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phospholipase/fetma

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Secreted phospholipase A2 inhibitor modulates fatty acid composition and reduces obesity-induced inflammation in Beagle dogs.

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Secreted phospholipase A2 inhibitor (sPLA2i) has been reported to have an anti-inflammatory function by blocking the production of inflammatory mediators. Obesity is characterized by low-grade inflammation and oxidative stress. The aim of this study was to investigate the effects of dietary
BACKGROUND Lipoprotein-associated phospholipase A2 activity (Lp-PLA2) is a good marker of cardiovascular risk in adults. It is strongly associated with stroke and many others cardiovascular events. Despite this, the impact of obesity on this enzyme activity and its relation to biomarkers of
Objectives: Glypican4 (GPC4) is a novel adipokine associated with obesity and insulin resistance. GPC4 was cleaved by the glycosylphosphatidylinositol-specific phospholipase D (GPLD1) in an anchored site of the

Elevated circulating levels of lipoprotein-associated phospholipase A2 in obese children.

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BACKGROUND Obesity and cardiovascular disease (CVD) often co-exist, but the pathophysiologic mechanisms that link the two are not fully understood. Lipoprotein-associated phospholipase A2 (Lp-PLA2) is involved in the modification of lipids within atheromatous plaques. Recently, circulating Lp-PLA2

Phospholipases D1 and D2 Suppress Appetite and Protect against Overweight.

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Obesity is a major risk factor predisposing to the development of peripheral insulin resistance and type 2 diabetes (T2D). Elevated food intake and/or decreased energy expenditure promotes body weight gain and acquisition of adipose tissue. Number of studies implicated phospholipase D (PLD) enzymes

Critical role for cytosolic group IVA phospholipase A2 in early adipocyte differentiation and obesity.

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Adipogenesis is the process of differentiation of immature mesenchymal stem cells into adipocytes. Elucidation of the mechanisms that regulate adipocyte differentiation is key for the development of novel therapies for the control of obesity and related comorbidities. Cytosolic group IVA

Genetic defect in phospholipase Cδ1 protects mice from obesity by regulating thermogenesis and adipogenesis.

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OBJECTIVE Regulation of obesity development is an important issue to prevent metabolic syndromes. Gene-disrupted mice of phospholipase Cδ1 (PLCδ1), a key enzyme of phosphoinositide turnover, seemed to show leanness. Here we examined whether and how PLCδ1 is involved in obesity. METHODS Weight gain,
BACKGROUND The aim of this study was to examine the relationship between subclinical inflammation and weight loss by laparoscopic adjustable gastric banding (LAGB). METHODS Plasma concentrations of intercellular adhesion molecule-1 (ICAM-1), vascular adhesion molecule-1 (VCAM-1), sensitive

Phospholipase C-related catalytically inactive protein can regulate obesity, a state of peripheral inflammation.

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Obesity is defined as abnormal or excessive fat accumulation. Chronic inflammation in fat influences the development of obesity-related diseases. Many reports state that obesity increases the risk of morbidity in many diseases, including hypertension, dyslipidemia, type 2 diabetes, coronary heart
BACKGROUND Obesity is associated with non-alcoholic fatty liver disease (NAFLD), and the patatin-like phospholipase 3 (PNPLA3) rs738409 (Ile148Met, C>G) gene polymorphism is one of the most important genetic determinants of NAFLD. Carriers have been reported to better respond to lifestyle
Although circulating glycosylphosphatidylinositol-specific phospholipase D (GPI-PLD), a minor high-density lipoprotein-associated protein, is elevated in patients with insulin resistance or high triglycerides, no information is available on the effect of weight loss or changes in insulin sensitivity
Glycosylphosphatidylinositol-anchored proteins (GPI-AP) with the complete glycolipid anchor attached are present in rat and human serum at amounts which are lower in insulin-resistant/obese rats compared to normal ones. These findings prompted further evaluation of the potential of full-length
BACKGROUND Increased concentration of small dense LDL cholesterol (sdLDL-C) and activity of lipoprotein-associated phospholipase A2 (Lp-PLA(2)) are considered as emerging cardiovascular risk factors and are commonly encountered in subjects with metabolic syndrome (MetS). OBJECTIVE The primary

Activation of phospholipase A2 is associated with generation of placental lipid signals and fetal obesity.

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BACKGROUND Obesity and diabetes during pregnancy are associated with increased insulin resistance and higher neonatal adiposity. In turn, insulin resistance triggers inflammatory pathways with accumulation of placental cytokines. OBJECTIVE To determine placental signals that translate into
BACKGROUND Platelet-activating factor acetylhydrolase (PAF-AH or Lp-PLA(2)) is a Ca(2+)-independent phospholipase A(2) primarily associated in plasma with low density lipoproteins (LDL), especially with small dense LDL (sdLDL) particles. Increased plasma Lp-PLA(2) levels have been associated with
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