Oleic acid activates peroxisome proliferator-activated receptor δ to compensate insulin resistance in steatotic cells

Wu, Hung Tsung; Chen, Wency; Cheng, Kai‐Chun; Ku, Po Ming; Yeh, Ching‐Hua; Cheng, Juei Tang

doi:10.1016/j.jnutbio.2011.07.006

Cited by 36 publications

(27 citation statements)

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“…The mice showed improvement of insulin sensitivity in IPITT. These results agree with other previous reports (29,30). Especially, it is reported that oleic acid-enriched diet might decrease levels of inflammation markers [tumor necrosis factor (TNF)-a, interleukin (IL)-1b] in the adipose tissues and up-regulate the expression of enzymes involved in muscle mitochondrial b-oxidation [medium-chain acyl-CoA dehydrogenase (MCAD), carnitine palmitoyltransferase (CPT)-1b], which likely contributed to the improved muscle insulin sensitivity in an animal study (31).…”

Section: Discussionsupporting

confidence: 94%

Palmitic acid-rich diet suppresses glucose-stimulated insulin secretion (GSIS) and induces endoplasmic reticulum (ER) stress in pancreatic islets in mice

et al. 2015

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The objective was to clarify whether dietary palmitic acid supplementation affects glucose-stimulated insulin secretion (GSIS) and the endoplasmic reticulum (ER) stress pathway in pancreatic islets in mice. Eight-week-old male C57BL/6J mice were randomly divided into three treatment diet groups: control diet, palmitic acid-supplemented diet (PAL) and oleic acid-supplemented diet (OLE). After 2 weeks of treatment, intraperitoneal glucose tolerance test and intraperitoneal insulin tolerance test were performed. GSIS was assessed by pancreatic perfusion in situ with basal (100 mg/dL) glucose followed by a high (300 mg/dL) glucose concentration. We measured mRNA levels of ER stress markers such as C/EBP homologous protein (CHOP), immunoglobulin heavy-chain binding protein (BIP) and X-box binding protein (XBP)-1 using real-time polymerase chain reaction (PCR) analyses in isolated islets. Immunohistochemical staining was also performed. Mice fed PAL showed significantly decreased glucose tolerance (p < 0.05). In the perfusion study, GSIS was significantly suppressed in the PAL group (p < 0.05). Semi-quantitative RT-PCR revealed that islet CHOP, BIP, and XBP-1 mRNA expression were significantly increased in the PAL group (p < 0.05). TUNEL-positive β-cells were not detected in all groups. Dietary palmitic acid-supplementation for 2 weeks might suppress GSIS and induce ER stress in pancreatic islets in mice, in the early stage of lipotoxicity.

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Section: Discussionsupporting

confidence: 94%

Palmitic acid-rich diet suppresses glucose-stimulated insulin secretion (GSIS) and induces endoplasmic reticulum (ER) stress in pancreatic islets in mice

et al. 2015

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“…However, mechanisms of OA action are less understood. Involvement of CD36 and GPR40‐PLC‐calcium pathway has been described in vascular smooth muscle cells and steatotic cells, respectively . Moreover, PUFAs can act as antagonists for TLR4 agonists .…”

