Ambient fine particulate matter and ozone exposures induce inflammation in epicardial and perirenal adipose tissues in rats fed a high fructose diet

Abstract

BackgroundInflammation and oxidative stress play critical roles in the pathogenesis of inhaled air pollutant-mediated metabolic disease. Inflammation in the adipose tissues niches are widely believed to exert important effects on organ dysfunction. Recent data from both human and animal models suggest a role for inflammation and oxidative stress in epicardial adipose tissue (EAT) as a risk factor for the development of cardiovascular disease. We hypothesized that inhalational exposure to concentrated ambient fine particulates (CAPs) and ozone (O3) exaggerates inflammation and oxidative stress in EAT and perirenal adipose tissue (PAT).MethodsEight- week-old Male Sprague–Dawley rats were fed a normal diet (ND) or high fructose diet (HFr) for 8 weeks, and then exposed to ambient AIR, CAPs at a mean of 356 μg/m3, O3 at 0.485 ppm, or CAPs (441 μg/m3) + O3 (0.497 ppm) in Dearborn, MI, 8 hours/day, 5 days/week, for 9 days over 2 weeks.ResultsEAT and PAT showed whitish color in gross, and less mitochondria, higher mRNA expression of white adipose specific and lower brown adipose specific genes than in brown adipose tissues. Exposure to CAPs and O3 resulted in the increase of macrophage infiltration in both EAT and PAT of HFr groups. Proinflammatory genes of Tnf-α, Mcp-1 and leptin were significantly upregulated while IL-10 and adiponectin, known as antiinflammatory genes, were reduced after the exposures. CAPs and O3 exposures also induced an increase in inducible nitric oxide synthase (iNOS) protein expression, and decrease in mitochondrial area in EAT and PAT. We also found significant increases in macrophages of HFr-O3 rats. The synergetic interaction of HFr and dirty air exposure on the inflammation was found in most of the experiments. Surprisingly, exposure to CAPs or O3 induced more significant inflammation and oxidative stress than co-exposure of CAPs and O3 in EAT and PAT.ConclusionEAT and PAT are both white adipose tissues. Short-term exposure to CAPs and O3, especially with high fructose diet, induced inflammation and oxidative stress in EAT and PAT in rats. These findings may provide a link between air-pollution exposure and accelerated susceptibility to cardiovascular disease and metabolic complications.

Repeated ozone exposure exacerbates insulin resistance and activates innate immune response in genetically susceptible mice

“…Vella et al reported that overnight exposure to O 3 triggers insulin resistance by activating JNK pathway (Vella et al 2015). Study from our group also suggests O 3 exposure induces inflammation in epicardial and perirenal adipose tissues in rats (Sun et al 2013). Type 2 diabetes is a chronic disorder involving both genetic and environmental factors.…”

“…Although several studies have indicated acute (hours to 2 days) and chronic/sub-chronic (months) O 3 exposure may induce insulin resistance (Bass et al 2013; Sun et al 2013; Vella et al 2015), the effect of sub-acute exposure to O 3 on insulin sensitivity is not clear. In addition, the effect of O 3 exposure on diabetes susceptible individuals has not been reported.…”

“…Mice (8/group) were exposed to filtered air (FA), or O 3 (O 3 ; 0.5 ppm target) for 13 consecutive weekdays (Monday to Friday, 4 h/day). Choice of the O 3 exposure regimen was made on previously reported rodent studies in our group and others (Katre et al 2011; Last et al 2004; Sun et al 2013; Wagner et al 2014; Ying et al 2016). The magnitude of O 3 -induced airway epithelial injury and inflammation are exposure (e.g., concentration, time, and frequency) and species dependent.…”

Exposure to fine airborne particulate matters induces hepatic fibrosis in murine models

“…Recent studies indicated that exposure to fine ambient particulate matter (aerodynamic diameter < 2.5 µm, PM 2.5 ) is a risk factor for pulmonary and cardiovascular diseases as well as metabolic syndrome [1–3]. Traffic-related airborne PM 2.5 is a complex mixture of particles and gases from gasoline and diesel engines, together with dust from wear of road surfaces, tires, and brakes [4, 5].…”

Long-Term Exposure to Ambient Air Pollution and Serum Leptin in Older Adults

“…A recent clinical study found that exposure to even low levels of PM 2.5 may reduce metabolic insulin sensitivity (12). Animal toxicological studies also suggest that long-term exposure to particulate matter can induce insulin resistance and mitochondrial dysfunction, inflammation in adipose tissue, and up-regulation of leptin gene expression in adipose tissue (13–15). …”