Palmitoleic acid (PMA) has anti-inflammatory and antidiabetic activities. Here we tested whether these effects of PMA on glucose homeostasis and liver inflammation, in mice fed with high-fat diet (HFD), are PPAR-α dependent. C57BL6 wild-type (WT) and PPAR-α-knockout (KO) mice fed with a standard diet (SD) or HFD for 12 weeks were treated after the 10th week with oleic acid (OLA, 300 mg/kg of b.w.) or PMA 300 mg/kg of b.w. Steatosis induced by HFD was associated with liver inflammation only in the KO mice, as shown by the increased hepatic levels of IL1-beta, IL-12, and TNF-α; however, the HFD increased the expression of TLR4 and decreased the expression of IL1-Ra in both genotypes. Treatment with palmitoleate markedly attenuated the insulin resistance induced by the HFD, increased glucose uptake and incorporation into muscle in vitro, reduced the serum levels of AST in WT mice, decreased the hepatic levels of IL1-beta and IL-12 in KO mice, reduced the expression of TLR-4 and increased the expression of IL-1Ra in WT mice, and reduced the phosphorylation of NF 𝜅B (p65) in the livers of KO mice. We conclude that palmitoleate attenuates diet-induced insulin resistance, liver inflammation, and damage through mechanisms that do not depend on PPAR-α.

Although dietary fatty acids can modulate metabolic and immune responses, the effects of palmitoleic acid (16:1n-7) remain unclear. Since this monounsaturated fatty acid is described as a lipokine, studies with cell culture and rodent models have suggested it enhances whole body insulin sensitivity, stimulates insulin secretion by β cells, increases hepatic fatty acid oxidation, improves the blood lipid profile, and alters macrophage differentiation. However, human studies report elevated blood levels of palmitoleic acid in people with obesity and metabolic syndrome. These findings might be reflection of the level or activity of stearoyl-CoA desaturase-1, which synthesizes palmitoleate and is enhanced in liver and adipose tissue of obese patients. The aim of this review is to describe the immune-metabolic effects of palmitoleic acid observed in cell culture, animal models, and humans to answer the question of whether palmitoleic acid is a plausible nonpharmacological strategy to prevent, control, or ameliorate chronic metabolic and inflammatory disorders. Despite the beneficial effects observed in cell culture and in animal studies, there are insufficient human intervention studies to fully understand the physiological effects of palmitoleic acid. Therefore, more human-based research is needed to identify whether palmitoleic acid meets the promising therapeutic potential suggested by the preclinical research.

The stimulation with LPS increased the production of IL-6 and IL-1β while PM decreased the production of IL-6 in WT macrophages. In KO macrophages, LPS increased the production of TNF-α and IL-6 and PM decreased the production of TNFα.The expression of inflammatory markers such NFκB and IL1β were increased by LPS and decreased by PM in both WT and KO macrophages. PM reduced the expression of MyD88 and caspase-1 in KO macrophages, and the expression of TLR4 and HIF-1αin both WT and KO macrophages, although LPS had not effect. CD86, an inflammatory macrophage marker, was reduced by PM independently of genotype. PM increased PPARγ and reduced PPARβ gene expression in macrophages of both genotypes, and increased ACOX-1 expression in KO macrophages. In conclusion, PM promotes anti-inflammatory effects in macrophages exposed to LPS through inhibition of inflammasome pathway, which was independent of PPARα, PPARϒ and AMPK, thus the molecular mechanisms of anti-inflammatory response caused by PM is still unclear.

In mice fed with a high-fat diet, palmitoleic acid supplementation stimulated the uptake of glucose in liver through activation of AMPK and FGF-21, dependent on PPARα. J. Cell. Physiol. 232: 2168-2177, 2017. © 2016 Wiley Periodicals, Inc.

POA has anti-inflammatory effects on ECs stimulated with TNF-α and may counter endothelial dysfunction.

The aim of this study was to analyze performance, time structure, technical actions, and perceptual responses in Brazilian jiu-jitsu athletes during a simulated competition. For this purpose, 10 athletes were analyzed in a simulated competition (4 matches of 10 minutes). Physical tests and scales of the perception of effort and recovery were applied. The matches were recorded for the purpose of technical-tactical analysis and to determine the time structure. The main results show that in the simulated competition, reaction time (F(2.5,17.6) = 2.7; p = 0.087; η² = 0.28) and flexibility (F(7,63) = 1.5; p = 0.172; η² = 0.15) were unchanged across the matches. An analysis of variance showed a significant difference for grip endurance using the kimono (F(2.0,15.9) = 8.1; p = 0.004; η² = 0.50), which was not confirmed by the Bonferroni test. Jump height indicated postactivation potentiation after match 2 (F(7,63) = 3.5; p = 0.003; η² = 0.28). The maximal isometric handgrip strength in the dominant hand (F(3.2,28.6) = 2.9; p = 0.049; η² = 0.24) and in the nondominant hand (F(7,63) = 3.8; p = 0.002; η² = 0.30) showed a decline after matches 3 and 4. Although these data indicate the onset of fatigue, the effort/pause ratio of the matches was not altered (F(3,12) = 0.6; p = 0.624; η² = 0.13). The perceptions of effort (F(3,27) = 0.9; p = 0.469; η² = 0.09) and recovery (F(1.9,17.0) = 2.4; p = 0.125; η² = 0.21) and the degree of fatigue reported (F(1.5,13.8) = 0.5; p = 0.588; η² = 0.05) did not change during the simulated competition. Thus, it may be concluded that the execution of successive matches causes a decline in maximal isometric handgrip strength. No changes in the time structure of the matches or in the perceptual responses were observed.

• Marine-derived fatty acids (EPA and DHA) had potent anti-inflammatory effects in EA.hy926 endothelial cells. • Plant-derived fatty acids (-linolenic and stearidonic acids) modulated some inflammatory responses in EA.hy926 endothelial cells. • Of the two plant-derived fatty acids, stearidonic acid had greater anti-inflammatory effects.

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