of Type I and Type V Hyperlipoproteinemia

Association between serum lipoprotein lipase mass concentration and subcutaneous fat accumulation during neonatal period

Intravascular Free Tissue Factor Pathway Inhibitor Is Inversely Correlated With HDL Cholesterol and Postheparin Lipoprotein Lipase but Proportional to Apolipoprotein A-II

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