Disconnect between adipose tissue inflammation and cardiometabolic dysfunction in Ossabaw pigs

Objective The Ossabaw pig is emerging as an attractive model of human cardiometabolic disease because of its size and susceptibility to atherosclerosis, among other characteristics. The relationship between adipose tissue inflammation and metabolic dysfunction in this model was investigated here. Me...

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Published inObesity (Silver Spring, Md.) Vol. 23; no. 12; pp. 2421 - 2429
Main Authors Vieira‐Potter, Victoria J., Lee, Sewon, Bayless, David S., Scroggins, Rebecca J., Welly, Rebecca J., Fleming, Nicholas J., Smith, Thomas N., Meers, Grace M., Hill, Michael A., Rector, R. Scott, Padilla, Jaume
Format Journal Article
LanguageEnglish
Published United States Blackwell Publishing Ltd 01.12.2015
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Summary:Objective The Ossabaw pig is emerging as an attractive model of human cardiometabolic disease because of its size and susceptibility to atherosclerosis, among other characteristics. The relationship between adipose tissue inflammation and metabolic dysfunction in this model was investigated here. Methods Young female Ossabaw pigs were fed a Western‐style high‐fat diet (HFD) (n = 4) or control low‐fat diet (LFD) (n = 4) for a period of 9 months and compared for cardiometabolic outcomes and adipose tissue inflammation. Results The HFD‐fed “OBESE” pigs were 2.5 times heavier (P < 0.001) than LFD‐fed “LEAN” pigs and developed severe obesity. HFD feeding caused pronounced dyslipidemia, hypertension, and insulin resistance (systemic and adipose), as well as induction of inflammatory genes, impairments in vasomotor reactivity to insulin, and atherosclerosis in the coronary arteries. Remarkably, visceral, subcutaneous, and perivascular adipose tissue inflammation (via FACS analysis and RT‐PCR) was not increased in OBESE pigs, nor were circulating inflammatory cytokines. Conclusions These findings reveal a disconnect between adipose tissue inflammation and cardiometabolic dysfunction induced by Western diet feeding in the Ossabaw pig model.
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Funding agencies
The authors declare no conflict of interest.
Funding was provided by NIH K01HL125503 (J.P.), University of Missouri Mizzou Advantage (R.S.R.), VA‐CDA2‐1299 (salary support to R.S.R.), and a grant from the Allen Foundation Inc. (R.S.R.). We acknowledge the support of NIH RR013223 and HL062552 to Dr. Michael Sturek and the Comparative Medicine Center of IUSM and Purdue University for the female Ossabaw swine used in this study.
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ISSN:1930-7381
1930-739X
DOI:10.1002/oby.21252