Expression of Inflammatory Markers in Visceral Fat of Obesity‐prone Rats is Increased by High Fat Diet Consumption

Abstract

Listen

Translate article

Excess visceral adiposity, rather than total adiposity, is associated with obesity‐related increases in the risk for developing cardiovascular disease (CVD). As a consequence of expanding visceral adiposity, inflammation is prevalent and may link obesity and CVD. The current study tested the hypothesis that high fat diet (HFD) consumption leads to an increase in the expression of inflammatory markers in visceral fat, not subcutaneous fat, in obesity‐prone, Osborne‐Mendel (OM), rats. OM rats were fed either a HFD (60% fat; n=6) or low fat diet (LFD, 10% fat; n=6) for 7 weeks. As expected, body weight and % adiposity were increased by HFD intake. A multiplex rat cytokine/chemokine panel was used to assess the expression of inflammatory markers in epididymal fat, mesenteric fat and subcutaneous fat. Expression of IL‐1α, IL‐1ᵦ, IL‐6, IL‐10, TNF‐α, GM‐CSF, MIP‐1α (CCL3) and MIP‐2 (CXCL2) was increased by HFD intake in the epididymal fat of OM rats (p<.05). In mesenteric fat, the expression of IL‐1α, IL‐6 and IL‐10 was increased by the consumption of HFD (p<.05). GM‐CSF and MIP‐2 (CXCL2) were undetectable in the mesenteric fat of LFD fed OM rats. Subcutaneous fat expression of MIP‐2 (CXCL2) was decreased in the HFD fed group, compared to the LFD fed group (p<.05). An increase in cytokine/chemokine expression in the visceral adipose depots, but not in the subcutaneous fat, of obesity‐prone OM rats following HFD intake supports the role of visceral fat in the deleterious effects of obesity. These data suggest that HFD‐induced inflammation in obesity‐prone rats will enhance the risk for cardiovascular disease. Support: NIH 1P30GM106392‐01A1.