Oleic acid protects insulin-secreting INS-1E cells against palmitic acid-induced lipotoxicity along with an amelioration of ER stress

Liu, Xiaohong; Zeng, Xin; Chen, Xuanming; Luo, Ruixi; Li, Linzhao; Wang, Chengshi; Liu, Jingping; Cheng, Jun; Liu, Yanrong; Chen, Younan

doi:10.1007/s12020-019-01867-3

Cited by 26 publications

(31 citation statements)

References 48 publications

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“…It is well demonstrated that the Mediterranean diet, rich of monounsaturated fatty acid, can reduce liver fat even without weight loss, so it is a greatly recommended dietary pattern for NAFLD. In consistence with other reports, our previous study has demonstrated the great protective effects of monounsaturated OA against saturated FFAs induced hepatic lipotoxicity in both hepatocytes and NASH rats [24]. In the present study, we aimed to further explore the underlying mechanisms, and we demonstrated that OA was able to effectively suppress PA induced ER stress and downstream pyroptosis activation, implying a novel mechanism for monounsaturated fatty acids mediated protection for lipotoxicity.…”

Section: Discussionsupporting

confidence: 69%

Oleic acid ameliorates palmitic acid induced hepatocellular lipotoxicity by inhibition of ER stress and pyroptosis

et al. 2020

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Background: Pyroptosis is a novel programmed cell death. It is identified as caspase-1 dependent and characterized by plasma-membrane rupture and release of proinflammatory intracellular contents inculuding IL-1 beta and IL-18. Pyroptosis is distinct from other forms of cell death, especially apoptosis that is characterized by nuclear and cytoplasmic condensation and is elicited via activation of a caspase cascade. In pyroptosis, gasdermin D (GSDMD) acts as a major executor, while NLRP3 related inflammasome is closely linked to caspase-1 activation. Given that pyroptosis has played a critical role in the progression of non-alcoholic steatohepatitis (NASH), here, we investigated whether the regulation of pyroptosis activation is responsible for the protective role of monounsaturated oleic acids in the context of hepatocellular lipotoxicity. Methods: Human hepatoma cell line HepG2 cells were exposed to palmitic acid (PA) with or without oleic acids (OA) or/and endoplasmic reticulum (ER) stress inhibitor tauroursodeoxycholic acid (TUDCA) for 24 h. Besides, the cells were treated with the chemical ER stressor tunicamycin (TM) with or without OA for 24 h as well. The expressions of pyroptosis and ER stress related genes or proteins were determined by real-time PCR, Western blot or immunofluorescence. The morphology of pyroptosis was detected by acridine orange and ethidium bromide (AO/EB) staining. The release of IL-1 beta and tumor necrosis factor alpha (TNF-α) was determined by ELISA. Sprague-Dawley (SD) rats were fed with high fat diet (HFD) for 16 w, then, HFD was half replaced by olive oil to observe the protective effects of olive oil. The blood chemistry were analyzed, and the liver histology and the expressions of related genes and proteins were determined in the liver tissues. Results: We demonstrated that PA impaired the cell viability and disturbed the lipid metabolism of HepG2 cells (P < 0.01), but OA robustly rescued cells from cell death (P < 0.001). More importantly, we found that instead of cell apoptosis, PA induced significant pyroptosis, evidenced by remarkably increased mRNA and protein expressions of inflammasome marker NLRP3, Caspase-1 and IL-1beta, as well as cell membrane perforation driving protein GSDMD (P < 0.05). Furthermore, we demonstrated that the PA stimulated ER stress was causally related to pyroptosis. The enhanced expressions of ER stress markers CHOP and BIP were found subcellular co-located to pyroptosis markers NLRP3 and ASC. Additionally,TM was able to induce pyroptosis like PA did, and ER stress inhibitor TUDCA was able to inhibit both PA and TM induced ER stress as well as pyroptosis. Furthermore, we demonstrated that OA substantially alleviated either PA or TM induced ER stress and pyroptosis in HepG2 cells (P < 0.01). In vivo, only olive oil supplementation did not cause significant toxicity, while HFD for 32 w obviously induced liver steatosis and inflammation in SD rats (P < 0.05). Half

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Section: Discussionsupporting

confidence: 69%

Oleic acid ameliorates palmitic acid induced hepatocellular lipotoxicity by inhibition of ER stress and pyroptosis

et al. 2020

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“…Oleic acid is essential to human nutrition and has a protective effect on beta cells that are insulin producers. The mechanisms involved in the action are based on the anti-inflammatory and anti-oxidation capacity of unsaturated fatty acids, such as oleic (Liu et al, 2019). In addition to pancreatic B cells, anti-inflammatory activity extends to other tissues, such as the epithelial (Pegoraro et al, 2019) and intestinal (Reddy & Naidu, 2016).…”

