Absence of Hyperlipidemia in LDL Receptor-Deficient Mice Having Apolipoprotein B100 Without the Putative Receptor-Binding Sequences

To examine the effects of apoB100 structure, specifically a mutation in the LDLr binding region, on the production of LDL and development of atherosclerosis in vivo

Dietary Supplements and Sports Performance: Amino Acids

This is the third in a series of six articles to discuss the major classes of dietary supplements (vitamins; minerals; amino acids; herbs or botanicals; metabolites, constituents/extracts, or combinations). The major focus is on efficacy of such dietary supplements to enhance exercise or sport performance

Palmitoleate Induces Hepatic Steatosis but Suppresses Liver Inflammatory Response in Mice

The interaction between fat deposition and inflammation during obesity contributes to the development of non-alcoholic fatty liver disease (NAFLD). The present study examined the effects of palmitoleate, a monounsaturated fatty acid (16∶1n7), on liver metabolic and inflammatory responses, and investigated the mechanisms by which palmitoleate increases hepatocyte fatty acid synthase (FAS) expression. Male wild-type C57BL/6J mice were supplemented with palmitoleate and subjected to the assays to analyze hepatic steatosis and liver inflammatory response. Additionally, mouse primary hepatocytes were treated with palmitoleate and used to analyze fat deposition, the inflammatory response, and sterol regulatory element-binding protein 1c (SREBP1c) activation. Compared with controls, palmitoleate supplementation increased the circulating levels of palmitoleate and improved systemic insulin sensitivity. Locally, hepatic fat deposition and SREBP1c and FAS expression were significantly increased in palmitoleate-supplemented mice. These pro-lipogenic events were accompanied by improvement of liver insulin signaling. In addition, palmitoleate supplementation reduced the numbers of macrophages/Kupffer cells in livers of the treated mice. Consistently, supplementation of palmitoleate decreased the phosphorylation of nuclear factor kappa B (NF-κB, p65) and the expression of proinflammatory cytokines. These results were recapitulated in primary mouse hepatocytes. In terms of regulating FAS expression, treatment of palmitoleate increased the transcription activity of SREBP1c and enhanced the binding of SREBP1c to FAS promoter. Palmitoleate also decreased the phosphorylation of NF-κB p65 and the expression of proinflammatory cytokines in cultured macrophages. Together, these results suggest that palmitoleate acts through dissociating liver inflammatory response from hepatic steatosis to play a unique role in NAFLD

Mobilization of ectopic yolk in Gallus gallus domesticus: a novel reverse lipid transport process

Summary In many oviparous animals, bursting type atresia of ovarian follicles occurs during the reproductive cycle resulting in the escape of yolk into the extracellular compartment. In birds, this ectopic yolk is rapidly cleared by an unknown process that involves the appearance of yolk-engorged macrophage-like cells. To study this unique type of lipid transport, we injected young male chickens intra-abdominally with egg yolk. Absorption of egg yolk from the body cavity markedly increased the triacylglyceride-rich fraction (TRL) of plasma lipoproteins and was coincident with increased levels of plasma triacylglycerides (TAG) but not non-esterified fatty acids (NEFA). Thus, the transport of yolk lipids from the abdominal cavity appears to occur in lipoproteins and be more similar to the transport of hepatic TAG to the periphery via lipoproteins than to transport of adipose TAG to the periphery via NEFA released by the action of lipases. When macrophages were exposed to yolk in vitro, they quickly phagocytized yolk; however, it is unclear if this level of phagocytosis contributes significantly to total yolk clearance. Instead, the chicken macrophage may function more as a facilitator of yolk clearance through modification of yolk lipoproteins and the regulation of the local and systemic immune response to ectopic yolk. Yolk appears to be anti-inflammatory in nature. Yolk did not increase inflammatory cytokines IL-1, IL-6 and IFNγ either in vivo or in vitro; in fact, yolk dampened many inflammatory changes caused by lipopolysaccharide (LPS). Conversely, LPS-induced inflammation retarded yolk clearance from the abdominal cavity and plasma TAG levels.</jats:p