Flaxseed supplementation improved insulin resistance in obese glucose intolerant people: a randomized crossover design

Obesity leads to an increase in inflammation and insulin resistance. This study determined antioxidant activity of flaxseed and its role in inflammation and insulin resistance in obese glucose intolerant people. Using a randomized crossover design, nine obese glucose intolerant people consumed 40 g ground flaxseed or 40 g wheat bran daily for 12 weeks with a 4-week washout period. Plasma inflammation biomarkers (CRP, TNF-a, and IL-6), glucose, insulin, and thiobaribituric acid reactive substance (TBARS) were measured before and after of each supplementation. Flaxseed supplementation decreased TBARS (p = 0.0215) and HOMA-IR (p = 0.0382). Flaxseed or wheat bran supplementation did not change plasma inflammatory biomarkers. A positive relationship was found between TBARS and HOMA-IR (r = 0.62, p = 0.0003). The results of the study weakly support that decreased insulin resistance might have been secondary to antioxidant activity of flaxseed. However, the mechanism(s) of decreased insulin resistance by flaxseed should be further determined using flaxseed lignan. (Authors abstract)

Studies have reported that pro-inflammatory cytokines, tumor necrosis factor (TNF)-a and interleukin (IL)-6 are associated with an increased hepatic C-reactive protein (CRP) synthesis, inflammation, and insulin resistance in humans and animals. TNF-a has been positively related to factors associated with metabolic syndrome. Antioxidants have been reported to attenuate inflammatory response, insulin resistance, and diabetes development. The active ingredient of flaxseed (lignan, secoisolariciresinol diglucoside (SDG)) has significant antioxidant effects by inhibiting DNA scissions and lipid peroxidation and decreasing ROS.  The current study was conducted to determine the mechanism(s) by which flaxseed offers the protection against insulin resistance and inflammation via regulation of oxidative stress. The results showed that flaxseed supplementation decreased insulin resistance. Although the plasma insulin concentration did not change significantly, an HOMA-IR index significantly decreased, suggesting a decrease in insulin resistance or decreased glucose concentration following flaxseed supplementation. No significant changes in plasma insulin concentration following flaxseed might be related to small sample sizes which warrant the need of future study with a larger sample size. Flaxseed supplementation significantly decreased TBARS concentration which suggests decreased lipid peroxidation. TNF-a, IL-6, and CRP remained within normal ranges. The results suggest that these obese participants did not have low grade systemic inflammation, but these participants are classified as a high cardiovascular disease risk group. While CRP concentration in flaxseed supplementation group remained the same as the baseline, it increased following wheat bran (control) supplementation. The results support that high glucose concentrations increase oxidative stress as shown increased TBARS. The present results indicate that obese participants were glucose intolerant without low grade systemic inflammation. Since these participants did not have an identified inflammatory condition, flaxseed supplementation may have not affected these inflammation biomarkers. If these participants had systemic inflammation secondary to obesity or impaired glucose tolerance, flaxseed effects on inflammation may have been seen. This suggests the need of future study using either animal models with inflammation or people with systemic inflammation to determine flaxseed effects on inflammation. (Editors comments)