title: Ambient fine particulate matter and ozone exposures induce inflammation in epicardial and perirenal adipose tissues in rats fed a high fructose diet.
abstract: BACKGROUND
  Inflammation 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).
  
  
  METHODS
  Eight- 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.
  
  
  RESULTS
  EAT 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.
  
  
  CONCLUSIONS
  EAT 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.
authors: Lixian
authors: L
authors: Sun
authors: Cuiqing
authors: C
authors: Liu
authors: Xiaohua
authors: X
authors: Xu
authors: Zhekang
authors: Z
authors: Ying
authors: Andrei
authors: A
authors: Maiseyeu
authors: Aixia
authors: A
authors: Wang
authors: Katryn
authors: K
authors: Allen
authors: Ryan P
authors: RP
authors: Lewandowski
authors: Lori A
authors: LA
authors: Bramble
authors: Masako
authors: M
authors: Morishita
authors: James G
authors: JG
authors: Wagner
authors: J
authors: J
authors: Dvonch
authors: Zhichao
authors: Z
authors: Sun
authors: Xiaowei
authors: X
authors: Yan
authors: Robert D
authors: RD
authors: Brook
authors: Sanjay
authors: S
authors: Rajagopalan
authors: Jack R
authors: JR
authors: Harkema
authors: Qinghua
authors: Q
authors: Sun
authors: Zhongjie
authors: Z
authors: Fan
mesh_terms: D054392:Adipokines / Q000235:genetics / Q000378:metabolism; D002001:Adipose Tissue, Brown / Q000187:drug effects / Q000378:metabolism / Q000648:ultrastructure; D052436:Adipose Tissue, White / Q000187:drug effects* / Q000378:metabolism / Q000648:ultrastructure; D000818:Animals; D004040:Dietary Carbohydrates; D005632:Fructose; D005786:Gene Expression Regulation; D018836:Inflammation Mediators / Q000378:metabolism; D019570:Inhalation Exposure / Q000009:adverse effects*; D007668:Kidney; D008264:Macrophages / Q000187:drug effects / Q000378:metabolism; D008297:Male; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects; D010126:Ozone / Q000633:toxicity*; D015434:Panniculitis / Q000139:chemically induced* / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D052638:Particulate Matter / Q000633:toxicity*; D010496:Pericardium; D012333:RNA, Messenger / Q000378:metabolism; D017207:Rats, Sprague-Dawley; D018570:Risk Assessment; D013997:Time Factors
chemical_list: D054392:Adipokines; D004040:Dietary Carbohydrates; D018836:Inflammation Mediators; D052638:Particulate Matter; D012333:RNA, Messenger; D005632:Fructose; D010126:Ozone; D052247:Nitric Oxide Synthase Type II; C496318:Nos2 protein, rat
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