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Adipose Inflammation and Cardiovascular Disease Risk Factors in Obesity‐Prone Osborne‐Mendel and Obesity‐Resistant S5B/Pl Rats
Author(s) -
Primeaux Stefany,
SouzaSmith Flavia,
Poret Jonquil,
Mouton Alan,
Marcell Shawn,
Battle Claire,
Braymer H. Douglas,
HarrisonBernard Lisa
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.1293.10
Subject(s) - medicine , endocrinology , adipose tissue , obesity , adipocyte , triglyceride , inflammation , cholesterol
Obesity‐related increases in visceral adipose deposition and inflammation, circulating triglyceride (TRG), LDL cholesterol, and C‐reactive protein (CRP) enhance the risk for CVD. These effects may be intensified by the consumption of an energy dense, high fat diet (HFD). The current study tested the hypothesis that HFD consumption would exacerbate CVD risk factors in obesity‐prone Osborne‐Mendel (OM) rats, compared to obesity‐resistant S5B/Pl (S5B) rats. OM and S5B rats were fed either a HFD (60% fat; n=6/strain) or low fat diet (LFD, 10% fat; n=6/strain) for 7 weeks. A multiplex rat cytokine/chemokine panel was used to assess the expression of inflammatory markers in epididymal fat and subcutaneous fat depots. Circulating TNF‐α and CRP levels were determined by ELISA and circulating TRG, HDL, LDL and total cholesterol were assessed. Cardiac hypertrophy was assessed by total heart and left ventricular mass. As expected, body weight, % visceral adiposity (OM‐HFD 5.3% vs. S5B‐HFD 1.2%) and adipocyte size were increased by HFD intake to a greater extent in the obesity‐prone OM rats. Higher basal levels of IL‐6, TNF‐α, IL‐1α, and IL‐1β were detected in the epididymal fat depots of obesity‐prone rats. Consumption of a HFD increased Il‐6, TNF‐α, IL‐1α, and IL‐1β in the epididymal fat of both OM and S5B rats. HFD intake synergistically increased TNF‐α expression in OM rats (2‐fold vs. S5B‐HFD; p<.05). However, circulating levels of TNF‐α were decreased in OM rats fed the HFD. In subcutaneous fat, HFD intake did not alter inflammatory marker expression in either OM or S5B rats, though basal expression of IL‐6, IL‐1α, and IL‐1β was higher in subcutaneous fat of OM rats, compared to S5B rats (p<.05). Circulating TRG was increased and HDL cholesterol was decreased in OM rats, regardless of diet. Circulating CRP levels were increased by HFD in both strains, suggesting an inflammatory response to the HFD (p<.05). Left ventricle/heart ratio was lower in OM rats, but increased with HFD consumption in this strain, suggesting cardiac hypertrophy. A HFD‐induced increase in pro‐inflammatory cytokine expression in the visceral adipose depot, but not in subcutaneous fat, supports the role of visceral fat in the deleterious effects of dietary fat. Higher basal levels of pro‐inflammatory cytokines in adipose tissue and TRG and lower levels of HDL cholesterol in obesity‐prone rats suggest that this strain is at a greater risk for developing CVD compared to the obesity‐resistant rats. Support or Funding Information COBRE 1P30GM106392