Triterpene-enriched fractions from Eucalyptus tereticornis ameliorate metabolic alterations in a mouse model of diet-induced obesity

Acı́n, Sergio; Muñoz, Diego A.; Guillen, Alis; Soscue, Duberney; Castaño, Adriana; Echeverri, Fernándo; Balcazar, Norman

doi:10.1016/j.jep.2020.113298

Cited by 15 publications

(8 citation statements)

References 31 publications

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“…1g). A notable finding was that the serum adiponectin levels did not decrease after 8 weeks of HFD feeding, which was similar to the results of Acín et al [35]. This finding may be associated with disordered adipose tissue metabolism in obese BALB/c mice (shown in Fig.…”

Section: Establishment Of Obesity Model Induced By Hfdsupporting

confidence: 89%

High-Fat Diet-Induced Obesity Aggravates Food Allergy by Intestinal Barrier Destruction and Inflammation

Gu¹,

Guo²,

Sun³

et al. 2021

Int Arch Allergy Immunol

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Introduction: The increase in high-fat diet (HFD)-induced obesity and food allergy leads to an assumption that the 2 are related. This study aims to (1) systematic verification of HFD-induced obesity aggravates food allergy and (2) explore the correlation and molecular mechanisms of HFD-induced obesity promotes food allergy. Methods: Female BALB/c mice are divided into the control group (control), the ovalbumin (OVA)-sensitized group (OVA), the HFD-induced obesity group (HFD), and HFD-induced allergic obesity group (HFD + OVA). Results: In vivo data showed that HFD feed enhance clinical symptoms and intestinal mucosa villi shed on allergic mice. Moreover, we found that HFD and OVA irritation enhanced levels of mast cell degranulation and Th2 humoral response. Additionally, Western blot analysis showed the potentiation of peroxisome proliferator-activated receptor γ (PPAR γ) remarkably reduced on intestinal in HFD and OVA group, thereby inhibiting the expression of nuclear factor kappa B (NF-κB)/PPAR γ signal the phosphorylation of NF-κB P65. Conclusions: Overall, our results suggest that HFD-induced obesity is a potential risk factor for food allergy, which related to intestinal barrier destruction and inflammation through the PPAR γ/NF-κB signaling pathway.

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Section: Establishment Of Obesity Model Induced By Hfdsupporting

confidence: 89%

High-Fat Diet-Induced Obesity Aggravates Food Allergy by Intestinal Barrier Destruction and Inflammation

Gu¹,

Guo²,

Sun³

et al. 2021

Int Arch Allergy Immunol

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“…To further elucidate the potential mechanism based on TMAO acting on hepatocytes, we focused on NF-κB signaling pathway meditated in ammatory activation. ABCG5, PPAR gamma and SERBP1 are crucial proteins of lipid metabolism in liver so that they are widely used in hepatitis steatosis researches [31][32][33].…”

Section: Discussionmentioning

confidence: 99%

TMAO Stimulate Inflammation and Lipid Accumulation via NF-κB Signaling Pathway in Nonalcoholic Fatty Liver Disease

chen

Zhang

Qian

et al. 2021

Preprint

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Background Nonalcoholic fatty liver disease (NAFLD) is a common disease and it is commonly associated with obesity. Trimethylamine N-oxide (TMAO) is a metabolite of intestinal flora generated in liver by flavin-containing monooxygenase 3 (FMO3), which has been widely studied in cardiovascular diseases and obesity. However, the mechanism of TMAO reacted on liver remains unclear. This study aimed to determine TMAO activated hepatitis inflammation and lipid accumulation which was associated with nuclear factor kappa B (NF-κB) signaling pathway in vitro. ResultsThe present study showed that TMAO in 50μM markedly increased the LO2 cells function and decreased the cells inflammation. However, over the concentration of 200μM in TMAO, cells inflammation was increased and function was declined apparently. In addition, TMAO promoted lipid accumulation. Mechanistically, this change was accompanied by the activation of NF-κB signaling pathway. Furthermore, blocking NF-κB by SN50 was significantly increased in lipid accumulation and apoptosis. SN50 was markedly decreased the protein expression stimulating by TMAO.ConclusionsOverall, the result suggested that TMAO promotes cells inflammation and lipid accumulation in hepatocytes and it might be associated with NF-κB signaling pathway.

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“…Furthermore, OA may reduce obesity via the suppression of the adipogenic factors PPARα, SREBP1, and FAS [ 19 ]. OA has been shown to reduce the synthesis of fat and accelerate the utilization of fat through the alteration of hepatic PPARα, recombinant carnitine palmitoyltransferase 1A (CPT1A), SREBP-1, the acetyl coenzyme A carboxylase, and coupled protein 1 (UCP1) [ 20 ]. In addition, OA can reduce blood glucose and lipid levels by promoting carbohydrate and fat metabolism [ 21 ].…”

Section: Anti-metabolic Syndromes’ Effectsmentioning

confidence: 99%

“…Furthermore, OA could accelerate fat utilization by reducing PPARα, inhibiting CPT1, and promoting UCP1. It was also observed that OA suppressed fat accumulation via the regulation of the level of SERBP1 and ACACA [ 20 ].…”

Section: Signaling Pathways Of Oa For the Treatment Of Mets And Cvdsmentioning

confidence: 99%

The Effect and Mechanism of Oleanolic Acid in the Treatment of Metabolic Syndrome and Related Cardiovascular Diseases

Luo,

Wei,

et al. 2024

Molecules

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Metabolic syndromes (MetS) and related cardiovascular diseases (CVDs) pose a serious threat to human health. MetS are metabolic disorders characterized by obesity, dyslipidemia, and hypertension, which increase the risk of CVDs’ initiation and development. Although there are many availabile drugs for treating MetS and related CVDs, some side effects also occur. Considering the low-level side effects, many natural products have been tried to treat MetS and CVDs. A five-cyclic triterpenoid natural product, oleanolic acid (OA), has been reported to have many pharmacologic actions such as anti-hypertension, anti-hyperlipidemia, and liver protection. OA has specific advantages in the treatment of MetS and CVDs. OA achieves therapeutic effects through a variety of pathways, attracting great interest and playing a vital role in the treatment of MetS and CVDs. Consequently, in this article, we aim to review the pharmacological actions and potential mechanisms of OA in treating MetS and related CVDs.

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Triterpene-enriched fractions from Eucalyptus tereticornis ameliorate metabolic alterations in a mouse model of diet-induced obesity

Cited by 15 publications

References 31 publications

High-Fat Diet-Induced Obesity Aggravates Food Allergy by Intestinal Barrier Destruction and Inflammation

High-Fat Diet-Induced Obesity Aggravates Food Allergy by Intestinal Barrier Destruction and Inflammation

TMAO Stimulate Inflammation and Lipid Accumulation via NF-κB Signaling Pathway in Nonalcoholic Fatty Liver Disease

The Effect and Mechanism of Oleanolic Acid in the Treatment of Metabolic Syndrome and Related Cardiovascular Diseases

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