lipase/necrosis

To investigate the effects of cytokines on adipocyte lipolysis, a macrophage cell line (RAW 264.7) was treated with Escherichia coli lipopolysaccharide (1 microgram/ml) for 18 h to induce cytokine release. Conditioned medium (5%, vol/vol) from these cells was added to rat epididymal adipocytes

The aim of the present study was to (1) evaluate the responsiveness of human mononuclear cells to lipoprotein lipase (LPL), as assessed by tumor necrosis factor-alpha (TNFalpha) production, during the process of differentiation of monocytes to macrophages, and (2) determine the mechanisms by which

When added to murine adipocytes in culture, tumor necrosis factor (TNF) decreases the levels of lipoprotein lipase (LPL). Semb et al (1987. J. Biol Chem. 262: 8390-8394) have shown that administration of murine TNF to rats decreases lipoprotein lipase (LPL) in the epididymal fat pad with maximal

The regulation of macrophage lipoprotein lipase (LPL) by cytokines is of potentially crucial importance in the pathogenesis of atherosclerosis. The effect of combinations of interleukin 1 (IL-1), 6 (IL-6), and 11 (IL-11), interferon gamma (INF-gamma), leukaemia inhibitory factor (LIF) and tumour

Post-heparin plasma activity of lipoprotein lipase (LPL) and hepatic lipase (HL), and fat and muscle activity of LPL were measured in neutered lean and obese cats. Lipoprotein lipase, hormone-sensitive lipase (HSL), and tumor necrosis factor a (TNF) mRNA were measured in muscle and fat tissue with

Lipopolysaccharide (LPS), the active principle of certain endotoxins, protein-free perfused in rat hearts leads in 3 h to a considerable loss of lipoprotein lipase (LPL) activity. In the presence of albumin LPS has virtually no effect. Tumor necrosis factor (TNF) added instead of LPS had no effects

Previous studies have demonstrated that cachectin/tumor necrosis factor (TNF) inhibits lipoprotein lipase (LPL) activity in cultures of 3T3-L1 cells. To determine whether TNF also inhibits LPL in human adipocytes, primary cultures of isolated human adipocytes were exposed to a spectrum of

Tumour necrosis factor (TNF) has previously been shown to decrease lipoprotein lipase (LPL) activity and mRNA levels in 3T3-L1 cells and in adipose tissue from rats and guinea pigs when injected in vivo, but not to alter LPL activity in human adipocytes incubated in vitro. The effect of recombinant

This study was initiated to compare the temporal response of serum lipoprotein lipase-suppressing mediator (LSM) and tumor necrosis factor (TNF) in lipopolysaccharide (LPS) -infused or -injected rats. Serial blood samples were obtained over a 5-day period from rats implanted with vascular catheters.

Human monocyte-derived macrophages secrete lipoprotein lipase (LPL) in culture. The regulation of human macrophage LPL production is poorly understood. Since bacterial lipopolysaccharide (LPS) alters production of several macrophage secretory products, its effect on human monocyte-derived macrophage

We have previously found that lipoprotein lipase (LPL) induces tumor necrosis factor alpha (TNF alpha) mRNA expression and TNF alpha protein production in the ANA-1 macrophage cell line and in resident murine macrophages. The present study was designed to elucidate the intracellular signalling

OBJECTIVE To explore the correlation between the single nucleotide polymorphism (SNP) in the promotor of hepatic lipase (HL) gene and nontraumatic avascular necrosis of the femoral head (ANFH). METHODS Between January 2007 and June 2009, 243 patients with ANFH were treated (case group), including

Levels of mRNA for lipoprotein lipase (LPL) in guinea pig epididymal adipose tissue, heart and liver were determined by dot blot analysis of total RNA using a cDNA probe complementary to the coding region, and compared to the LPL activity. For adipose tissue we also measured the incorporation of

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is found throughout the environment in industrialized countries, and most people have had some exposure. TCDD has very high lipid solubility and is concentrated in adipose tissue. Because an epidemiologic association between TCDD exposure and diabetes has

Lipopolysaccharide (LPS) modulates macrophage functions and induces the synthesis and secretion of tumor necrosis factor (TNF) and interleukin 1 (IL-1) in these cells. The latter two factors but not LPS suppress lipoprotein lipase (LPL) synthesis and secretion in adipocytes. Since the regulation of