Fine particles cause the abnormality of cardiac ATP levels via PPARɑ-mediated utilization of fatty acid and glucose using in vivo and in vitro models

Jin, Xiaoting; Xue, Bin; Ahmed, Rifat Zubair; Ding, Guo-Bin; Li, Zhuoyu

doi:10.1016/j.envpol.2019.02.083

Cited by 20 publications

(7 citation statements)

References 52 publications

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“…How this changes occur is ukknonwn, nevertheless, we presented evidence that a metabolic effect of PM 2.5 exposure is compromised oxidation of glucose compensated by the use of alternative fuels. In line with our results, reported effects of acute PM 2.5 exposure are decreased ATP in cardiomyocytes, decreased of fumarate accumulation in the liver, and the lungs 27,33,34,49 . However, we recognized that our assessment is limited to the liver metabolism of a single time point, that is insufficient to describe without ambiguity the kinetics and directionality of the metabolic reactions.…”

Section: Discussionsupporting

confidence: 93%

Air pollution-derived particulate matter dysregulates hepatic Krebs cycle, glucose and lipid metabolism in mice

Reyes-Caballero

Rao

Sun

et al. 2019

Sci Rep

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Exposure to ambient air particulate matter (PM2.5) is well established as a risk factor for cardiovascular and pulmonary disease. Both epidemiologic and controlled exposure studies in humans and animals have demonstrated an association between air pollution exposure and metabolic disorders such as diabetes. Given the central role of the liver in peripheral glucose homeostasis, we exposed mice to filtered air or PM2.5 for 16 weeks and examined its effect on hepatic metabolic pathways using stable isotope resolved metabolomics (SIRM) following a bolus of 13C6-glucose. Livers were analyzed for the incorporation of 13C into different metabolic pools by IC-FTMS or GC-MS. The relative abundance of 13C-glycolytic intermediates was reduced, suggesting attenuated glycolysis, a feature found in diabetes. Decreased 13C-Krebs cycle intermediates suggested that PM2.5 exposure led to a reduction in the Krebs cycle capacity. In contrast to decreased glycolysis, we observed an increase in the oxidative branch of the pentose phosphate pathway and 13C incorporations suggestive of enhanced capacity for the de novo synthesis of fatty acids. To our knowledge, this is one of the first studies to examine 13C6-glucose utilization in the liver following PM2.5 exposure, prior to the onset of insulin resistance (IR).

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Section: Discussionsupporting

confidence: 93%

Air pollution-derived particulate matter dysregulates hepatic Krebs cycle, glucose and lipid metabolism in mice

Reyes-Caballero

Rao

Sun

et al. 2019

Sci Rep

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“…The result of fatty acid metabolism is the generation of ATP [45]. This experiment shows that after VAP regulates fatty acid metabolism in aging mice, it further increases the ATP content of aging mice and improves energy metabolism in aging mice [46,47]. Although the mitochondrial and peroxisomal fatty acid oxidation decomposition products are the same, they are catalyzed by different enzymes.…”

Section: Discussionmentioning

confidence: 89%

The anti-aging effect of velvet antler polypeptide is dependent on modulation of the gut microbiota and regulation of the PPARα/APOE4 pathway

Liu

Yang

et al. 2021

J. Integr. Neurosci.

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We investigated the anti-aging effects of velvet antler polypeptide on D-galactose (D-gal)-induced aging mice. D-gal-induced aging mice were established and randomly divided into five groups, the control, model, vitamin E (VE), velvet antler polypeptide low-dose and velvet antler polypeptide high-dose groups. The Morris water maze test was used to evaluate the learning and memory abilities of aging mice. Hippocampal neurons were observed via hematoxylineosin staining and transmission electron microscopy. Biochemical methods were used to detect the activities of superoxide dismutase, malonaldehyde and other enzymes and evaluate the influence of velvet antler polypeptide on the antioxidant capacity of aging mice. Using 16S rRNA gene sequencing and meristem technology, we assessed the effect of velvet antler polypeptide on aging mice's intestinal flora and fatty acid metabolism. The experimental results showed that velvet antler polypeptide could significantly improve aging mice's learning and cognitive abilities, increase the activities of superoxide dismutase, glutathione peroxidase, and catalase in the serum decrease the malonaldehyde content. Intestinal microecological analysis showed that velvet antler polypeptide could significantly increase the beneficial bacterial genus Lactobacillus abundance. Western blot analysis further demonstrated that velvet antler polypeptide could promote fatty acid metabolism by activating peroxisome proliferator-activated receptor α (PPARα) and upregulating the expression of the downstream enzymes carnitinepalmitoyl transferase-1 A and acyl-CoA oxidase 1 while downregulating that of apolipoprotein E4 (APOE4), thereby reducing fatty acid accumulation and increasing adenosine-triphosphate (ATP) production. Therefore, velvet antler polypeptide improves the intestinal microecology and activates the PPARα/APOE4 pathway to regulate fatty acid metabolism.

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“…Cells were harvested following incubation with different coated 5 nm and 50 nm AuNPs (5 μg/mL) for 24 h. The intracellular ATP content was quantified by a commercial kit according to the manufacturer's instructions (Nanjing Jiancheng Biological Product, Nanjing, China), as described in our previous study [ 68 ]. The absorbance value was measured using a fluorescence microplate reader (Thermo Fisher Scientific, Waltham, MA, USA) at 636 nm.…”

Section: Methodsmentioning

confidence: 99%

Surface charge-dependent mitochondrial response to similar intracellular nanoparticle contents at sublethal dosages

Jin

Zhang

et al. 2021

Part Fibre Toxicol

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Background Considering the inevitability for humans to be frequently exposed to nanoparticles (NPs), understanding the biosafety of NPs is important for rational usage. As an important part of the innate immune system, macrophages are widely distributed in vital tissues and are also a dominant cell type that engulfs particles. Mitochondria are one of the most sensitive organelles when macrophages are exposed to NPs. However, previous studies have mainly reported the mitochondrial response upon high-dose NP treatment. Herein, with gold nanoparticles (AuNPs) as a model, we investigated the mitochondrial alterations induced by NPs at a sublethal concentration. Results At a similar internal exposure dose, different AuNPs showed distinct degrees of effects on mitochondrial alterations, including reduced tubular mitochondria, damaged mitochondria, increased reactive oxygen species, and decreased adenosine triphosphate. Cluster analysis, two-way ANOVA, and multiple linear regression suggested that the surface properties of AuNPs were the dominant determinants of the mitochondrial response. Based on the correlation analysis, the mitochondrial response was increased with the change in zeta potential from negative to positive. The alterations in mitochondrial respiratory chain proteins indicated that complex V was an indicator of the mitochondrial response to low-dose NPs. Conclusion Our current study suggests potential hazards of modified AuNPs on mitochondria even under sublethal dose, indicates the possibility of surface modification in biocompatibility improvement, and provides a new way to better evaluation of nanomaterials biosafety.

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Fine particles cause the abnormality of cardiac ATP levels via PPARɑ-mediated utilization of fatty acid and glucose using in vivo and in vitro models

Cited by 20 publications

References 52 publications

Air pollution-derived particulate matter dysregulates hepatic Krebs cycle, glucose and lipid metabolism in mice

Air pollution-derived particulate matter dysregulates hepatic Krebs cycle, glucose and lipid metabolism in mice

The anti-aging effect of velvet antler polypeptide is dependent on modulation of the gut microbiota and regulation of the PPARα/APOE4 pathway

Surface charge-dependent mitochondrial response to similar intracellular nanoparticle contents at sublethal dosages

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