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Gut inflammation as a contributing factor for the development of insulin resistance in obesity
Author(s) -
Schwerbrock Nicole MJ,
Smith Alexia G,
Cole Kathryn,
Scull Brookes,
Lund Kay,
Coleman Rosalind A,
Beck Melinda A
Publication year - 2007
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.21.5.a375-c
Subject(s) - inflammation , adipose tissue , insulin resistance , medicine , endocrinology , tumor necrosis factor alpha , obesity , biology
Adipose tissue in obese animals and humans produces a low level of cytokines and chemokines leading to a state of chronic, low grade inflammation. This inflammation is hypothesized to play a role in the development of insulin resistance associated with obesity. However, the intestine as a potential site of production of pro‐inflammatory cytokines during obesity has been largely overlooked. To address the contribution that gut inflammation may have on the development of inflammation during weight gain, we fed C57BL/6 mice a diet either low (10.5% fat: 38% soybean, 62% coconut oil) or high (58% fat: 93% coconut oil, 7% soybean oil) in fat. Preliminary data from our laboratory demonstrates that gut inflammation precedes weight gain and adipose tissue inflammation. Upregulation of the mRNA expression of the inflammatory mediator TNF‐α; occurred in the intestine within 2 weeks of feeding C57BL/6 mice a high fat diet. Enhanced expression of TNF‐α; mRNA in adipose tissue did not occur until week 8 on the high fat diet. Impaired glucose tolerance occurred between weeks 6 and 8, after the gut inflammation and prior to adipose inflammation. Therefore, we hypothesize that intestinal inflammation may be a contributing factor to chronic inflammation of obesity, leading to the development of insulin resistance.