Chronic inflammation and increased visceral adipose tissue (VAT) are key elements
of the metabolic syndrome. Both are considered to play a pathogenic role in the development
of liver steatosis and insulin resistance. The aim of the present study was to investigate
the hypothesis that an inflamed intestine, induced both by diet and chemical irritation,
could induce persistent inflammation in VAT. Female C57BL/6JOlaHsd mice were used.
In study I, groups of mice (n = 6 per group) were given an obesity-inducing cafeteria
diet (diet-induced obesity) or regular chow only (control) for 14 weeks. In study
II, colitis in mice (n = 8) was induced by 3% dextran sulfate sodium in tap water
for 5 days followed by 21 days of tap water alone. Healthy control mice (n = 8) had
tap water only. At the end of the studies, all mice were killed; and blood and tissues
were sampled and processed for analysis. Body weight of diet-induced obese mice was
greatly increased, with evidence of systemic inflammation, insulin resistance, and
liver steatosis. Tissue inflammation indexed by proinflammatory cytokine expression
was recorded in liver, mesenteric fat, and proximal colon/distal ileum, but not in
subcutaneous or perigonadal fat. In dextran sulfate sodium-induced colitis mice, mesenteric
fat was even more inflamed than the colon, whereas a much milder inflammation was
seen in liver and subcutaneous fat. The studies showed both diet- and colitis-initiated
inflammation in mesenteric fat. Fat depots contiguous with intestine and their capacity
for exaggerated inflammatory responses to conditions of impaired gut barrier function
may account for the particularly pathogenic role of VAT in obesity-induced metabolic
disorders.