Catabolism of lipoprotein-X induced by infusion of 10% fat emulsion

Abe, M; Kawano, Motoharu; Tashiro, Tsuguhiko; Yamamori, Hideo; Takagi, Kazuya; Morishima, Yasuo; Shirai, Kohji; Saitou, Yukio; Nakajima, Nobuyuki

doi:10.1016/s0899-9007(97)91279-x

Cited by 16 publications

(8 citation statements)

References 15 publications

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“…Lp-X is postulated to be related to biliary lipid vesicles, but the mechanism of Lp-X generation remains unclear. The role of Lp-X in atherogenesis has also not been clarified; Lynn et al [29] have only reported that Lp-X enhanced FC formation in rat Mφs, whereas other reports have demonstrated that Lp-X did not enhance [42,43] but rather suppressed [1,2] FC formation. More studies are needed to reveal whether the abnormal lipoprotein seen in this study is Lp-X, and its pathological significance in this model.…”

Section: Discussionmentioning

confidence: 99%

APA Hamster Model for Diabetic Atherosclerosis. 2. Analysis of Lipids and Lipoproteins.

et al. 2000

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Syrian hamsters of the APA strain (APA hamsters) have recently been shown to have atheromatous lesions in the aortic arches under diabetic condition induced by a single injection of streptozotocin (SZ). In that model, fatty streaks, which are the initial lesions of atherogenesis, develop by 6 weeks after the injection (WAI). In this study, we evaluated plasma lipid concentrations and lipoprotein profiles in diabetic APA hamsters at 6 WAI to reveal the early stage of atherogenesis clinicopathologically. As a result, by biochemical analysis, hyperglycemic APA hamsters showed signs of hypercholesterolemia and hypertriglyceridemia. Low-density lipoprotein (LDL) cholesterol significantly increased, but high-density lipoprotein (HDL) cholesterol significantly decreased. Agarose gel electrophoresis showed an obvious increase in the fractions of chylomicron, LDL and abnormal lipoprotein. Plasma LDL in diabetic animals was in a state more susceptible to oxidization. In addition, a significant increase in glycated LDL was also found in the diabetic animals by enzyme linked immunosorbent assay (ELISA). Moreover, lipid peroxidation product (4-hydroxynonenal (4 HNE))-adducted proteins and advanced glycation end-products (AGE) were immunohistochemically detected in the foam cells of the fatty streaks. These results revealed that diabetic APA hamsters had hyperlipidemia characterized by increases in chylomicron, LDL and abnormal lipoprotein, and suggested that oxidized LDL and/or glycated LDL might be actively uptaken by macrophages and play an important role in the initial stage of atherogenesis.

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Section: Discussionmentioning

confidence: 99%

APA Hamster Model for Diabetic Atherosclerosis. 2. Analysis of Lipids and Lipoproteins.

et al. 2000

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“…Precisely what accounts for these discrepant results is not known. However, differences between the metabolism of lipoproteins versus lipid emulsions [43][44][45][46] and the kinetics of LPS binding by triglyc- Interestingly, the liver is not directly stimulated by circulating LPS, but is instead activated by the cytokine products of LPS-responsive cells (4). Consequently, the liver responds to the endotoxic challenge with a dramatic alteration in hepatic protein synthesis termed "the acute-phase response."…”

Section: Serum Proteins Regulate Lipoprotein-lps Interactionsmentioning

confidence: 99%

Triglyceride-Rich Lipoproteins as Agents of Innate Immunity

Barcia

Harris

2005

Clinical Infectious Diseases

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Bacterial endotoxin (i.e., lipopolysaccharide [LPS]) elicits dramatic responses in the host, including elevated plasma lipid levels due to increased synthesis and secretion of triglyceride-rich lipoproteins by the liver and inhibition of lipoprotein lipase. This cytokine-induced hyperlipoproteinemia, clinically termed the "lipemia of sepsis," was customarily thought to involve the mobilization of lipid stores to fuel the host response to infection. However, because lipoproteins can also bind and neutralize LPS, we have long postulated that triglyceride-rich lipoproteins (very-low-density lipoproteins and chylomicrons) are also components of an innate, nonadaptive host immune response to infection. Recent research demonstrates the capacity of lipoproteins to bind LPS, protect against LPS-induced toxicity, and modulate the overall host response to this bacterial toxin.

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“…70 Precisely what accounts for these discrepant results is uncertain. But, differences between the metabolism of lipoproteins versus lipid emulsions, [71][72][73][74] and the kinetics of LPS binding by TGrich lipoproteins are likely, in part, responsible. 21,54 The catabolism of TG-rich fat emulsions is complex and includes the generation of phospholipid-rich discoid particles termed lipoprotein-X.…”

Section: Lipoproteins Protect Against Endotoxinmentioning

confidence: 99%

Review: The lipemia of sepsis: triglyceride-rich lipoproteins as agents of innate immunity

Harris

Gosnell

Kumwenda

2000

Journal of Endotoxin Research

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Bacterial endotoxin (LPS) elicits dramatic responses in the host including elevated plasma lipid levels due to the increased synthesis and secretion of triglyceride (TG)-rich lipoproteins by the liver, and the inhibition of lipoprotein lipase. This cytokine-induced hyperlipoproteinemia, clinically termed the "lipemia of sepsis", was customarily thought to represent the mobilization of lipid stores to fuel the host response to infection. However, since lipoproteins can also bind and neutralize LPS, we hypothesize that TG-rich lipoproteins (VLDL and chylomicrons) are also components of an innate, non-adaptive host immune response to infection. Herein we review data demonstrating the capacity of lipoproteins to bind LPS, protect against LPS-induced toxicity, and modulate the overall host response to this bacterial toxin. Lastly, we propose a pathway whereby lipoprotein-bound LPS may represent a novel, endogenous mechanism for regulating the hepatic acute phase response.

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Catabolism of lipoprotein-X induced by infusion of 10% fat emulsion

Cited by 16 publications

References 15 publications

APA Hamster Model for Diabetic Atherosclerosis. 2. Analysis of Lipids and Lipoproteins.

APA Hamster Model for Diabetic Atherosclerosis. 2. Analysis of Lipids and Lipoproteins.

Triglyceride-Rich Lipoproteins as Agents of Innate Immunity

Review: The lipemia of sepsis: triglyceride-rich lipoproteins as agents of innate immunity

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