Chronic Oleoylethanolamide Treatment Decreases Hepatic Triacylglycerol Level in Rat Liver by a PPARγ/SREBP-Mediated Suppression of Fatty Acid and Triacylglycerol Synthesis

Romano, Adele; Friuli, Marzia; Coco, Laura Del; Longo, Serena; Vergara, Daniele; Boccio, Piero Del; Valentinuzzi, Silvia; Cicalini, Ilaria; Fanizzi, Francesco Paolo; Gaetani, Silvana; Giudetti, Anna Maria

doi:10.3390/nu13020394

Cited by 17 publications

(16 citation statements)

References 75 publications

(113 reference statements)

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“…Oxidative stress can modulate metabolic pathways by activating transcription factors, among which Nrf1 and Nrf2 play a key role [ 49 , 50 , 51 , 52 , 53 , 54 , 55 ]. We measured the protein expression of Nrf1, Nrf2, and PPARγ, this latter being an Nrf2-downstream transcriptional factor [ 56 ], involved in the regulation of lipid metabolism [ 34 , 57 ].…”

Section: Resultsmentioning

confidence: 99%

“…PPARγ is a regulator of lipid metabolism in hepatocytes; changes in the expression of this protein have been associated with non-alcoholic fatty liver diseases through the induction of lipogenic factors [ 57 ]. Recently, we demonstrated a PPARγ-mediated effect of OEA on reducing hepatic lipid accumulation in control rats [ 34 ]. Here, we found that HFD increased PPARγ expression ( Figure 3 D), and induced liver steatosis, both restored by OEA administration.…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, it has been demonstrated that OEA reduces lipid synthesis and lipoprotein secretion in hepatocytes [ 30 ] and improves HFD-induced liver steatosis in rats [ 31 ] and humans [ 32 , 33 ]. Recently, we demonstrated that OEA decreases hepatic lipid accumulation through a peroxisome proliferator-activated receptor γ (PPARγ)-mediated inhibition of hepatic fatty acid uptake and triacylglycerol synthesis [ 34 ].…”

Section: Introductionmentioning

confidence: 99%

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Oleoylethanolamide Reduces Hepatic Oxidative Stress and Endoplasmic Reticulum Stress in High-Fat Diet-Fed Rats

et al. 2021

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Long-term high-fat diet (HFD) consumption can cause weight gain and obesity, two conditions often associated with hepatic non-alcoholic fatty liver and oxidative stress. Oleoylethanolamide (OEA), a lipid compound produced by the intestine from oleic acid, has been associated with different beneficial effects in diet-induced obesity and hepatic steatosis. However, the role of OEA on hepatic oxidative stress has not been fully elucidated. In this study, we used a model of diet-induced obesity to study the possible antioxidant effect of OEA in the liver. In this model rats with free access to an HFD for 77 days developed obesity, steatosis, and hepatic oxidative stress, as compared to rats consuming a low-fat diet for the same period. Several parameters associated with oxidative stress were then measured after two weeks of OEA administration to diet-induced obese rats. We showed that OEA reduced, compared to HFD-fed rats, obesity, steatosis, and the plasma level of triacylglycerols and transaminases. Moreover, OEA decreased the amount of malondialdehyde and carbonylated proteins and restored the activity of antioxidant enzymes superoxide dismutase, catalase, and glutathione peroxidase, which decreased in the liver of HFD-fed rats. OEA had also an improving effect on parameters linked to endoplasmic reticulum stress, thus demonstrating a role in the homeostatic control of protein folding. Finally, we reported that OEA differently regulated the expression of two transcription factors involved in the control of lipid metabolism and antioxidant genes, namely nuclear factor erythroid-derived 2-related factor 1 (Nrf1) and Nrf2, thus suggesting, for the first time, new targets of the protective effect of OEA in the liver.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Oleoylethanolamide Reduces Hepatic Oxidative Stress and Endoplasmic Reticulum Stress in High-Fat Diet-Fed Rats

et al. 2021

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“…Li et al [ 45 ] demonstrated that the protein expression and activity of ACC, FAS, and SCD-1 were suppressed when the aberrant expression of SREBP-1 was suppressed. Furthermore, Romano et al [ 46 ] demonstrated that downregulation of SREBP-1 and PPAR-γ suppressed lipogenesis-specific gene expression. Whether the expression of these major lipogenic factors is regulated is one of the main indicators to determine the inhibitory effect of pharmacologically active substances on lipogenesis [ 47 ].…”

