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|標題:||Effect of weight loss on proinflammatory state of mononuclear cells in obese women|
|期刊/報告no：:||Obesity, Volume 16, Issue 5, Page(s) 1033-1038.|
|摘要:||In order to investigate whether weight loss can lead to improvement of the mononuclear cell (MNC) proinflammatory state, 21 nondiabetic obese women with mean age 34 +/- 2 years (mean +/- s.e.m.) and BMI 32.5 +/- 1.2 kg/m(2) were enrolled in a 12-week caloric restriction and light exercise-based weight loss program. Ten lean women served as controls. Reverse transcription-PCR of proinflammatory cytokines and adipocytokines as well as homeostasis model assessment of insulin resistance (HOMA-IR) were determined before and after weight reduction. Nuclear factor kappa B (NF-kappa B) binding to DNA and inhibitors of NF-kappa B (I kappa B-beta and I kappa B-beta) obtained from peripheral MNCs were measured. Overall, subjects lost a mean of 4.0 +/- 0.4 kg (5.0 +/- 0.3% of their initial body weight) (P < 0.01). In addition to significant reductions in BMI, fasting glucose and insulin concentrations, mean serum high-sensitivity C-reactive protein (hs-CRP), migration inhibitor factor (MIF), leptin and visfatin levels decreased by 49.0, 66.6, 17.2, and 50.2%, respectively (all P < 0.05), while adiponectin concentrations rose by 33.9% (P < 0.05). The DNA binding of the transcriptionally active NF-kappa B from (p65/p50) decreased by 38.1% (P < 0.05). Elevated levels of mRNA of NF-kappa B related proinflammatory genes, tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), MIF, and matrix metalloproteinase-9 (MMP-9), decreased significantly after weight loss. Although mRNA expression of Rel-A, p105, I kappa B-alpha, I kappa B-alpha decreased significantly, their protein levels did not change after weight loss. As a group, NF-kappa B binding activity correlated with HOMA-IR (r = 0.332, P = 0.049) and marginally with values of BMI (r = 0.308, P = 0.059). In conclusion, weight loss by 5% of initial weight in nondiabetic obese women led to significant improvement in activated intranuclear NF-kappa B binding as well as several transcriptions of proinflammatory genes regulated by NF-kappa B.|
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