Section: Msmentioning

confidence: 99%

Analysis of the chemical profile of cerrado pear fixed compounds by mass spectrometry with paper spray and volatile ionization by SPME-HS CG-MS

Mariano¹,

Ramos²,

Augusti³

et al. 2020

RSD

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Eugenia klotzschiana Berg is a native fruit of the cerrado, belonging to the Myrtaceae family, known as the cerrado pear and very little explored. The present study's objective was to obtain the profile of the fixed and volatile chemical constituents of the fruit. Mass spectrometry with ambient ionization paper spray (PS-MS) was used in positive and negative mode for fixed compounds. For volatiles, solid-phase microextraction by head space and gas chromatography was employed. The PS-MS identified 31 compounds, 21 in the negative and 10 in the positive mode, including fatty acids, flavonoids, phenolic acids, tannins and sugars. The solid-phase microextraction method was used in head space mode, using the polydimethylsiloxane-divinylbenzene fiber to extract volatile organic compounds (VOCs). The volatiles detected totaled 11 substances, belonging to the class of monoterpenes, sesquiterpenes, and esters. PS-MS was capable and efficient in determining the fixed compounds present in the cerrado pear pulp, providing the chemical profile of the fruit, which contains essential compounds with potential antioxidant bioactivity. The volatile profile was obtained with success, indicating menthol, fruity and vanilla notes in the pulp of the cerrado pear.

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“…It is reported that the effect of specific fatty acids on β cells is directly related to the degree of their saturation ( Janikiewicz et al 2015 , Liu et al 2019 ). According to the Prospective Metabolism and Islet Cell Evaluation (PROMISE) survey, an impaired β-cell function and a higher risk of T2DM were correlated with the serum saturate lipid levels ( Johnston et al 2016 ).…”

Section: Discussionmentioning

confidence: 99%

“…According to the Prospective Metabolism and Islet Cell Evaluation (PROMISE) survey, an impaired β-cell function and a higher risk of T2DM were correlated with the serum saturate lipid levels ( Johnston et al 2016 ). Besides, chronic exposure of β cells to unsaturated fatty acids significantly increases β-cell survival ( Liu et al 2019 ). Additionally, Busch et al (2005) reported that the level of stearoyl-CoA desaturase ( SCD ), an important gene in the regulation of cholesterol unsaturation, was increased in PA-resistant Min6 cells.…”

Section: Discussionmentioning

confidence: 99%

Circ-Tulp4 promotes β-cell adaptation to lipotoxicity by regulating soat1 expression

Xiong

Jin

et al. 2020

Journal of Molecular Endocrinology

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This study aimed to identify circular RNAs differentially expressed in the islets of type 2 diabetes (T2DM) models and clarify their roles in the control of β-cell functions. Circular RNAs dysregulated in the islets of diabetic db/db mice were identified by high-throughput RNA sequencing. Then, the expression level of the selected circular RNA circ-Tulp4 was confirmed by real-time PCR in the islets of diabetic models and Min6 cells. MTS, EdU, western blot, flow cytometric analysis, and luciferase assay were performed to investigate the impact of circ-Tulp4 on β-cell functions. This study identified thousands of circular RNAs in mouse pancreatic islets. The circ-Tulp4 level significantly decreased in the diabetic models and altered in the Min6 cells under lipotoxic condition. The modulation of circ-Tulp4 level in Min6 cells regulated cell proliferation. Furthermore, an interaction was demonstrated between circ-Tulp4 and miR-7222-3p, which suppressed the expression of cholesterol esterification related gene, sterol O-Acyltransferase 1 (SOAT1). The accumulation of soat1 activated cyclin D1 expression, thus promoting cell cycle progression. These findings showed that circ-Tulp4 regulated β-cell proliferation via miR-7222-3p/soat1/cyclin D1 signaling. Our research suggested that circ-Tulp4 might be a potential therapeutic intervention for T2DM. Besides, soat1 might be important for β-cell adaptation to lipotoxicity.

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Oleic acid protects insulin-secreting INS-1E cells against palmitic acid-induced lipotoxicity along with an amelioration of ER stress

Cited by 26 publications

References 48 publications

Oleic acid ameliorates palmitic acid induced hepatocellular lipotoxicity by inhibition of ER stress and pyroptosis

Oleic acid ameliorates palmitic acid induced hepatocellular lipotoxicity by inhibition of ER stress and pyroptosis

Analysis of the chemical profile of cerrado pear fixed compounds by mass spectrometry with paper spray and volatile ionization by SPME-HS CG-MS

Circ-Tulp4 promotes β-cell adaptation to lipotoxicity by regulating soat1 expression

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