Exercise improves high fat diet-impaired vascular function

Fang, Jun; Tang, Man‐Lai

doi:10.3892/br.2017.972

Cited by 8 publications

(8 citation statements)

References 27 publications

(30 reference statements)

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“…Vegf, a key pro‐angiogenic regulator gene increased with high‐fat diet exposure, however, decreased significantly with exercise in accordance with the literature (Fang & Tang, 2017 ), with and without change in diet. Angiogenesis is a key event in the progression of NAFLD (Lefere et al, 2020 ), and VEGF, supported by the activation of hypoxia‐inducible factors, is a key pro‐angiogenic regulator of this process.…”

Section: Discussionsupporting

confidence: 90%

The effect of endurance training on non‐alcoholic fatty liver disease in mice

et al. 2021

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Chronic endurance exercise is a therapeutic strategy in the treatment of non‐alcoholic fatty liver disease (NAFLD). Metabolic, cardiorespiratory, and endocrine pathways targeted by chronic endurance exercise have been identified; however, the specific cellular and molecular pathways modified by exercise in the steatotic liver remain unresolved. In this study, we show hepatic gene expression, and the structure, characteristics, and clinical differences between sedentary and exercised mice, by an endurance exercise model with wheels with a controlled velocity that allows for the quantification of a human‐relevant endurance “dosage,” after exposure to regular and high‐fat diet. Chronic exercise modified the transcription of hepatic genes related to liver nuclear receptors, cell growth, fibrosis, inflammation, and oxidative stress, and decreased the amount of lipid accumulation in the liver. Moreover, the combination of endurance training with the change in diet differentially modified the genetic expression of the biomarkers relative to the separate interventions. Even though exercise by itself showed counteract NAFLD development, the combined intervention was sufficient to convert the structure and clinical aspects of the liver from steatotic to healthy. Given our findings, the combination of endurance exercise and change in diet should be considered a therapeutic option for NASH.

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Section: Discussionsupporting

confidence: 90%

The effect of endurance training on non‐alcoholic fatty liver disease in mice

et al. 2021

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“…Endurance aerobic exercise or resistance training potentially contributes to the reduction in plasma resistin levels in the diabetic patients suffering from obesity and/or IR 32 . Similarly, exercise training protects against HFD-induced obesity by reducing oxidative stress and resistin and inhibiting vascular dysfunction 33 …”

Section: Discussionmentioning

confidence: 99%

Exercise Reduces Insulin Resistance in Type 2 Diabetes Mellitus via Mediating the lncRNA MALAT1/MicroRNA-382-3p/Resistin Axis

Liu

Fan

Xie

et al. 2019

Molecular Therapy - Nucleic Acids

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Insulin resistance (IR) is the primary pathological mechanism underlying type 2 diabetes mellitus (T2DM). Here, the study aimed to ascertain whether and how exercise mediates IR in T2DM. An in vivo mouse model of high-fat diet-induced IR and an in vitro high-glucose-induced IR model were constructed. High long non-coding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) expression was detected in T2MD and was positively correlated with HOMA-IR and resistin levels. Then, short hairpin RNA targeting MALAT1 (sh-MALAT1) or pcDNA-MALAT1 was delivered into human umbilical vein endothelial cells (HUVECs) to knock down or upregulate its expression, respectively. Silencing of MALAT1 resulted in reduced levels of resistin, Ang II, tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), soluble intercellular adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1), endothelin-1 (ET-1), and p-insulin receptor substrate-1 (p-IRS)/ISR-1, and decreased cell migration, as well as enhanced glucose uptake and levels of nitric oxide (NO) and p-Akt/Akt. In the IR mouse model, exercise was observed to downregulate MALAT1 to reduce resistin, whereby exercise reduced homeostatic model assessment-insulin resistance (HOMA-IR). Besides, exercise also elevated microRNA-382-3p (miR-382-3p) expression in the serum of IR mice. Dual-luciferase reporter and RNA binding protein immunoprecipitation (RIP) assays identified that MALAT1 could bind to miR-382-3p to upregulate resistin. Collectively, the key observations of the study provide evidence that inhibition of MALAT1 elevates miR-382-3p to repress resistin, which consequently underlies the mechanism of exercise protecting against IR, highlighting a direction for T2DM therapy development.

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“…In the present study, the H 2 O 2 -induced oxidative stress model and HFD-induced atherosclerosis model were used to explore the effect of AEE on vascular endothelial cell dysfunction. HFD-fed rats and H 2 O 2 -induced vascular endothelial cells are rapid, invaluable and sensitive models of evoked vascular endothelial dysregulation in vivo and in vitro, respectively [33,34,35,36]. In vitro, after exposure to 200 µM H 2 O 2 for 22 h, the percentage of early apoptotic HUVECs and E-selectin expression in HUVECs were significantly increased.…”

Section: Discussionmentioning

confidence: 99%

Cellular Metabolomics Reveal the Mechanism Underlying the Anti-Atherosclerotic Effects of Aspirin Eugenol Ester on Vascular Endothelial Dysfunction

Huang

Yang

et al. 2019

IJMS

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Aspirin eugenol ester (AEE) possesses anti-thrombotic, anti-atherosclerotic and anti-oxidative effects. The study aims to clarify the mechanism underlying the anti-atherosclerotic effects of AEE on vascular endothelial dysfunction. Both the high-fat diet (HFD)-induced atherosclerotic rat model and the H2O2-induced human umbilical vein endothelial cells (HUVECs) model were used to investigate the effects of AEE on vascular endothelial dysfunction. UPLC/QTOF-MS coupled with a multivariate data analysis method were used to profile the variations in the metabolites of HUVECs in response to different treatments. Pretreatment of HUVECs with AEE significantly ameliorated H2O2-induced apoptosis, the overexpression of E-selectin and VCAM-1, and the adhesion of THP-1 cells. Putative endogenous biomarkers associated with the inhibition of endothelial dysfunction were identified in HUVECs pretreated with AEE in the absence or presence of H2O2, and these biomarkers were involved in important metabolic pathways, including amino acid metabolism, carbohydrate metabolism, and glutathione metabolism. Moreover, in vivo, AEE also significantly reduced vascular endothelial dysfunction and decreased the overexpression of VCAM-1 and E-selectin. Based on our findings, the mechanism underlying the anti-atherosclerotic effects of AEE might be related to a reduction in vascular endothelial dysfunction mediated by ameliorating alterations in metabolism, inhibiting oxidative stress, and decreasing the expression of adhesion molecules.

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Exercise improves high fat diet-impaired vascular function

Cited by 8 publications

References 27 publications

The effect of endurance training on non‐alcoholic fatty liver disease in mice

The effect of endurance training on non‐alcoholic fatty liver disease in mice

Exercise Reduces Insulin Resistance in Type 2 Diabetes Mellitus via Mediating the lncRNA MALAT1/MicroRNA-382-3p/Resistin Axis

Cellular Metabolomics Reveal the Mechanism Underlying the Anti-Atherosclerotic Effects of Aspirin Eugenol Ester on Vascular Endothelial Dysfunction

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