Serum amyloid A is found on ApoB-containing lipoproteins in obese humans with diabetes.

Objective: In murine models of obesity/diabetes, there is an increase in plasma serum amyloid A (SAA) levels along with redistribution of SAA from high-density lipoprotein (HDL) to apolipoprotein B (apoB)-containing lipoprotein particles, namely, low-density lipoprotein and very low-density lipoprotein. The goal of this study was to determine if obesity is associated with similar SAA lipoprotein redistribution in humans.

Design And Methods: Three groups of obese individuals were recruited from a weight loss clinic: healthy obese (n = 14), metabolic syndrome (MetS) obese (n = 8), and obese with type 2 diabetes (n = 6).

Elevated IgG levels against specific bacterial antigens in obese patients with diabetes and in mice with diet-induced obesity and glucose intolerance.

High fat diets increase the risk for insulin resistance by promoting inflammation. The cause of inflammation is unclear, but germfree mouse studies have implicated commensal gut bacteria. We tested whether diet-induced obesity, diabetes, and inflammation are associated with anti-bacterial IgG.

Nascent HDL formation by hepatocytes is reduced by the concerted action of serum amyloid A and endothelial lipase.

Inflammation is associated with significant decreases in plasma HDL-cholesterol (HDL-C) and apoA-I levels. Endothelial lipase (EL) is known to be an important determinant of HDL-C in mice and in humans and is upregulated during inflammation. In this study, we investigated whether serum amyloid A (SAA), an HDL apolipoprotein highly induced during inflammation, alters the ability of EL to metabolize HDL.

ATP binding cassette G1-dependent cholesterol efflux during inflammation.

ATP binding cassette transporter G1 (ABCG1) mediates the transport of cellular cholesterol to HDL, and it plays a key role in maintaining macrophage cholesterol homeostasis. During inflammation, HDL undergoes substantial remodeling, acquiring lipid changes and serum amyloid A (SAA) as a major apolipoprotein. In the current study, we investigated whether remodeling of HDL that occurs during acute inflammation impacts ABCG1-dependent efflux.

High-density lipoprotein and the acute phase response.

Purpose Of Review: Inflammation and the concomitant acute phase response induce marked changes in the lipoprotein profile, particularly the high-density lipoprotein (HDL) fraction. The present review describes the transfer proteins and lipases that remodel HDL and regulate its plasma levels, discusses the changes occurring in their activities during inflammation, and the influence of this altered remodeling on HDL function. The review will also discuss the contribution of the ATP-binding-membrane-cassette transporters to the protective actions of HDL.

SR-BI selective lipid uptake: subsequent metabolism of acute phase HDL.

Objective: The purpose of this study was to investigate the interaction of SAA and SR-BI in remodeling of acute phase HDL (AP HDL).

Methods And Results: We used SAA and SR-BI adenoviral vector expression models to study the interaction between these entities. SR-BI processing of mouse AP HDL generated progressively smaller discreet HDL particles with distinct apolipoprotein compositions.

Scavenger receptor class B type I protein as an independent predictor of high-density lipoprotein cholesterol levels in subjects with hyperalphalipoproteinemia.

Context: In mice, scavenger receptor class B, type I (SR-BI) receptor protein deficiency is associated with elevated high-density lipoprotein (HDL)-cholesterol (HDL-C) levels.

Objective: Our objective was to determine the relationship between SR-BI protein and HDL-C levels in humans.

Design: This was a prospective study of adults with hyperalphalipoproteinemia.

HDL remodeling during the acute phase response.

Objective: The purpose of this study was to examine the interactive action of serum amyloid A (SAA), group IIA secretory phospholipase A(2) (sPLA(2)-IIA), and cholesteryl ester transfer protein (CETP) on HDL remodeling and cholesterol efflux during the acute phase (AP) response elicited in humans after cardiac surgery.

Methods And Results: Plasma was collected from patients before (pre-AP), 24 hours after (AP-1 d), and 5 days after cardiac surgery (AP-5 d). SAA levels were increased 16-fold in AP-1 d samples.

Dietary fish oil alters cardiomyocyte Ca2+ dynamics and antioxidant status.

The n-3 polyunsaturated fatty acids (PUFAs) found in fish oil (FO) have been shown to protect against reperfusion arrhythmias, a manifestation of reperfusion injury, which is believed to be induced by the formation of reactive oxygen species (ROS) and intracellular calcium (Ca2+) overload. Adult rats fed a diet supplemented with 10% FO had a higher proportion of myocardial n-3 PUFAs and increased expression of antioxidant enzymes compared with the saturated fat (SF)-supplemented group. Addition of hydrogen peroxide (H2O2) to cardiomyocytes isolated from rats in the SF-supplemented group increased the proportions of cardiomyocytes contracting in an asynchronous manner, increased the rate of Ca2+ influx, and increased the diastolic and systolic [Ca2+]i compared with the FO group.

Apolipoproteins regulate the kinetics of endothelial lipase-mediated hydrolysis of phospholipids in reconstituted high-density lipoproteins.

Endothelial lipase (EL) is a newly identified member of the triglyceride lipase gene family that hydrolyzes high-density lipoprotein (HDL) phospholipids. This study investigates the ability of the major apolipoproteins of rHDL to regulate the kinetics of EL-mediated phospholipid hydrolysis in well-characterized, homogeneous preparations of spherical rHDL. The rHDL contained either apoA-I as the only apolipoprotein, (A-I)rHDL, apoA-II as the only apolipoprotein, (A-II)rHDL, or apoA-I as well as apoA-II, (A-I/A-II)rHDL.

Dietary fish oil increases acetylcholine- and eicosanoid-induced contractility of isolated rat ileum.

The long-chain (n-3) polyunsaturated fatty acids (PUFA) have been reported to exhibit health benefits and healing properties for the gastrointestinal tract. The aim of this study was to investigate the effects of dietary fish oil supplementation on the in vitro contractility of gut tissue. Rats (9 wk old) were fed synthetic diets supplemented with 170 g/kg Sunola oil (SO; 850 g/kg as oleic acid [18:1(n-9)]) or with 100 g/kg of the SO replaced by saturated animal fat (SF) or fish oil (FO) for 4 wk.