palmitoleic/nekroos

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Disassociated relation between plasma tumor necrosis factor-alpha, interleukin-6 and increased body weight in Amerindian women: A long-term prospective study of natural body weight variation and impaired glucose tolerance.

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BACKGROUND Inflammatory cytokines are linked to obesity-related insulin resistance and may predict type 2 diabetes independently of obesity. We previously reported that a majority of a cohort of 73 non-diabetic women with normal plasma (p-)glucose with Amerindian heritage in Lima, Peru, during a

Changes in rat plasma-free fatty acid composition under oxidative stress induced by carbon tetrachloride: decrease of polyunsaturated fatty acids and increase of palmitoleic acid.

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In order to measure the changes in antioxidant levels and the composition of plasma-free fatty acids resulting from oxidative stress, male Fisher rats were given a twice weekly subcutaneous injection of a 50% solution of carbon tetrachloride (CCl4) in corn oil for a period of 2 to 13 weeks. The

Insulin protects pancreatic acinar cells from palmitoleic acid-induced cellular injury.

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Acute pancreatitis is a serious and sometimes fatal inflammatory disease where the pancreas digests itself. The non-oxidative ethanol metabolites palmitoleic acid (POA) and POA-ethylester (POAEE) are reported to induce pancreatitis caused by impaired mitochondrial metabolism, cytosolic Ca(2+)

Palmitoleic acid prevents palmitic acid-induced macrophage activation and consequent p38 MAPK-mediated skeletal muscle insulin resistance.

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Obesity and saturated fatty acid (SFA) treatment are both associated with skeletal muscle insulin resistance (IR) and increased macrophage infiltration. However, the relative effects of SFA and unsaturated fatty acid (UFA)-activated macrophages on muscle are unknown. Here, macrophages were treated

Palmitoleic acid reduces the inflammation in LPS-stimulated macrophages by inhibition of NFκB, independently of PPARs.

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Palmitoleic acid (PM, 16:1n-7) has anti-inflammatory properties that could be linked to higher expression of PPARα, an inhibitor of NFκB. Macrophages play a major role in the pathogenesis of chronic inflammation, however, the effects of PM on macrophages are underexplored. Thus, we aimed to

Palmitoleic Acid has Stronger Anti-Inflammatory Potential in Human Endothelial Cells Compared to Oleic and Palmitic Acids.

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Fatty acids (FAs) may affect endothelial cell (EC) function, influencing atherogenesis and inflammatory processes. Palmitoleic acid (POA) has been described as an anti-inflammatory FA. However, its effects on ECs are underexplored. This study compares the effects of POA with those of palmitic acid

Differential protective effects of palmitoleic acid and cAMP on caspase activation and cell viability in pancreatic beta-cells exposed to palmitate.

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Saturated and mono-unsaturated fatty acids exert differential effects on pancreatic beta-cell viability during chronic exposure. Long chain saturated molecules (e.g. palmitate) are cytotoxic to beta-cells and this is associated with caspase activation and induction of apoptosis. By contrast,

Relationships between serum fatty acid composition and multiple markers of inflammation and endothelial function in an elderly population.

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BACKGROUND Fatty acid (FA) composition in serum has been associated with C-reactive protein (CRP), but associations with other markers of inflammation and endothelial function, e.g. adhesion molecules are unknown. We recently suggested a possible role of the lipogenic enzyme stearoyl coenzymeA

Saturated fatty acids enhance TLR4 immune pathways in human trophoblasts.

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OBJECTIVE What are the effects of fatty acids on placental inflammatory cytokine with respect to toll-like receptor-4/nuclear factor-kappa B (TLR4/NF-kB)? CONCLUSIONS Exogenous fatty acids induce a pro-inflammatory cytokine response in human placental cells in vitro via activation of TLR4 signaling

Activation of α7nACh receptor protects against acute pancreatitis through enhancing TFEB-regulated autophagy

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Acute pancreatitis (AP) is associated with impaired acinar cell autophagic flux, intracellular zymogen activation, cell necrosis and inflammation. Activation of the cholinergic system of vagus nerve has been shown to attenuate AP, but the effect of organ-intrinsic cholinergic system on pancreatitis

Blockade of kinin B(1) receptor reverses plasma fatty acids composition changes and body and tissue fat gain in a rat model of insulin resistance.

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OBJECTIVE Kinin B(1) receptor (B(1) R) contributes to insulin resistance through a mechanism involving oxidative stress. This study examined the effect of B(1) R blockade on the changes in plasma fatty acids composition, body and tissue fat mass and adipose tissue inflammation that influence insulin

Effects of 7-MEGATM 500 on Oxidative Stress, Inflammation, and Skin Regeneration in H2O2-Treated Skin Cells.

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Environmental stimuli can lead to the excessive accumulation of reactive oxygen species (ROS), which is one of the risk factors for premature skin aging. Here, we investigated the protective effects of 7-MEGATM 500 (50% palmitoleic acid, 7-MEGA) against oxidative stress-induced cellular damage and

Cytotoxic allelochemicals induce ultrastructural modifications in Cassia tora L. and mitotic changes in Allium cepa L.: a weed versus weed allelopathy approach.

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The stress induced by allelochemicals present in stem aqueous extract (SAE) of Nicotiana plumbaginifolia on alterations in growth, ultrastructure on Cassia tora L., and mitotic changes on Allium cepa L. were inspected. Application of SAE at different concentrations (0.5, 1, 2, and 4%) expressively

Fatty acids from Plasmodium falciparum down-regulate the toxic activity of malaria glycosylphosphatidylinositols.

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Plasmodium falciparum malaria kills roughly 2.5 million people, mainly children, annually. Much of this mortality is thought to arise from the actions of a malarial toxin. This toxin, identified as glycosylphosphatidylinositol (GPI), is a major pathogenicity determinant in malaria. A malarial

Protective effects of seabuckthorn pulp and seed oils against radiation-induced acute intestinal injury.

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Radiation-induced gastrointestinal syndrome, including nausea, diarrhea and dehydration, contributes to morbidity and mortality after medical or industrial radiation exposure. No safe and effective radiation countermeasure has been approved for clinical therapy. In this study, we aimed to

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