Isoflavones may ease obesity-related inflammation

By Nathan Gray

- Last updated on GMT

Related tags: Insulin resistance, Obesity, Inflammation

Isoflavones may reduce chronic inflammation and insulin resistance in fat cells, according to researchers.

The study, published in Food Chemistry​, suggests that isoflavones from soybeans could reduce chronic inflammation and insulin resistance associated with obesity by blocking key pro-inflammatory signals from immune cells in adipose tissue.

“Our main finding is that a chronic treatment with isoflavones down regulates expression of cytokines and reduces the … secretion of inflammatory molecules,”​ wrote the researchers, led by Dr. Lluís Arola, professor of biochemistry and molecular biology at the Universitat Rovira i Virgili, Spain.

Promoting health

Isoflavones are mainly derived from soybeans. Recent epidemiological data strongly suggests they promote health in humans, with consumption related to breast and prostate cancer prevention, reduced risk of cardiovascular diseases, and the relief of post-menopausal complaints such as hot flashes and bone density loss.

They have also been suggested to have potential beneficial in the prevention of obesity and diabetes, both of which are associated to a low level, chronic inflammation.

Fat tissue (adipose tissue) is categorized by a high level of immune cells called macrophages - which produce pro-inflammatory proteins like tumor necrosis factor alpha (TNF-a), and other molecules (cytokines) that provoke insulin resistance and aggravate inflammation .

Isoflavones have been observed to cut pro-inflammatory secretions in macrophages, however there is little known about how isoflavones may affect fat cells’ (adipocytes) secretion of pro-inflammatory factors.

The new study investigated how isoflavone affects the adipocyte reaction to inflammation, testing three isoflavones (genistein, daidzein and equol) effects on the secretion of inflammatory molecules in fat cells.

Reduced inflammation

The researchers reported exposure to isoflavones prevented the secretion of key pro-inflammatory factors.

Isoflavones also were also seen to down regulate cytokine and gene expression of pro-inflammatory factors in TNF-a- stressed cells, and even reduced inflammatory signals in non-stressed cells.

The authors reported equol and daidzein to reverse the pro-inflammatory effects of TNF-a on inflammatory signals such as the Jak/stat cascade and NFkB pathway.

Equol and daidzein also showed a slight reduction in TNF-a-induced insulin resistance, whilst genistein was found to down-regulate the expression genes associated with lipid metabolism.

The researchers added that the effects of isoflavones extended to most of the genes and cytokines “with a meaningful role in inflammation”, noting that isoflavones down regulated molecules linked to cell infiltration, adhesion molecules, and pro-inflammatory mediators including interleukin-6 (IL-6), PGE2, and prostaglandins.

“Our results show no significant differences between the 3 tested isoflavones in terms of their effects on inflammatory factor gene expression, but equol was the most effective at reducing inflammatory factors secretion, suggesting that equol would promote an anti-inflammatory role in an additional way besides altering gene expression,”​ wrote the researchers.

Beneficial role?

In conclusion the researchers stated that isoflavones have a beneficial role in improving inflammation and reducing insulin resistance.

“The most important finding of this paper is that soy isoflavones reduced the secretion of inflammatory molecules and down-regulated the expression of several inflammatory factors,”​ stated the authors.

But the researchers warned that the role of soy isoflavones in humans must still be considered “more controversial”​, because of the unaccounted-for effects of human metabolism on isoflavones.

Source: Food Chemistry
Published online ahead of print, doi: 10.1016/j.foodchem.2010.09.042
“Isoflavones reduce inflammation in 3T3-L1 adipocytes”
Authors: M. Pinent, A.E. Espinel, M.A. Delgado, I. Baiges, C. Bladé, L. Arola

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