Section: Discussionmentioning

confidence: 99%

Free fatty acids sensitize dendritic cells to amplify TH1/TH17‐immune responses

et al. 2016

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Obesity is associated with body fat gain and impaired glucose metabolism. Here, we identified both body fat gain in obesity and impaired glucose metabolism as two independent risk factors for increased serum levels of free fatty acids (FFAs). Since obesity is associated with increased and/or delayed resolution of inflammation observed in various chronic inflammatory diseases such as psoriasis, we investigated the impact of FFAs on human monocyte-derived and mouse bone marrow-derived dendritic cell (DCs) functions relevant for the pathogenesis of chronic inflammation. FFAs such as palmitic acid (PA) and oleic acid (OA) did not affect the pro-inflammatory immune response of DCs. In contrast, PA and OA sensitize DCs resulting in augmented secretion of TH1/TH17-instructive cytokines upon pro-inflammatory stimulation. Interestingly, obesity in mice worsened a TH1/TH17-driven psoriasis-like skin inflammation. Strong correlation of the amount of total FFA, PA, and OA in serum with the severity of skin inflammation points to a critical role of FFA in obesity-mediated exacerbation of skin inflammation. Our data suggest that increased levels of FFAs might be a predisposing factor promoting a TH1/TH17-mediated inflammation such as psoriasis in response to an inflammatory danger signal.Keywords: Dendritic cells r Diet r Free fatty acids r Inflammation r Metabolism r TH1 r TH17 Additional supporting information may be found in the online version of this article at the publisher's web-site IntroductionHuman and mouse studies demonstrate that immune responses are dysregulated in obesity. In particular, obesity in mice is associated with increased inflammation and/or its delayed resolution Correspondence: Dr. Anja Saalbach e-mail: Anja. Saalbach@medizin.uni-leipzig.de in models of acute pancreatitis, arthritis, and neutrophil-mediated peritonitis [1][2][3][4]. Kanemaru et al. described a worsening of psoriasis from dermatitis in mice by upregulating IL-17A, IL-22, and Reg3c in skin [5]. Likewise human psoriasis, a chronic TH1/TH17-driven inflammatory skin disease, shows a significant positive * These authors contributed equally to this work. Eur. J. Immunol. 2016Immunol. . 46: 2043Immunol. -2053 correlation between body mass index (BMI) and the onset and severity of the disease as well as a weaker response to treatment [6,7]. Obesity is associated with low-grade chronic inflammation reflected by increased levels of acute-phase proteins and pro-inflammatory mediators as well as by a pro-inflammatory state of circulating mononuclear cells in obese compared to lean subjects [3,8]. Enlarged adipocytes change their secretion pattern and release more pro-inflammatory mediators such as TNF-α and MCP-1, while the release of anti-inflammatory mediators such as adiponectin is reduced [9][10][11]. Thus, white adipose tissue could link metabolism and inflammation [12]. Moreover, in obesity, visceral adipose tissues as well as subcutaneous fat depots enlarge and adipocyte production of free fatty acids (FFAs), mainly palmitic acid (PA)...

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“…The molecular mechanism of avocado oil for controlling lipids levels might be related with peroxisomes proliferator activated receptors (PPARs). It has been reported that C18:1 is capable to induce PPAR-δ (Wu et al 2012), which has been associated with degradation of lipids by enhancing fatty acid catabolism (Wang et al 2003). Another interesting characteristic of avocado oil is the relative high concentration of linolenic acid (around 10.1 %), an omega-3 fatty acid precursor of long chain fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA).…”

Section: Discussionmentioning

confidence: 99%

Protective effects of dietary avocado oil on impaired electron transport chain function and exacerbated oxidative stress in liver mitochondria from diabetic rats

Ortiz‐Avila

Gallegos‐Corona

Sánchez‐Briones

et al. 2015

J Bioenerg Biomembr

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Electron transport chain (ETC) dysfunction, excessive ROS generation and lipid peroxidation are hallmarks of mitochondrial injury in the diabetic liver, with these alterations also playing a role in the development of non-alcoholic fatty liver disease (NAFLD). Enhanced mitochondrial sensitivity to lipid peroxidation during diabetes has been also associated to augmented content of C22:6 in membrane phospholipids. Thus, we aimed to test whether avocado oil, a rich source of C18:1 and antioxidants, attenuates the deleterious effects of diabetes on oxidative status of liver mitochondria by decreasing unsaturation of acyl chains of membrane lipids and/or by improving ETC functionality and decreasing ROS generation. Streptozocin-induced diabetes elicited a noticeable increase in the content of C22:6, leading to augmented mitochondrial peroxidizability index and higher levels of lipid peroxidation. Mitochondrial respiration and complex I activity were impaired in diabetic rats with a concomitant increase in ROS generation using a complex I substrate. This was associated to a more oxidized state of glutathione, All these alterations were prevented by avocado oil except by the changes in mitochondrial fatty acid composition. Avocado oil did not prevented hyperglycemia and polyphagia although did normalized hyperlipidemia. Neither diabetes nor avocado oil induced steatosis. These results suggest that avocado oil improves mitochondrial ETC function by attenuating the deleterious effects of oxidative stress in the liver of diabetic rats independently of a hypoglycemic effect or by modifying the fatty acid composition of mitochondrial membranes. These findings might have also significant implications in the progression of NAFLD in experimental models of steatosis.

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Oleic acid activates peroxisome proliferator-activated receptor δ to compensate insulin resistance in steatotic cells

Cited by 36 publications

References 50 publications

Palmitic acid-rich diet suppresses glucose-stimulated insulin secretion (GSIS) and induces endoplasmic reticulum (ER) stress in pancreatic islets in mice

Palmitic acid-rich diet suppresses glucose-stimulated insulin secretion (GSIS) and induces endoplasmic reticulum (ER) stress in pancreatic islets in mice

Free fatty acids sensitize dendritic cells to amplify TH1/TH17‐immune responses

Protective effects of dietary avocado oil on impaired electron transport chain function and exacerbated oxidative stress in liver mitochondria from diabetic rats

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