Section: Discussionmentioning

confidence: 99%

Bee Venom and Its Major Component Melittin Attenuated Cutibacterium acnes- and IGF-1-Induced Acne Vulgaris via Inactivation of Akt/mTOR/SREBP Signaling Pathway

Gwon

et al. 2022

IJMS

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Acne vulgaris is the most common disease of the pilosebaceous unit. The pathogenesis of this disease is complex, involving increased sebum production and perifollicular inflammation. Understanding the factors that regulate sebum production is important in identifying novel therapeutic targets for the treatment of acne. Bee Venom (BV) and melittin have multiple effects including antibacterial, antiviral, and anti-inflammatory activities in various cell types. However, the anti-lipogenic mechanisms of BV and melittin have not been elucidated. We investigated the effects of BV and melittin in models of Insulin-like growth factor-1 (IGF-1) or Cutibacterium acnes (C. acnes)-induced lipogenic skin disease. C. acnes or IGF-1 increased the expression of sterol regulatory element-binding protein-1 (SREBP-1) and proliferator-activated receptor gamma (PPAR-γ), transcription factors that regulate numerous genes involved in lipid biosynthesis through the protein kinase B (Akt)/mammalian target of rapamycin (mTOR)/SREBP signaling pathway. In this study using a C. acnes or IGF-1 stimulated lipogenic disease model, BV and melittin inhibited the increased expression of lipogenic and pro-inflammatory factor through the blockade of the Akt/mTOR/SREBP signaling pathway. This study suggests for the first time that BV and melittin could be developed as potential natural anti-acne agents with anti-lipogenesis, anti-inflammatory, and anti-C. acnes activity.

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“…PPARs are important transcriptional factors in modulating liver inflammation [67], lipid metabolism [68], and cancer growth [69]. All three PPAR subtypes, including PPARα [70], PPARβ/δ [71], and PPARγ [72], play important roles in lipid metabolism, either in the liver or adipose tissues. For example, hepatocyte-specific PPARα deficiency mice showed a significant increase in oleic acid and linoleic acid compared with wild-type mice in fasting, partly due to a fasting-induced increase in fibroblast growth factor 21 (FGF21) expression [73].…”

Section: Pparsmentioning

confidence: 99%

The Emerging Factors and Treatment Options for NAFLD-Related Hepatocellular Carcinoma

Zhang

Yang

2021

Cancers

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Hepatocellular carcinoma (HCC) is the most common type of primary liver cancer, followed by cholangiocarcinoma (CCA). HCC is the third most common cause of cancer death worldwide, and its incidence is rising, associated with an increased prevalence of obesity and nonalcoholic fatty liver disease (NAFLD). However, current treatment options are limited. Genetic factors and epigenetic factors, influenced by age and environment, significantly impact the initiation and progression of NAFLD-related HCC. In addition, both transcriptional factors and post-transcriptional modification are critically important for the development of HCC in the fatty liver under inflammatory and fibrotic conditions. The early diagnosis of liver cancer predicts curative treatment and longer survival. However, clinical HCC cases are commonly found in a very late stage due to the asymptomatic nature of the early stage of NAFLD-related HCC. The development of diagnostic methods and novel biomarkers, as well as the combined evaluation algorithm and artificial intelligence, support the early and precise diagnosis of NAFLD-related HCC, and timely monitoring during its progression. Treatment options for HCC and NAFLD-related HCC include immunotherapy, CAR T cell therapy, peptide treatment, bariatric surgery, anti-fibrotic treatment, and so on. Overall, the incidence of NAFLD-related HCC is increasing, and a better understanding of the underlying mechanism implicated in the progression of NAFLD-related HCC is essential for improving treatment and prognosis.

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Chronic Oleoylethanolamide Treatment Decreases Hepatic Triacylglycerol Level in Rat Liver by a PPARγ/SREBP-Mediated Suppression of Fatty Acid and Triacylglycerol Synthesis

Cited by 17 publications

References 75 publications

Oleoylethanolamide Reduces Hepatic Oxidative Stress and Endoplasmic Reticulum Stress in High-Fat Diet-Fed Rats

Oleoylethanolamide Reduces Hepatic Oxidative Stress and Endoplasmic Reticulum Stress in High-Fat Diet-Fed Rats

Bee Venom and Its Major Component Melittin Attenuated Cutibacterium acnes- and IGF-1-Induced Acne Vulgaris via Inactivation of Akt/mTOR/SREBP Signaling Pathway

The Emerging Factors and Treatment Options for NAFLD-Related Hepatocellular Carcinoma

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