Background: High ambient levels of ozone (O3) and fine particulate matter (PM2.5) are associated with cardiovascular morbidity and mortality, especially in people with preexisting cardiopulmonary diseases. Enhanced susceptibility to the toxicity of air pollutants may include individuals with metabolic syndrome (MetS).

Objective: We tested the hypothesis that cardiovascular responses to O3 and PM2.5 will be enhanced in rats with diet-induced MetS.

Methods: Male Sprague-Dawley rats were fed a high-fructose diet (HFrD) to induce MetS and then exposed to O3, concentrated ambient PM2.5, or the combination of O3 plus PM2.5 for 9 days. Data related to heart rate (HR), HR variability (HRV), and blood pressure (BP) were collected.

Results: Consistent with MetS, HFrD rats were hypertensive and insulin resistant, and had elevated fasting levels of blood glucose and triglycerides. Decreases in HR and BP, which were found in all exposure groups, were greater and more persistent in HFrD rats compared with those fed a normal diet (ND). Coexposure to O3 plus PM2.5 induced acute drops in HR and BP in all rats, but only ND rats adapted after 2 days. HFrD rats had little exposure-related changes in HRV, whereas ND rats had increased HRV during O3 exposure, modest decreases with PM2.5, and dramatic decreases during O3 plus PM2.5 coexposures.

Conclusions: Cardiovascular depression in O3- and PM2.5-exposed rats was enhanced and prolonged in rats with HFrD-induced MetS. These results in rodents suggest that people with MetS may be prone to similar exaggerated BP and HR responses to inhaled air pollutants.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3888573PMC
http://dx.doi.org/10.1289/ehp.1307085DOI Listing

Publication Analysis

Top Keywords

hfrd rats
12
rats
11
cardiovascular depression
8
particulate matter
8
metabolic syndrome
8
air pollutants
8
decreases pm25
8
pm25
7
cardiovascular
4
depression rats
4

Similar Publications

Background: A growing body of evidence links a high-fructose diet (HFrD) to metabolic disturbances, including inflammation, dyslipidemia, insulin resistance and also endothelial dysfunction, yet its role in allergic asthma remains underexplored. Considering that obesity and hypercholesterolemia exacerbate asthma by promoting systemic inflammation, investigating interventions with dual metabolic and anti-inflammatory effects is essential. This study aimed to evaluate the potential modulatory effects of rosuvastatin in ameliorating the effects of HFrD-induced metabolic and vascular dysfunction in the context of allergic asthma.

View Article and Find Full Text PDF

Neuroprotective effect of niacin in a rat model of obesity induced by high-fat-rich diet.

Naunyn Schmiedebergs Arch Pharmacol

December 2024

Department of Pharmaceutics, College of Pharmacy, King Saud University, 11451, Riyadh, Saudi Arabia.

This study investigates the impact of a high-fat-rich diet (HFRD) on behavioral, biochemical, neurochemical, and histopathological studies using the hypothalamus of rats following niacin (NCN) administration. The rats were divided into HFRD and normal diet (ND)-fed groups and administered selected doses of NCN, i.e.

View Article and Find Full Text PDF

Background: Intrahepatic lipid accumulation (IHL), a hallmark of metabolic disorders, is closely associated with de novo lipogenesis (DNL). Notably, fructose feeding increased the DNL. Lifestyle modifications resulting from dietary changes and increased physical activity/exercise can decrease the IHL content.

View Article and Find Full Text PDF

High fructose diet (HFrD) has been approved to be involved in the pathogenesis of insulin resistance. Mesenchymal stem cells have a vital role in the treatment of various diseases including metabolic disturbances. We investigated the effect of Adipose-derived mesenchymal stem cells (ADMSCs) against HFrD-induced metabolic disorders and the molecular mechanisms for this effect.

View Article and Find Full Text PDF
Article Synopsis
  • Abnormal lipid deposition plays a key role in the progression of metabolic dysfunction-associated steatotic liver disease (MASLD), with microRNA-411-5p (miR-411-5p) and eukaryotic translation initiation factor 4γ2 (EIF4G2) being linked to this process.
  • Research utilized different high-fat diets to create MASLD models in rats and mice, then applied miR-411-5p and EIF4G2 manipulation techniques to study their effects on liver function.
  • Findings revealed that increasing miR-411-5p reduced lipid deposition and liver damage by targeting EIF4G2, which in turn inhibited fatty acid synthesis pathways, suggesting a potential therapeutic approach for MASLD.
View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!